Unit 5: Unit 5: Respiration, Internal Environment, Coordination and Gene Technology

UNIT 5
Unit 5: Respiration, Internal Environment, Coordination and Gene Technology
Topic 7 – Respiration, Muscles and the Internal Environment
CELLULAR RESPIRATION
- This is a chemical reaction in the cell that breaks down respiratory substrates such as glucose to produce ATP.
- So, cellular respiration is a metabolic reaction as it takes place in the cell.
- Respiration is a metabolic pathway/metabolic process. This is the sequence of chemical reactions in a cell and each of
these reactions is controlled by specific enzymes.
- Metabolism is all chemical reactions in the cell. These chemical reactions are divided into two;
a) Anabolism/anabolic reactions
b) Catabolism/ catabolic reactions
- Anabolism is the synthesis of complex molecules from simpler ones. For example, protein synthesis is an anabolic
reaction where protein, being a complex molecule, is synthesized from amino acids that are simpler molecules.
- Catabolism is the breakdown of complex molecules into simpler ones. For example, cellular respiration is a catabolic
reaction where glucose, being a complex molecule, is broken down into simpler molecules such as ATP.
Enzymes in metabolic pathway

1. Oxidoreductases
 These are a class of enzymes that catalyze redox reactions, that is, they catalyze the transfer of hydrogen or electrons
from one molecule (the oxidant) to another molecule (the reductant).
 In respiration, the most common oxidoreductases are dehydrogenases that oxidize a substrate by transferring
hydrogen to a hydrogen acceptor such as NAD+/coenzyme. So, they are involved in oxidation, because the substrate
loses hydrogen to become oxidized.
2. Hydrolases
 These are enzymes that catalyze hydrolysis of chemical bonds to break them down.
 Hydrolysis reactions involve addition of water molecules to a chemical bond to break it.
 Example of hydrolase is ATPase that catalyzes the hydrolysis of ATP to ADP, Pi and 34kJ of energy.
ATPase
ATP +H20 ADP + Pi + 34kJ
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Adenosine Triphosphate (ATP)
 ATP is a high-energy molecule that stores the energy that is released when it is hydrolyzed.
 The energy is stored in the phosphate bonds. It is released when the terminal phosphate bond breaks down to form ADP, Pi and
34 kJ of energy.
 ATP molecules are produced by;
a) Cellular respiration
b) Light dependent reaction of photosynthesis, through photophosphorylation
 ATP is considered to be a universal energy currency of life because;
1. All cells synthesize it.
2. All cells hydrolyze it to produce energy.
3. When hydrolyzed, it releases energy
4. When hydrolyzed it produces a lot of energy i.e. 34kJ.
5. It is easily hydrolyzed to produce energy.
6. The turnover of ATP production is large.
7. Soluble hence forms hydrogen bonds with water in the cytoplasm of cells.
Structure of ATP molecule

 A molecule of ATP consist of;
a) Pentose sugar called ribose and a nitrogenous base called adenine, collectively called adenosine
b) Three inorganic phosphate molecules joined by phosphate bonds.
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- It is the hydrolysis (break down in presence of water), of the terminal phosphate bond that produces a lot of energy
(34kJ)
ATPase
ATP + H2O ADP + Pi + 34kJ.
Uses of energy from hydrolysis of ATP in cells

1. for active transport of molecules.
2. for anabolism e.g. protein synthesis
3. for muscle contraction hence movement
4. for cell division hence growth
5. for light independent reaction of photosynthesis
6. for secretion of substances by the cell
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7. for activating reactions
Types of cellular respiration

1. Aerobic respiration
 Chemical reaction in the cell that breaks down respiratory substrates such as glucose in presence of oxygen to
produce a lot of ATP. It takes place in the cytoplasm and mitochondria of cells.
2. Anaerobic respiration
 Chemical reaction in the cell that breaks down respiratory substrates such as glucose in absence of oxygen to
produce less ATP. It takes place in the cytoplasm of the cell.
AEROBIC RESPIRATION
- It has 4 stages;
a) Glycolysis
b) Link reaction
c) Krebs cycle
d) Oxidative phosphorylation/Electron Transport Chain (ETC)
The following table summarizes the stages, site and products of aerobic respiration
Stage Site Products
Glycolysis Cytoplasm Reduced NAD/NADH/NADH2/NADH+H+ :
ATP
Pyruvate
Link reaction Matrix of Mitochondria CO2
Acetyl CoA
Reduced NAD
Krebs cycle Matrix of mitochondria CO2
ATP
Reduced NAD
Reduced FAD (FADH2)
Oxidative Inner mitochondrial membrane ATP
phosphorylation/ETC Water
Glycolysis
- This is an enzyme-controlled reaction in the cytoplasm where hexose molecules are converted to pyruvate
molecules and in the process reduced NAD and ATP are also formed.
- So, the products of glycolysis are pyruvate, ATP and reduced NAD.
- Glycolysis occurs in all organisms whether aerobic or anaerobic.
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Stages of glycolysis
(i) Phosphorylation
- Phosphorylation is the addition of a phosphate group to an organic compound. Two ATP molecules are
hydrolyzed to get 2 phosphates that are added to hexose to form hexose 1, 6 bisphosphate. The hydrolysis of ATP
to get phosphates that phosphorylate hexoses is pump-priming reaction. In other words, the ATP expenditure in
the beginning of the preparative phase is sometimes called priming the pump/ pump-priming
- The importance of phosphorylation of hexose are:
a) For glucose to remain in the cell because the plasma membranes are impermeable to sugar phosphates.
b) To make hexose more reactive because phosphorylation reduces the activation energy.
(ii) Lysis
- This is the splitting of hexose 1, 6 bisphosphate into 2 triose phosphate molecules (GALP).
(iii) Oxidation
- Atoms of hydrogen are removed from each triose phosphate. In this oxidation reaction, energy is released which is
carried by the hydrogen atom. This is called energy of oxidation. NAD is the hydrogen carrier/acceptor
(coenzyme) that accepts the hydrogen atom.
(iv) Substrate level phosphorylation (ATP formation)
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- Substrate level phosphorylation is the process in which a phosphate group from a substrate molecule (a molecule
other than ATP, ADP, AMP) is transferred to ADP to form ATP. This takes place in glycolysis and Krebs cycle.
Net gain of ATP during glycolysis

- During glycolysis, 2 ATP molecules are hydrolyzed so that glycolysis can run.
- 4 ATP molecules are formed /synthesized.
- Because 2 ATP molecules were hydrolyzed during phosphorylation, then the net gain of ATP is 2 i.e. 4 – 2 = 2
Products of glycolysis
1. Reduced NAD
2. ATP molecules
3. Pyruvate molecules
Question
In the first reaction of glycolysis, a phosphate group from an ATP molecule is transferred to the oxygen at the
carbon-6 of glucose. Glucose-6-phosphate and ADP are produced. The diagram below shows a summary of this
process.
(a) State
which form of glucose is shown in the diagram. (1)
α / alpha
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(b) Explain why the phosphorylation of glucose by ATP, shown in the diagram above, allows the reactions of
glycolysis to continue. (2)
 Making hexose more reactive by lowering activation energy ;
 Prevents loss of hexose from cell because the CSM is impermeable to sugar
phosphates
(c) State the final products of glycolysis. (3)

 pyruvate / pyruvic acid
 ATP
 NADH / reduced NAD
The transfer of the phosphate group is catalysed by the enzyme hexokinase. As glucose- 6-phosphate
concentration increases, it acts as a non-active site-directed inhibitor of hexokinase. The diffusion of glucose
into a cell is regulated as a result of this inhibition.
(d) (i) Suggest how an increase in the concentration of glucose-6-phosphate leads to increased inhibition of
hexokinase. (3)
 Glucose-6-phosphate binds to any other part of hexokinase apart from active site
 This changes shape of active site so that hexose/glucose no longer fits.
 High concentration of glucose-6-phosphate causes more molecules of enzymes to
be inhibited
(ii) Suggest why the inhibition of hexokinase regulates the diffusion of glucose into a cell (3)
 Phosphorylation of glucose to form glucose- 6-phosphate slows down or it is stopped.
 So, glucose remains in the cell as it is not being converted to glucose- 6-phosphate
 This reduces concentration gradient of glucose between the cell and the outside
environment
 Diffusion of glucose into the cell stops (when equilibrium has been reached) or
slows down due to reduced concentration gradient.
What happens to products of glycolysis in aerobic respiration?

(i) ATP
- It is a source of heat energy when hydrolyzed.
(ii) Reduced NAD
- It diffuses into the inner mitochondrial membrane where it undergoes oxidative phosphorylation in the
electron transport chain.
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(iii) Pyruvate molecules
- Pyruvate molecules diffuse into the matrix of mitochondria where they undergo Link reaction and
Krebs cycle.
LINK REACTION
- It takes place in the matrix of mitochondria.
- Pyruvate (3C) undergoes oxidative decarboxylation
- Oxidative decarboxylation consists of;
(i) Oxidation – this is catalyzed by dehydrogenase enzyme, where NADH is formed
(ii) Decarboxylation - this is the removal of carbon in form of CO2 and it is
catalyzed by decarboxylase enzyme.
- The products of link reaction are
a) Acetyl CoA (2C)
b) CO2
c) Reduced NAD
Acetyl group +
coenzyme A
(CoA)=Acetyl
CoA (2C)
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Krebs cycle/Citric acid cycle
- It takes place in the matrix of mitochondria.
- In Krebs cycle, acetyl CoA (2c) combines with oxaloacetate (4c) to form citrate (6c). Citrate is converted back to
oxoloacetate in the enzyme controlled reactions called decarboxylation to form CO 2; oxidation to form reduced NAD
& reduced FAD; and ATP formation (substrate level phosphorylation) to form ATP.
- The products of Krebs cycle are:
a) CO2
b) ATP
c) Reduced NAD
d) Reduced FAD
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OXIDATIVE PHOSPHORYLATION
What happens to reduced NAD and FAD: Oxidative phosphorylation?
- Reduced NAD comes from glycolysis, link reaction and Krebs cycle.
- Reduced FAD comes from Krebs cycle.
- Oxidative phosphorylation takes place in the electron transport chain in the inner mitochondrial membrane.
- It involves oxidation of reduced NAD and FAD.
- When reduced NAD is oxidized, 3 ATP molecules are formed and when reduced FAD is oxidized, 2 ATP molecules
are formed.
- The process of oxidative phosphorylation is as follows:

 Reduced NAD and FAD move to the inner mitochondrial membrane where they release hydrogen atoms.
 The H atoms split into electrons and protons (H+).
 Electrons diffuse into the ETC in the inner mitochondrial membrane. As these electrons move from one
carrier to another, they release energy that activates proton pump in the membrane that moves H + from the
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matrix into the inter membrane space causing H + gradient between the matrix and the intermembrane
space and this causes the H+ to diffuse back to the matrix through ATP synthase/stalked particle.
 As the H+ flow through the ATP synthase, they release energy which combines ADP and P i catalysed ATP
synthase, forming ATP. This is oxidative phosphorylation/Chemiosmosis .
 In the matrix, electrons combine with H+ to form Hydrogen atom that reduces oxygen to form water
 The products of oxidative phosphorylation are: ATP & Water
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NB
- Oxidative phosphorylation is the synthesis of ATP from ADP and P i using energy released by electrons as they move
along the ETC in the inner mitochondrial membrane and protons as they move through ATP synthase.
- There are two process of forming ATP during respiration;
(i) Substrate –level phosphorylation – glycolysis and Krebs cycle.
(ii) Oxidative phosphorylation – produces the highest number of ATP molecules.
Chemiosmosis
It is the synthesis of ATP; by the diffusion of protons, down their electrochemical gradient, from the
inter-membrane space into the matrix through ATP synthase/ stalked particle; on the selectively-
permeable inner mitochondrial membrane. The diffusion of protons is due to a proton gradient that
forms across the inner mitochondrial membrane.
ANAEROBIC RESPIRATION
- This is the breakdown of respiratory substrates such as glucose without oxygen.
- Only glycolysis takes place in anaerobic respiration.
- All the stages of respiration that take place in the mitochondria cannot function. These stages are;
(i) Link reaction – matrix of mitochondria.
(ii) Krebs cycle – matrix of mitochondria.
(iii) Oxidative phosphorylation – inner mitochondrion membrane.
- The 3 stages above do not take place because oxygen is the final acceptor of H atom in the ETC, so lack of
oxygen causes ETC not to function hence no oxidative phosphorylation. So, NAD and FAD remain reduced as
they cannot be oxidized. They accumulate in the matrix of mitochondrion and therefore Link reaction and
Krebs cycle do not function.
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What happens to pyruvate in anaerobic respiration in human muscles?
- This involves two stages;
(i) Glycolysis
(ii) Reduction of pyruvate to lactate/NAD+ regeneration
- Pyruvate in the cytoplasm is directly reduced by NADH to form lactate. In the process, NAD + is regenerated so
that it can allow glycolysis to continue.
- The products of anaerobic respiration in human muscles are;
a) ATP
b) Lactate
c) NAD+
- Accumulation of lactic acid in the human muscle causes cramps.

 Animal tissue can tolerate quite high levels of lactate but lactate forms lactic acid in solution and therefore the pH
of the cell falls inhibiting the enzymes involved in glycolysis which then stops.
 Lactate diffuses from the muscle cell into the blood and is transported to the liver
 In the liver, lactate is converted/oxidized to pyruvate by NAD catalyzed by lactate
dehydrogenase
 Pyruvate is converted to glucose through gluconeogenesis and this requires extra oxygen
that comes from oxygen debt.
 Glucose diffuses into the blood and transported back to muscle for glycolysis, link and
Krebs cycle to produce carbon dioxide and water
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 Excess glucose is converted into glycogen and stored in liver cells
OXYGEN DEBT
 The demand for oxygen when muscle is contracting (during exercise) exceeds the supply of oxygen to these
muscles.
 This triggers anaerobic respiration during exercise, producing lactic acid that builds up in the muscle.
 Oxygen debt is the volume of oxygen required to oxidize/break down lactate (conversion of pyruvate to glucose in
liver cells). It is normally obtained through frequent and deep breathing after the exercise.
 It is also called post exercise oxygen consumption
Why are athletes in training advised not to simply stop or lie down after vigorous exercise but rather to aim for active
recovery through gentle exercise?
To maintain rapid flow of oxygen through muscles to remove lactate
What happens to pyruvate in anaerobic respiration in yeast cells?

- Anaerobic respiration involves;
1. Glycolysis
2. Decarboxylation (pyruvate converted into ethanal/acetaldehyde)
3. Reduction of ethanal into ethanol by reduced NAD
- Pyruvate undergoes decarboxylation, catalyzed by decarboxylase enzyme to form ethanal (acetaldehyde) that is
reduced by NADH to ethanol and in the process; NAD + is regenerated that makes glycolysis to continue.
- The products of anaerobic respiration in yeast cells are;

(i) ATP
(ii) Ethanol
(iii) NAD+
(iv) CO2
- The commercial applications of anaerobic respiration in
yeast are;
a) Beer making –
ethanol
b) Bread making – CO2 to raise the dough
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Question
Florence (Flo-Jo) Griffith-Joyner’s world record of 10.49 seconds for the 100 m women’s sprint in 1988 is unbeaten. In
this short time, a sprinter such as Flo-Jo could not deliver enough oxygen to her muscles to maintain aerobic respiration.
(i) Describe how a sprinter is able to release sufficient energy for the 100 m sprint without having enough oxygen
available for her muscles. (6)
 They have fast twitch muscle fibres

 energy is obtained from ATP
 ATP molecules are already in muscle cells e.g. ATP store
 Some aerobic respiration takes place due to some oxygen present providing some ATP.
 ATP comes from glycolysis of anaerobic respiration which produces ATP rapidly. Glycolysis occurs in cytoplasm.
To recycle NAD, + pyruvate is converted to lactate by reduced NAD. The fast twitch muscle fibres are lactate
tolerant(fatigue resistant)
 They have a lot of creatine phosphate to assist in rapid formation of ATP
(ii) Lactate (lactic acid) can build up in the muscles of a sprinter. Suggest why the build-up of lactate may
prevent any further increase in speed. (2)
 lactate build up causing a drop in pH (more acidic)

 This denatures respiratory enzymes, slowing down anaerobic respiration hence less ATP
 With less ATP muscle contraction reduces, reducing speed
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(iii) Explain the fate of lactate following a sprint (4)
 Lactate diffuses in the blood and is transported to the liver

 In the liver, lactate is converted/oxidized to pyruvate by NAD catalyzed by lactate dehydrogenase
 Pyruvate is converted to glucose through gluconeogenesis and this requires extra oxygen that comes
from oxygen debt.
 Glucose diffuses in the blood and transported back to muscle for glycolysis, link and Krebs cycle to
produce carbon dioxide and water
 Excess glucose is converted into glycogen and stored in liver cells
FATTY ACID OXIDATION

- In addition to glucose, fats can also be respired to release energy
- Fats are digested into glycerol and fatty acids by lipases.
- The fatty acids are broken down to get 2c acetyl groups which are fed into the Krebs cycle for oxidation.
- Because fatty acids can only be respired through the Krebs cycle, fatty acids can only become fuel for aerobic
respiration and not anaerobic respiration and cannot be used when oxygen is not available. However, glucose can be
respired aerobically and anaerobically.
Efficiency of respiration
- In an ideal condition (no heat loss) one glucose molecule (180g) generates 2880kJ of energy.
a) Calculate efficiency of aerobic respiration;
38 ATP× 34
efficiency = ×100=44.9 %
2880
b) Calculate efficiency of anaerobic respiration;
2 ATP× 34
efficiency = × 100=2.4 %
2880
Questions
Describe what is meant by phosphorylation
This is the addition of phosphate group to an organic molecule such as glucose.
Describe two importance of phosphorylation
(i) The hexose sugar becomes more reactive by reducing the activation energy.
(i) The sugar phosphate remains in the cell as csm are impermeable to sugar phosphates.
In aerobic respiration, describe two processes that synthesize ATP
(i) Substrate-level phosphorylation

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It is the process in which a phosphate group from a substrate molecule other than AMP, ADP and ATP is
transferred to ADP to form ATP. This form of phosphorylation occurs in glycolysis and Krebs cycle
(ii) Oxidative phosphorylation

This is the synthesis of ATP from ADP and phosphate using energy from redox reactions (energy of oxidation).
What happens to the electrons released at the end of ETC

The electrons are passed to the matrix of mitochondria where they combine with H+ ion to form hydrogen atom that
reduces oxygen to form water.
What is the role of NADH when respiration takes place in aerobic respiration?
It moves to the inner mitochondrial membrane where it releases hydrogen atom that is ionized into electrons and protons.
Electrons enter the ETC along the inner mitochondrial membrane, and as they move from one electron carrier to another
they release energy that activates proton pump to move H+ from the matrix into inter membrane space creating H+
gradient between the space and matrix. H+ diffuse to the matrix through ATP synthase/ stalked particle and release energy
that phosphorylates ADP to ATP catalyzed by ATP synthase. This is oxidative phosphorylation.
Why do Krebs cycle and link reaction fail to take place in anaerobic respiration?
Oxygen in the matrix is the final acceptor of H atom in oxidative phosphorylation. Without oxygen, ETC is nonfunctional
and oxidative phosphorylation cannot take place. So NAD and FAD remain reduced and Krebs cycle and link reaction fail.
What happens to H atom released from substrate during aerobic respiration

Dehydrogenase enzyme catalyzes the transfer of Hydrogen atom to NAD and FAD which pass them to the ETC in the
inner mitochondrial membrane for oxidative phosphorylation
Describe the role of the mitochondrion in aerobic respiration

- Outer membrane is partially permeable to substances e.g. allows pyruvate to enter from the cytoplasm
- Intermembrane space is a reservoir for H+
- Inner membrane has electron carriers for oxidative phosphorylation
- Inner membrane has cristae to increase surface area for respiration
- Inner membrane has stalked/ATP synthase involved in oxidative phosphorylation.
- Matrix is the site for link reaction and Krebs cycle.
List the substances that diffuse into the mitochondrion

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- reduced NAD from glycolysis
- Pyruvate
- ADP
- PI
- O2
List substances that diffuse out of the mitochondria
- H2O
- ATP
- CO2
Describe how oxidation of reduced NAD and FAD gives 5ATP molecules
During oxidative phosphorylation reduced NAD produces 3ATP and reduced FAD produces 2 ATP
In one glucose molecule, account for the number of ATP molecules formed in aerobic respiration
SLP OP Total
Glycolysis 2 6 8
Link 0 6 6
Kreb’s cycle 2 22 24
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Describe the reasons why aerobic respiration produces more ATP than anaerobic respiration from one glucose
molecule.
In anaerobic respiration, only 2 ATP are produced in glycolysis through substrate level phosphorylation. In aerobic
respiration, a lot of ATP molecules are produced through substrate level phosphorylation in glycolysis, Krebs cycle and
through oxidative phosphorylation where oxidation of reduced NAD and FAD produces 3ATP and 2 ATP, respectively.
So, 38 ATP molecules are produced in aerobic respiration and only 2 are produced in anaerobic respiration.
Describe how human muscle ensures that glycolysis continues to take place in anaerobic respiration
 This is by regenerating NAD+
 NADH directly reduces pyruvate into lactate
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 In this reduction, NAD+ is regenerated for glycolysis to continue.
Describe how yeast cell ensures that glycolysis continues to take place in anaerobic respiration
 This is by regenerating NAD+
 Pyruvate is first converted to ethanol/acetaldehyde through decarboxylation where carbon is released as carbon
dioxide.
 Ethanal is reduced by NADH into ethanol. In this reduction, NAD + is regenerated for glycolysis to continue.
List the processes in anaerobic respiration in human muscle.

 Glycolysis
 Reduction/NAD+ regeneration
List the processes in anaerobic respiration in yeast cells.
 Glycolysis
 Decarboxylation
 Reduction/ NAD+ regeneration
Suggest reasons why fat can only be used as a respiratory substrate in aerobic respiration.
- In addition to glucose, fats can also be respired to release energy
- In fatty acid oxidation, the glycerol and fatty acids that make up triglyceride are separated
- The fatty acids are broken down to acetyl groups which combine with CoA to form acetyl CoA that are fed into the
Krebs cycle for oxidation.
- Because fatty acids can only be respired through the Krebs cycle, fats can only become fuel for aerobic respiration and
not anaerobic respiration and cannot be used when oxygen is not available. However, glucose can be respired
aerobically and anaerobically.
Describe and explain the functions of enzymes in metabolic process such as respiration as shown below
 Each step is controlled by a specific enzyme which converts one intermediate into the next e.g. enzyme
1 converts DHAP to 2-PG
 This product becomes the substrate of the next stage/enzyme where the substrate has a specific shape
to fit into a complementary active site of the enzyme
 These enzymes speed up the conversion by lowering the activation energy
 Pyruvate is only produced if all enzymes are active.
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The diagram below shows the electron transport chain, which is part of aerobic
respiration.
Using the diagram and your own knowledge, describe the role of carrier B. (3)
 Carrier B picks electron from carrier A and passes it to carrier C; through redox reaction
 As electrons move from one carrier to another, energy is released; that this is used to pump
protons from the matrix into intermembrane space
Name structure X and explain its role in aerobic respiration. (3)

 Structure X is stalked particle / ATP synthase
 Protons flow through stalked particle down their electrochemical gradient; and release energy that
combines ADP and Pi to form ATP
(ii) Name substance X and w

X is ATP
W is NAD+
Explain the link between the formation of substance X and the H+ shown on the diagram. (3)
 Substance X is ATP
 H+ pass through stalked particle down their electrochemical gradient ; to release energy
that joins ADP and Pi to form ATP
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Respiratory Quotient
 RQ is the ratio of CO2 produced to oxygen consumed when food is being metabolized.
 RQ = volume of carbon dioxide given out in unit time

volume of oxygen taken in in unit time
RQ for Carbohydrate
 The RQ for carbohydrate metabolism can be demonstrated by the chemical equation for oxidation of
glucose:
 C6H12O6 + 6O2  6CO2 + 6H2O
 Because the gas exchange in this reaction is equal, the respiratory quotient for carbohydrates is: RQ =
6CO2 / 6O2 = 1.0
RQ for Fats
 When the fatty acid oleic acid (from olive oil) is respired
aerobically, the equation is:
 C18H34O2 + 25.5O2 → 18CO2 + 17H2O + energy
 For the aerobic respiration of oleic acid:
RQ = CO2
O2
= 18
25.5
= 0.7
For the aerobic respiration of palmitic acid:
= 16
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=0.7
RQ for Proteins
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 RQ for Oxidation of Albumin:
= 63
77
= 0.8
Question
Calculate the RQ for the aerobic respiration of the fatty acid stearic acid (C18H36O2)?
C18H36O2 + 26O2  18CO2 + 18H2O
= 18
26
= 0.69
RQ in Anaerobic Respiration
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RESPIROMETER
Describe the term respirometer
 It is an apparatus that measures the oxygen uptake by an organism

 It consists of an experimental tube/respirometer tube with an organism placed on the gauze and below the gauze is KOH solution
to absorb carbon dioxide so that only oxygen uptake is measured. It also consists of a manometer. This is a device that consists of
coloured liquid and it’s role is to measure pressure difference usually by the difference in height of 2 coloured liquid columns
 In summary, a simple respirometer consists of:
 Experimental tube consisting of living organism and KOH
 Control tube consisting of non-living substance and KOH.
 U – tube manometer consisting of coloured liquid and it is connected to the 2 tubes.
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To make the experiment by respirometers valid, another tube with everything the experimental tube has minus the living organism is
set up. The experimental tube and control tube are connected to the U – tube manometer. The control tube compensates for any change
in pressure or temperature within the apparatus
 As the organism respires, it produces heat, which causes expansion of the air in the tubes and therefore cause an
increase in pressure in the experimental tube. This causes the liquid in the manometer to move in the opposite direction
(left) instead, leading to an incorrect reading of the distance moved by the liquid.
 Movement of the liquid in the manometer is determined by the differential pressure that exists between the two tubes.
The control tube prevents a differential pressure being created as a result of the heat produced by the organism during
respiration. This occurs because there is always a constant pressure exerted by the fixed volume of gas trapped in the
control tube. So, any fluctuation in temperature or pressure affects both sides of the manometer equally, so that the
individual changes in pressure in each tube cancel each other out.
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 Therefore, the only difference in pressure that exists between the two tubes is due to the oxygen absorbed by the
respiring organism (and not due to any changes in temperature or pressure).
Explain the purpose of the syringe in the set up.
 reset / move the coloured oil

 allows collection of several measurements / repeated results
Suggest reasons for absorbing carbon dioxide in this apparatus.
 Carbon dioxide is produced in respiration

 This carbon dioxide affects volume / pressure of gas
 Absorption of carbon dioxide allows measurement of oxygen used
Suggest two reasons why a valid comparison cannot be made between the mean rates of respiration of the germinating seeds in air and
the insects. For each reason, suggest a modification that would allow a valid comparison. (4)
 Mass of organism may differ; so, use same mass

 Temperature changes; so, control temperature using a water bath
 Pressure may affect volume of gas: so, use of control with no organisms, at the same time
Describe how respirometer could be used to find the mean rate of respiration of woodlice. (6)
 Use of constant temperature by the use of water bath set at stated temperature.
 Place the setup with KOH and coloured liquid but no organism, beads and bungs.
 Leave the setup to equilibrate.
 Place the organism, beads and bungs. The mass of organisms and beads is the same. Beads act as a control.
 State the time for the investigation
 Measure the volume: cross section area of manometer tube multiplied by distance moved by the liquid
 Calculate the rate of respiration/ rate of oxygen uptake (volume divided by time)
 Replicate (repeat two more times)
Describe the function of the clip
 Opened to reset experiment/return colored liquid back to origin, that is, allows the pressure throughout the apparatus to
equilibrate with atmospheric pressure for another reading to be taken).
 Closed to start experiment to prevent the entry of atmospheric air that will affect movement of colored liquid.
State likely source of error when using respirometer and how the error can be minimized
 Apparatus not airtight, so less fall in pressure inside due to loss of air: apply grease to all connecting points
 Soda lime/KOH saturates/stops absorbing carbon dioxide: change the soda lime/KOH after each repeat/ replicate.
Respirometers are designed to measure the respiration rate. They do this by recording the volume of oxygen taken up by
respiring tissues. In most cases, where a tissue is undergoing aerobic respiration, the volume of oxygen taken up by the tissue is
equal to the volume of carbon dioxide released by the same tissue.
a) Explain how a respirometer is designed to overcome this problem

KOH is added to absorb carbon dioxide and this allows the coloured liquid to move towards the experimental tube. This
enables the measurement of oxygen absorbed by the organism.
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b) Changes in temperature can cause large deficits in the volume of a gas. Explain how temperature is controlled
when using a respirometer.
This is by the use of a water bath which needs to be equilibrated before sealing the apparatus
The best temperature is 20-40°C.
c) What would happen if KOH is not added

Coloured liquid in the manometer would not move as the volume of oxygen absorbed by the organism is equal to the
volume of carbon dioxide released hence no volume of oxygen to measure.
How would you use respirometer to measure the volume of oxygen absorbed by an organism?
- Measure the distance moved by the liquid in the manometer in the fixed time.
- Measure the diameter and divide by two to get the radius of the U – tube manometer
- Calculate the cross section area of the tube using π r 2
- To calculate the volume of oxygen absorbed, the cross section area is multiplied by the distance moved by the coloured liquid
in the U-tube manometer (d)
Volume of oxygen absorbed=π r 2d
- To calculate the rate of oxygen uptake: the volume is divided by time
volume
Rate of respiration=
time
- A student used a respirometer to compare the rates of respiration of yeast cells using 2 different sugars, glucose and
sucrose as substrates.
a) Suggest a suitable hypothesis for this investigation
Yeast cells respire faster using glucose as a substrate and not sucrose
b) Use your biological knowledge and understanding to explain and justify your hypothesis
Yeast will respire faster using glucose because glucose is the starting point for glycolysis in respiration. It is therefore the
first molecule to be phosphorylated.
Yeast will respire sucrose more slowly as it has to be hydrolysed to glucose and fructose before it enters glycolysis.
SKELETAL MUSCLE FIBRES OF THE SKELETAL MUSCLE

- These are cells that contract and relax.
- They form a tissue called skeletal muscle.
- The characteristics of skeletal muscle fibres are:
 Long cells
 Multinucleated cells
 They are made up of many myofibrils that lie parallel to each other and they are made up of sarcomeres.
 Sarcomere is a functional unit of a skeletal muscle fibre.
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 When they contract they shorten to do the work.
 When they relax they are pulled back to their original position.
- -
SKELETAL MUSCLE
 They are also called striated or voluntary muscle.

 They are made up of skeletal muscle fibres.
 They are attached to the bone through tendons
 They are involved in locomotion/movement.
 They are striated/striped.
 They are under the control of voluntary nervous system.
 They contract rapidly.
 They tire quickly.
 They are arranged in antagonistic pairs.
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ANTAGONISTIC PAIRS
 These are pairs of muscles which pull in opposite direction.

 Flexors contract to flex/bend a joint.
 Extensors contract to extend/straighten a joint.
 Skeletal muscles are arranged in antagonistic pairs because when muscles contract they cannot extend themselves
and therefore they need an opposing muscle to extend to original position. They therefore allow control of
movement.
 Examples of antagonistic muscles are:
 biceps in the arms( flexors) and triceps in the arms (extensors)
 quadriceps in the thigh (extensors) and hamstrings in the thigh (flexors)
The extensor muscle is relaxed and the flexor muscle is contracted
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(b) Name the structures that connect muscles to bones. (1)
Tendons
(c) Explain why muscles occur in antagonistic pairs. (2)
 muscles cannot extend themselves

 they need opposing muscle to extend
 antagonistic muscle allows control of movement
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Suggest how tendons and antagonistic muscles cause the lower leg to move in the direction shown by the arrow
in the diagram below.
 Antagonistic action is when muscles work in opposition, that is, when one contracts the
other relaxes
 Extensor muscles (quadriceps) contract / shorten / and the leg is straightened
 Flexor muscle (hamstring) relaxes and is stretched
 Tendons attach muscles to bones

Name of Function Example in sport
muscle
Triceps Extend the arm at the elbow Press-up, throwing a javelin
Biceps Flex the arm at the elbow Pull-up, drawing a bow in archery
Quadriceps Extend the leg at the knee Kicking a ball jumping upwards
Hamstrings Flex the leg at the knee Bending knee before kicking a ball
SARCOMERE
 This is the basic unit of contraction of skeletal muscle fibre.

 It consists of:
1. Proteins- actin, myosin, troponin, tropomyosin
2. The plasma membrane is called sarcolemma.
3. The cytoplasm inside the sarcomere is called sarcoplasm.
4. It has sarcoplasmic reticulum that stores and releases calcium ions.
5. It has a lot of mitochondria that produces ATP needed for muscle contraction.
6. A sarcomere is the region of the muscle fibre between two Z lines
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31
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- Sarcomere is the region of the myofibril between two Z-lines.
- I band (isotropic band)
 has actin filaments only.
- A band (Anisotropic band) has two sections;
 Dark region of A-band -has overlap of actin and myosin filaments.
 Light region of A-band (H-zone) -has myosin only.
Proteins in the skeletal muscle fibre.
Actin
Structure of actin
- These are two thin fibrous proteins twisted around one another.
- Has myosin binding sites at regular intervals where globular heads of the myosin fit or bind.
- Wrapping around the actin is another fibrous protein called tropomyosin. In a relaxed muscle, the tropomyosin chain
covers the myosin binding sites.
- Tropomyosin has another globular protein called troponin attached regularly along the tropomyosin chain
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Myosin
Structure of myosin
 These are two thick fibrous proteins with globular heads that project to the side.
 This head, called myosin head, has ADP, Pi and ATPase.
Tropomyosin
- Fibrous protein around the actin filament.

- In a relaxed muscle, tropomyosin covers the myosin binding sites in the actin.
Troponin
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- Globular protein.
- During muscle contraction, Ca2+ from sarcoplasmic reticulum bind to troponin so that troponin changes shape and
pulls away tropomyosin from the myosin binding sites.
- Troponin are attached regularly along the tropomyosin chain
Neuromuscular junction
 Neuromuscular junction is the point where a motor neurone meets a skeletal muscle fibre.
Contraction of skeletal muscles
 The model that explains how the skeletal muscle contracts is called sliding –filament model
 It involves the thick myosin filaments and the thin actin filaments. The actin filaments slide over the myosin
filaments and the muscle shortens.
Evidence of the sliding –filament mechanism
- Myofibrils appear darker in colour where the actin and myosin filaments overlap and lighter where they do not.
- There will be more overlap of actin and myosin in a contracted muscle (the width of overlap is great) than in a relaxed
one.
- When a muscle contracts, the following changes occur to a sarcomere;
(i) I bands (isotropic bands /light bands) become narrower /shorter due to increase in overlap of myosin and actin.
(ii) The z-lines move closer together (the sarcomere shortens) due to increase in overlap of myosin and actin.
(iii) The H-zone becomes narrower /shortens as the overlap of actin and myosin increases.
(iv) The A-band remains the same width as myosin do not move.
Muscle stimulation
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When action potential (nerve impulse) arrives at neuromuscular junction, sarcoplasmic reticulum is stimulated to release Ca 2+ that
flood the sarcomere to trigger muscle contraction.
Muscle contraction.
- Action potential arrives at the neuromuscular junction and stimulates sarcoplasmic reticulum to release Ca 2+ that flood the
sarcomere.
- Ca2+ bind to troponin causing it to change shape so that it causes tropomyosin to pull away from the myosin binding sites.
- The myosin head which has ADP, Pi and ATPase binds to its site on actin forming acto- myosin bridge.
- ADP and Pi leave and cause the myosin head to change shape and tilts or bends towards M line by 45 0. This causes the actin
filament to slide over along the myosin filaments by 10nm shortening the sarcomere (muscle) hence contraction.
Muscle relaxation
- ATP binds to myosin head in the acto-myosin bridge causing it to change shape so that it breaks away from its binding site on the
actin.
- Ca2+ activate ATPase so that it hydrolysis ATP to form ADP, P i and energy. This energy causes the myosin head to pull back to its
original position.
- ATP activates calcium pump so that this pump moves Ca2+ back into the sarcoplasmic reticulum.
Questions
Write down the roles of the following in muscle contraction and relaxation
a) ATP
- Binds to myosin head in the bridge so that it changes shape and breaks away from the bridge.
- It is hydrolysed to provide energy to pull back the myosin head to its original position.
- Activates calcium pump to move Ca2+ to sarcoplasmic reticulum during relaxation.
- ATP for synthesis of neurotransmitter
b) Ca2+
- Sarcoplasmic reticulum contain calcium ions

- These ions bind to troponin so that it change its shape and pulls tropomyosin away from the myosin binding sites on the actin so that myosin
head can bind
- It activates ATPase so that it hydrolysis ATP to provide energy to pull back the myosin head to its original position.
Q. Relate muscle contraction and rigor mortis
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o After death no more production of ATP
o Without ATP, the myosin head cannot break away from the acto-myosin bridge and so remains locked upright so that the muscle
remains stiff and rigid (rigor mortis)
TYPES OF SKELETAL MUSCLE FIBRES

 There are two types of skeletal muscle fibres in mammals which give them different levels of performance
(i) Slow twitch skeletal muscle fibres
(ii) Fast twitch skeletal muscle fibres
1. Slow twitch skeletal muscle fibres
- Slow twitch skeletal muscle fibres contract more slowly and produce less powerful contractions over a long period
of time.
- They are adapted for slow, sustained contraction to cope with long period of exercise. They play an important part in
maintaining body posture.
- The characteristics of these muscles are:
1. More mitochondria; provide a lot of ATP through aerobic respiration
2. More myoglobin; to store a lot of oxygen. Myoglobin is a red pigment in the muscle and it stores oxygen. It has
very high affinity for oxygen. It only releases oxygen to the muscle when the partial pressure of oxygen is very
low to prevent anaerobic respiration that produces lactic acid.
3. Less sarcoplasmic reticulum; do not need vigorous contraction of muscles hence needs less Ca 2+.
4. More capillaries; to deliver a lot of oxygen for aerobic respiration
5. Less (stored) glycogen, as fat is used as fuel
6. Less creatine phosphate; This is a molecule that rapidly donates phosphate to ADP to form ATP in anaerobic
conditions to provide energy for muscle contraction.
7. Greatly affected by low pH which is a result of accumulation of lactate
NB:
Slow twitch muscle fibres are also called oxidative skeletal muscle fibres (because they require a lot of oxygen) or red
skeletal muscle fibres (because they have a lot of myoglobin which is red)
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2. Fast twitch skeletal muscle fibres
- Fast twitch muscle fibres contract more rapidly and produce more powerful contractions for a short period of time.
- They are adapted for intense exercise, such as weight lifting and sprinting. As a result, they are more common in
muscles which need to do short burst of intense activity.
- Fast twitch muscles are adapted to their role by having:
1. Fewer mitochondria
2. Fewer myoglobin
3. More sarcoplasmic reticulum
4. Fewer capillaries
5. More (stored) glycogen, used as fuel
6. More creatine phosphate: This is a molecule that rapidly donates phosphate to ADP to form ATP in anaerobic
conditions to provide energy for muscle contraction
7. Less affected by low pH, as the muscle is anaerobic that produces lactate hence can continue
contracting at this low pH.
NB
Fast twitch muscles are also called glycolytic muscles (because ATP is produced from glycolysis only) or white
muscles (because of fewer myoglobin);
NB
The ATP used in these contractions is produced almost entirely from anaerobic glycolysis.
The table below summarizes the differences between slow and fast twitch muscles
Slow Fast
- Red ( a lot of myoglobin) - White (less myoglobin)
- More mitochondria - Less mitochondria
- Fewer sarcoplasmic reticulum - More sarcoplasmic reticulum
- More capillaries - Fewer capillaries
- Fatigue resistant - Fatigue quickly
- Fewer creatine phosphate - More creatine phosphate
- More fat, as fuel - Less fat, as fuel
- Less glycogen - More glycogen
- Thinner myosin filaments - Thicker myosin filaments
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Animals which are predators show bursts of very fast movement. Their prey are able to carry out sustained movement over longer periods of time. .Preys
have slow twitch muscles. Predators have fast twitch muscles because they need to be very fast to catch the prey and very powerful to kill their prey .
They therefore use anaerobic respiration to release ATP quickly.
Lactate (lactic acid) can build up in the muscles of a sprinter. Suggest why the build-up of lactate may prevent any further increase in speed.
 Lactate causes drop in pH / more acidic

 This low pH affects respiratory enzyme
 This slows down ATP production, affecting or reducing muscle contractions hence reducing speed.
The cheetah is the fastest land mammal. The cheetah needs to be within 50 m of its prey before starting to chase it. A cheetah runs at 27 m s –1
in an attempt to catch its prey. Explain why the muscle composition of a cheetah causes it to stop running if it fails to catch its prey within 50
m.
 Muscles of Cheetah have fast twitch fibres

 They have fewer capillaries / less myoglobin hence less oxygen supply
 They have fewer mitochondria so more anaerobic respiration takes place hence less ATP made
 Due to more anaerobic respiration, lactate is produced that lower pH that denature respiratory enzymes hence less ATP to
produce energy and this slows down the speed
Following anaerobic respiration, lactate dehydrogenase converts lactate to pyruvate and oxidised NAD to reduced NAD
Comparison of slow and fast twitch muscle fibers in humans
 Most people have roughly equal amounts of slow and fast twitch muscle fibres in their muscles.
 However, the proportions can vary in some people because of:
a) Training
For example, long distance runners, cyclists and swimmers have more slow twitch muscle fibres while weight lifters and sprinters have
more fast twitch muscle fibres in their muscles.
b) Genetics
Some people have 75% fast twitch and others have 75% slow twitch, although most have about 50% of each type
of muscle fibre. Super-fast twitch muscle fibres which contract even more quickly and strongly than usual. This is
as a result of sprint gene where it is believed that 70% of Jamaicans possess it.
c) Performance enhancing substances such as anabolic steroids or techniques such as gene doping and blood transfusion.
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CONNECTIVE TISSUE
Bones, cartilage, tendons & ligaments
Connective tissue connects/joins tissues, connects organs, supports other tissues and organs and transport substances
Bone
 Strong, hard and light connective tissue.

 It consists of matrix that consists of collagen fibres, bone salts and cells (osteocytes).
 Its roles are:
a) Allows movement.
b) Stores minerals.
c) Site for formation of blood cells (bone marrow).
Cartilage
 This is connective tissue made up of cells called chondrocytes.

 Has poor blood supply and so when injured or inflamed, repair is slow.
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 Are 3 types:
a) Hyaline cartilage
 Less elastic connective tissue
 Most abundant type of cartilage
 It covers the ends of long bones and parts of the ribs, nose, larynx, trachea and bronchi.
 It provides smooth surface for joint movement. So at joints it absorbs synovial fluid (lubricant)
and act as a shock absorber.
b) Fibrocartilage
 This is an inelastic connective tissue that has thick bundles of collagen fibres hence very strong.
 White in colour.
 Fibrocartilage discs are found in the intervertebral spaces and the knee joints.
c) Elastic cartilage
 Flexible/elastic
 Yellow due to elastic fibres.
 Makes up the malleable part of the external ear, the epiglottis and ligaments in the joints
Tendons
 Connective tissue that joins muscle to bone.

 Mainly made up of fibrocartilage (white) hence very strong due to collagen fibres and are inelastic.
Explain why tendons need to be inelastic. (3)

 tendons attach muscle to bone
 they should not stretch when muscle contracts so that all force is transferred to bone so that
the bone / skeleton moves.
Ligaments
 Connective tissue that joins bone to bone.

 Mainly made up of elastic tissue (Yellow) hence strong due to collagen fibres but more elastic/more
flexible.
 They are elastic to allow restricted/some movement of bones at a joint hence prevent dislocation.
What explains why ligaments are effective at keeping the knee joint stable.
They contain collagen making them inelastic
NB:
When talking about movement we say it is due to collagen that is more elastic
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When talking about stability we say it is due to collagen that is inelastic
Explain what is meant by the term cruciate ligament.
 Two cross shaped connective tissue

 In the knee, behind the knee cap
 Connects bone to bone, that is, tibia (shin bone) and femur (thigh bone)
in the knee.
A damaged cruciate ligament may require surgery. Explain the role of the cruciate ligament
1. Attaches bone to bone
2. Allows (some/restricted) movement
3. This gives added stability to prevent dislocation.
Ligament may become torn during some sporting activities. It may not be possible to join the torn parts together. Material
can be removed from tendon without causing any damage. This material can be used to join the damaged pieces of
ligament together. Suggest why the use of material from tendon will mean that recovery will be quite slow and require
careful physiotherapy.
Recovery will be quite slow because ligament has more elastic fibres and tendon has more inelastic/less flexible fibres
hence compatibility for quick repair is reduced.
Require careful physiotherapy to ensure that repaired tissue gradually stretch to avoid any damage.
Joints, muscles and movement

Joints
- A joint is where 2 bones meet/junctions between bones that allow movement
- The ends of the bones at a joint are shaped to move smoothly over each other.
- The way in which the 2 bones meet varies according to the type of movement required.
- The two main types of joints are;
(i) Ball and socket – found at the hip and shoulder
o It gives very free movement of 3600
(ii) Hinge joint – they are found in fingers, elbows and knees. They have less free movement – move at
1800
A synovial joint
They allow movement (articulation). They have 3 main parts;
1) Hyaline Cartilage: covering the surface of bones to reduce friction where they could rub against each
other.
2) Synovial fluid: between the cartilage-covered surfaces, to lubricate the joint and further reduce friction
3) Joint capsule: encloses/seals joints and holds in the synovial fluid
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THE HEART, ENERGY & EXERCISE
THE HEART
- The heart is a muscular pump.
- The heart is made up of cardiac muscles.
- This cardiac muscle is myogenic i.e. the impulse to contract the heart originates within the heart itself from the
sinoatrial node (SAN) or pace maker. So, the nervous system and hormonal system just modify the
contraction/heart beat to either slow down or speed up the contraction.
Cardiac cycle
- It is the sequence of events that take place in one heart beat and it last for 0.83 second. It is initiated at the sino-atrial
node (SAN) also called pacemaker. These events are: Atrial systole (0.11s), ventricular systole (0.31s) and complete
cardiac diastole (0.41s).
Events of the cardiac cycle

1. Atrial systole
- This is the contraction of the atria when they are filled up with blood.
- Its role is to pump blood into the ventricles from the atria via AV valves.
- It lasts for about 0.11s.
- During atrial systole, AV valves are open.
- During atrial systole, semi-lunar valves are closed.
- During atrial systole, atria are contracted and ventricles are relaxed.
2. Ventricular systole
- This is the contraction of the ventricles when they are filled up with blood.
- Its role is to pump blood into the aorta and the pulmonary artery from the ventricles.
- It lasts for 0.31s
- During ventricular systole, the AV valves close to prevent the backflow of blood from the ventricles into the atria and
to build up pressure in the ventricles.
- At the start of ventricular systole both semi-lunar and AV valves are closed
- During ventricular systole, semi-lunar valves are forced to open.
- During ventricular systole, atria are relaxed and ventricles are contracted.
3. Diastole (Complete cardiac diastole)

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- This is the relaxation of the heart after ventricular systole.
- During diastole the whole heart is relaxing, reducing pressure in the heart so that blood flows into the atria via the
vena cava and pulmonary vein, hence refilling the heart with blood.
- So, the role of the diastole is to refill the heart with blood.
- It lasts for 0.41 second.
- During diastole, the AV valves open.
- During diastole the semi-lunar valves are closed.
THE CONTROL OF THE CARDIAC CYCLE.

- The heart is myogenic.
- The SAN contracts and produces impulse.
- This impulse spreads over the atria walls, causing atrial systole that lasts for about 0.11 second.
- The impulses then pass to the atrio-ventricular node (AVN) where they are delayed for about 0.1 second.
- There are two importance of the 0.1 second delay at AVN:
(i) Atrial systole is completed before ventricular systole starts so that blood can flow from the atria into the
ventricles.
(ii) Ventricles are filled with blood before they contract.
- The bundle of His carries impulses from AVN to the apex of the heart along the septum.
- The Purkyne fibres carry the impulses from the apex of the heart to the walls of the ventricles causing contraction
from the apex upwards.
- Blood is squeezed into the arteries (pulmonary artery and aorta). This is ventricular systole.
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MEASUREMENT OF ELECTRICAL CHANGES IN THE HEART.
Explain what is meant by the term electrocardiogram (ECG)

It is a record that shows waves of electrical activity in the heart during cardiac cycle and this is detected on the skin. The
waves are called PQRST waves.
Describe how ECG is produced

 Electrodes are attached to the skin on the chest, wrist or ankle.
 These electrodes are connected to the ECG machine.
 The ECG machine sends the pattern of the electrical activity to the oscilloscope screen.
 This pattern or record is called ECG.
• P wave is caused by contraction (depolarization) of the

atria (atrial systole).
• QRS complex is caused by contraction (depolarization) of the ventricles (ventricular systole).
• T wave is caused by relaxation (repolarization) of the ventricles (diastole).
 The trace/record produced by the ECG machine is called ECG.
Explain how an electrocardiogram (ECG) can be used to calculate a person’s heart rate. (3)
 ECG shows wave of electrical activity of the heart during cardiac cycle.
 Time for one heart beat is the time from one P wave to the next; QRS complex to the
next; and T wave to the next
 To get heart rate, 60 seconds is divided by time taken for one beat.
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Doctors use ECG to diagnose heart problems. They compare the patient’s ECG with the normal trace (ECG).This helps
them to diagnose any problems with heart’s rhythm, which may indicate CVD. The heart problems diagnosed by ECG
include:
• Tachycardia
• Bradycardia
• Heart block
• Fibrillation
Tachycardia
 Tachycardia is a heart condition in which the heart beats very rapidly, even at rest,
around 120 beats per minute.
 Comparing the ECG of the normal person with a normal heartbeat with the ECG of the patient with
tachycardia the following is observed:
(i) Interval between QRS phase is longer in normal rhythm.
(ii) Lower voltage during QRS phase in normal rhythm.
Suggest what effects tachycardia could have

on cardiac output. Explain your answer
• Cardiac output(stroke volume x heart rate) could decrease if there was insufficient time to fill the ventricles (between
contractions).
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• Cardiac output could increase if ventricles fill sufficiently.
• The change in cardiac output will depend on whether the decrease in stroke volume is compensated by the increase in heart
rate.
Bradycardia
• This is the heart condition where the heart rate is less than 60 beats per minute. It is common in fit athletes at rest but can
also be a symptom of heart problem. In addition to fitness and bradycardia, the other causes of decreased heart rate
include hypothermia and drugs.
Heart block
 Heart block is abnormal conduction of impulse

 It is caused by damage to conducting systems of the heart.
 There are three types of heart blocks:
• 1st degree: The conduction of the nerve impulses from the atria to the ventricles is slow.
• 2nd degree: Some but not all of the impulses pass from the atria to the ventricles.
• 3rd degree: No impulses pass from the atria to the ventricles, so the atria and the ventricles beat at different rates.
Question
The co-ordination of the heart beat is disrupted when the conducting systems of the heart are damaged. This type of disease is
called heart block. Describe how an artificial pacemaker can be used to treat this condition.
 It is placed under the skin of the chest

 It is wired to the heart muscle.
 Just like SAN does, it generates impulses that cause cardiac muscle to contract rhythmically
Fibrillation
• Fibrillation is the rapid, irregular and unsynchronized (uncoordinated) contraction of cardiac muscle. Both the atria and the
ventricles lose their rhythm. There are two major classes of cardiac fibrillation:
1. Atrial fibrillation
2. Ventricular fibrillation.
Ischaemia is when the heart muscle does not receive enough blood due to plaques and clots in coronary arteries and subsequently the
tissues do not receive enough oxygenated blood.
INTRINSIC RHYTHM OF THE HEART AND EXERCISE

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Intrinsic rhythmicity
Intrinsic (built-in) rhythm is the rate at which the heart beats with no interference from the Central Nervous System.
The beating of the healthy heart arises in the SAN (Sino atrial node) in the right atrium. A normal resting heart rate is commonly
considered to be between 60 and 100 beats per minute. In some very well trained athletes or in periods of meditation a normal resting
heart rate may be less than 60.
When doing exercise, adequate supply of oxygen is maintained by;

(i) Increase in stroke volume (cardiac volume): more blood to move to muscles
(ii) Increase in heart rate: Quick delivery of more blood to muscles
(iii) Increase in rate of breathing: Quick delivery of Tidal Volume to muscles
(iv) Deep breathing: increased tidal volume to move to muscles
Exercise and cardiac output

- Cardiac output is the volume of blood pumped out of the heart per minute.
- The two components are;
a) Stroke volume (cardiac volume).
b) Heart rate
- Stroke volume – volume of blood leaving the heart per heart beat (dm3)
- Heart rate – number of beats per minute (beats per minute) ‘
- The equation for cardiac output is as follows:
Cardiac output = stroke volume x heart rate
(dm3/minute) (dm3) (beats/min)
- At rest, in a normal individual the heart rate is about 72 beats per minute and pumps about 4-6 dm 3 of blood per minute (cardiac
output).
- In a trained athlete the resting heart rate is about 60 bpm. During exercise, the cardiac output can go up to 30dm 3 per minute in a
trained athlete making maximum effort.
- Exercise demands for more glucose and oxygen. The body responds to this by increasing the cardiac output i.e. increasing the
stroke volume and heart rate. Increase in cardiac output increases volume of oxygenated blood reaching muscles.
Discuss the importance of thick cardiac muscles.

 Lower heart rate (fewer contractions) is required to deliver enough oxygenated blood to the muscle.
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 The lower the heart rate, the lower the chances of getting HBP.
HEART RATE
- This refers to beats per minute.
- The resting heart rate of a typical adult human is around 70 bpm
Control of heart rate

- It is essential that, the resting heart rate is altered to meet varying demands for oxygen. For example, during exercise,
the resting heart rate may need to be more than double.
- Changes to the heart rate are controlled by a region of the brain called cardiovascular control centre (cardiac
centre) in the medulla oblongata.
- The cardiovascular centre has 2 centres;
1. A centre that increases heart rate (Accelerator), which is linked to the sinoatrial node (SAN) by a sympathetic
nervous system.
2. A centre that decreases heart rate (Decelerator), which is linked to the SAN by the parasympathetic nervous
system.
These centers in the cardiovascular centre respond to the following changes.

(i) Chemical changes in blood which are detected by chemoreceptors in the walls of aorta and carotid arteries
(the arteries that serve the brain).
(ii) Pressure changes in the blood which is detected by pressure receptors/baroreceptors/stretch receptors in
the walls of right atrium, carotid arteries and the aorta.
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REGULATION OF HEART RATE
Baroreceptors/stretch
receptors in the walls of right
atrium, in the walls of aorta &
carotid arteries
Cardiovascular Control centre in the brain
Accelerator in the Cardiovascular Control Decelerator in the Cardiovascular Control

centre in the brain centre in the brain
Chemoreceptors in the walls of aorta &
carotid arteries
Sympathetic (accelerator) Parasympathetic (Vagus)

nerve nerve
Sino atrial node (SAN)
Increase heart rate Decrease heart rate
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Control of heart rate by chemoreceptors
- Chemoreceptors are found in the wall of the aorta and carotid arteries (the arteries that serve the brain). They are
sensitive to changes in the pH of the blood that result from changes in carbon dioxide concentration and lactic acid. In
solution, carbon dioxide forms carbonic acid and therefore lowers pH. The process of control works as follows;
1. When the blood has a higher than normal concentration of carbon dioxide, its pH is lowered.
2. The chemoreceptors in the wall of the carotid arteries and the aorta detect this and increase the frequency of
nerve impulses that are carried by sensory neurones to the accelerator of CVCC in the medulla oblongata that
then sends out impulses to the SAN via sympathetic nerve to increase the heart rate.
3. The increased blood flow leads to more carbon dioxide being removed by the lungs and so the carbon dioxide
level of the blood returns to normal
4. As a consequence, the pH of the blood rises to normal and the chemoreceptors in the wall of the carotid arteries
and aorta reduce the frequency of nerve impulses to the accelerator of CVCC in medulla oblongata
5. The accelerator of CVCC in medulla oblongata reduces the frequency of impulses to the sinoatrial node, which
therefore decreases the heart rate to normal.
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Control of heart rate by Baroreceptors/stretch receptors
At the start of exercise

 Contraction of skeletal muscles squeezes on veins causing increase in venous flow.
 This causes increase in blood volume in the vena cava and right atrium.
 This causes increase in blood pressure/ stretching of right atrium.
 Baroreceptors/Stretch receptors in the wall of the right atrium are stimulated generating impulse
 The impulses are sent to Accelerator of CVCC in the medulla
 The Accelerator of CVCC sends out sympathetic nerve impulses to SAN
 This increases heart rate.
During exercise
 During exercise, right heart reflex takes place

 Right heart reflex/Bainbridge reflex/ atrial reflex, is an increase in heart rate due to an increase in venous
pressure due to strenuous physical activity. Increased blood volume is detected by stretch receptors
(baroreceptors) located in the wall of the right atrium and impulse is produced. The impulses are sent to CVCC
in the medulla through sensory neurones. CVCC sends out sympathetic nerve impulses to SAN. This increases
heart rate.
At the end of the exercise

 Baroreceptors/Pressure receptors/ stretch receptors in the wall of carotid arteries and aorta detect rise in B.P.
 They produce nerve impulses and send to the cardiovascular control centre through sensory neurones, which sends
nerve impulses (inhibitory nerve impulses) to the SAN along the parasympathetic nerve to slow down the heart
rate.
 Aortic reflex takes place at the end of exercise

 Aortic reflex is decrease in heart rate due to increased B.P. in the aorta at the end of the exercise. At the end of
exercise baroreceptors/pressure receptors/ stretch receptors in the wall of aorta detect rise in B.P. They produce
nerve impulses and send it to the cardiovascular control centre, which sends nerve impulses (inhibitory nerve
impulses) to the SAN along the parasympathetic nerve to slow down the heart rate.
SUMMARY
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Decreased blood pH causes an increase in heart rate.
 A decrease in blood pH (caused by an increase in CO 2) is detected by chemoreceptors in aorta and
carotid arteries.
 The chemoreceptors send nerve impulses to the medulla.
 The medulla sends nerve impulses to the SAN along the sympathetic nerve to increase the heart rate.
Increased blood pressure causes a decrease in heart rate.
 Baroreceptors/Pressure receptors/ stretch receptors in the wall of carotid arteries and aorta detect
rise in B.P.
 They produce nerve impulses and send to the cardiovascular control centre, which sends nerve
impulses (inhibitory nerve impulses) to the SAN along the parasympathetic nerve to slow down
the heart rate.
Exercise triggers an increase in heart rate by decreasing blood pH.
 During exercise the level of CO2 in the blood increases. This decreases the pH of the blood, which
the Chemoreceptors detect and sends impulses to cardiovascular control centre that sends
impulses along the sympathetic nerve to the SAN to increase the heart rate.
Cardiac output increases with exercise.

 Cardiac output is the volume of blood pumped out of the heart per minute.
 Cardiac output (cm3/min)=heart rate(bpm) × stroke volume (cm3).
 Stroke volume is the volume of blood pumped out of the heart in one heartbeat.
 So, cardiac output increases during exercise because heart rate increases. Stroke volume also
increases because the heart pumps harder as well.
Questions
1. Name the region of the human brain involved in control of the heat rate
Cardiovascular centre in the medulla oblongata
2. Heart rate increased during exercise. Explain the mechanisms involved in controlling this increase in heart rate
- Respiration increases carbon dioxide and lactic acid
- Carbon dioxide and lactic acid lower the pH of blood
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- Chemoreceptors in the walls of carotid arteries and aorta detect the blood with low pH and send impulses to cardio
vascular centre in medulla.
- This centre increases the frequency of impulses a long sympathetic nerve to SAN, which in turn increases the heart
rate.
THE AUTONOMIC NERVOUS SYSTEM
- Autonomic means “self governing”
- The autonomic nervous system controls the involuntary activities of internal muscle and glands and it has 2 divisions.
(i) Sympathetic nervous system
In general, this stimulates effectors and so speeds up any activity
(ii) Parasympathetic nervous system
In general, this inhibits effectors and so slows down any activity
The actions of sympathetic and parasympathetic nervous systems normally oppose one another in other words, they are
antagonistic. If one system /nerve contracts a muscle, then the other relaxes it. The activities of internal glands and
muscles are therefore regulated by a balance of the two systems.
The following table summarizes the opposing effects of the sympathetic and parasympathetic nerves
Organ/tissue Effector of sympathetic nerve Effector of parasympathetic
nerve
Intercostal muscles Increase in breathing rate Decrease in breathing rate
Heart Increases cardiac output Decreases cardiac output
Hormonal control of the heart rate
Adrenaline
Released from adrenal glands into the blood and carried to the heart
Factors that cause its release:
(i) Fear
(ii) Excitement
(iii) Shock
(iv) Nervousness
(v) Anticipating exercise
(vi) Fright
- Adrenaline speeds up the heart rate
Nervous control of the heart rate

1. Sympathetic nervous system
55
- Increases heart rate
- Has noradrenaline (that now acts as a neurotransmitter) at its ends.
- Impulse causes noradrenaline to diffuse into SAN to increase heart rate.
2. Parasympathetic nervous system
- Decreases heart rate.
- Has a neurotransmitter substance at its ends called acetylcholine.
- Impulse causes acetylcholine to diffuse into SAN to decrease heart rate.
Investigation to measure the effect of increasing cardiac output on the systolic and diastolic pressures.
 Obtain 10 volunteers of same age, level of fitness and same body mass.
 Make them rest for 30 minutes.
 Measure their systolic and diastolic BP using digital blood pressure machine and obtain the mean.
 Have them exercise in a treadmill at 1km/hr, 2, 3, 4 and 5 speeds.
 Measure B.P. at each speed and get the mean.
 Repeat 2 more times for each speed to calculate the mean at each speed.
 Sketch what you would expect an ECG trace to look like if a patient suffered from ventricular fibrillation
(this is rapid and uncontrolled contractions in the ventricles sometimes caused by a patch of damaged
tissue in the ventricle acting as a pacemaker)
Repeated irregular QRS waves with very short P and T waves
 Suggest what might happen on the heart rate if the connection between sinoatrial node (SAN) and
parasympathetic nerve and sympathetic nerve was cut.
Heart would continue to beat because it is myogenic. However, it will not change in response to changes
in the body. But it will still be able to respond to hormonal changes such as the release of adrenaline.
BREATHING RHYTHMS
LUNG VOLUMES
1. Tidal volume (TV).
- The volume of air that enters and leaves the lungs per breath.
- The TV at rest is about 0.5dm3 (500cm3)
- After maximal exercise, it rises to about 3dm 3.
56
2. Inspiratory reserve volume (IRV)
- This is the extra volume of air (above the normal inspired tidal volume) that can be inhaled due to forced inhalation.
- It is about 3000-3300cm3.
3. Expiratory reserve volume (ERV)

- This is the extra volume of air (above the normal exhaled tidal air) that can be exhaled due to forced exhalation.
- It is about 1000-1200cm3.
4. Residual volume (RV)

- It is the volume of air left in the lungs after the strongest possible expiration.
- It is about 1200cm3.
LUNG CAPACITY
- This is the sum of lung volumes.
a) Vital capacity (VC)
- It is the maximum volume of air that can be taken in and out of the lungs by movement of diaphragm and ribs.
- It is the total of TV, IRV and ERV.
- In young men, the average is about 4.6dm3.
- In young women the average is about 3.1dm3.
- In trained athletes, the figure may be 6.0dm3 for men and 4.5dm3 for women.
b) Inspiratory capacity (IC)
- This is the total volume of air that can be inhaled; TV + IRV
c) Expiratory capacity (EC)
- Total volume of air that can be exhaled; TV +ERV.
d) Total lung
capacity
- Is the sum
of vital
capacity
(VC) and
RV
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Minute Volume/ ventilation rate/ Minute ventilation
- This is the total volume of air moved in the lungs in one minute.
- Ventilation rate = tidal volume x no. of breaths per minute
(dm3 min-1) (breathing rate)
- The ventilation rate is affected by 2 factors;
1) The volume of air taken into the lungs at each breath (TV).
2) The number of breaths per minute (breathing rate).
MEASURING LUNG VOLUMES USING A SPIROMETER.

- A spirometer is an apparatus that measures changes in lung volumes brought about by ventilation.
- In summary, a person using a spirometer breaches in and out of air tight chamber causing it to move up and
down and leaving a trace on a revolving drum (kymograph). This trace is called kymograph trace.
- 2 measurements can be obtained from the trace;
a) Tidal volume (TV)
b) Vital capacity (IRV, ERV and TV)
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i) Explain the importance of the soda lime in the spirometer. (2)
- Absorbs CO2 to avoid its accumulation in the spirometer. This has two major advantages;
1. So that only volume of O2 absorbed in the lungs is measured.
2. This is safe for humans because it is harmful to breath in increased volume of CO 2. It can cause
hyperventilation.
ii) Suggest how you could use the spirometer to measure the vital capacity of a person. (3)
- Put the nose clip. This prevents entry or exit of air through the nasal cavity to ensure accurate readings.
- Switch on the chart recorder.
- Breathe normally through the mouth piece to get TV.
- Inhale forcefully i.e. forced inhalation to get IRV
- Exhale forcefully i.e. forced exhalation to get ERV.
- The volumes are read from the chart (kymograph trace) on the rotating drum (kymograph).
- The vital capacity is calculated by adding up IRV, ERV and TV.
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A spirometer trace can be used to find the resting breathing rate in humans. Explain how a spirometer trace can be used to calculate
the mean resting breathing rate of a person. (3)
- One breath is peak to peak or trough to trough
- Count the number of peaks or troughs in a minute
- Repetition to obtain a mean or improve reliability
The figure below is a diagram of a spirometer, a piece of apparatus used to measure some aspects of
breathing, such as breathing rate and vital capacity.
c h a m b e r o f a ir
T
h in g e m o u th p ie c e
w a te r
v a lv e
d ir e c t io n o f
a ir f lo w
A person breathes through the mouthpiece of a spirometer. State what happens to the air chamber in the figure
above during inspiration.
it falls / goes down
Chamber T contains a chemical that absorbs carbon dioxide. Suggest a chemical that could be used in chamber T to
absorb carbon dioxide.
soda lime / sodium hydroxide / potassium hydroxide /
calcium hydroxide;
Explain why a person using the spirometer to measure their vital capacity should wear a nose clip.
- to ensure all air breathed comes from chamber
OR
to prevent, escape of air / entry of air, through nose;
State two other precautions that should be taken when using a spirometer to measure vital capacity.
 use (medical grade) oxygen / fresh air
 disinfect mouthpiece
 Soda lime absorbs CO2 to prevent it from accumulating in the spirometer as it is harmful to humans to breath in
increased volume of CO2
The diagram below shows the trace from a spirometer. A spirometer is a device designed to measure
the volume of air entering and leaving the lungs. A chamber in the spirometer contains soda lime to
absorb the carbon dioxide released by respiration. The measurements shown were recorded from a
60
healthy 17-year-old student at rest.
4
3
v o lu m e o f a ir
in s p ir o m e te r
/ dm 3 x
2
0
0 10 20 30 40 50 60 70 80
tim e / s
Explain why the volume of air in the spirometer drops slowly over the first minute.
oxygen is absorbed by the blood in the lungs to be used in respiration
respiration releases carbon dioxide.This carbon dioxide is absorbed by soda lime
After one minute, the student was asked to breathe in as deeply as possible and then breathe out as much as
possible. The resulting change in the trace is shown in the figure above as X. State the term given to measurement X.
Vital capacity;
The diagram below shows the trace from a spirometer. A spirometer is a device designed to measure the volume of
air entering and leaving the lungs. A chamber in the spirometer contains soda lime to absorb the carbon dioxide
released from respiration. The measurements shown were recorded from a healthy 16 year old student at rest.
4
3
v o lu m e o f
a ir in
s p ir o m e t e r
/ dm 3 2 X
0 0 10 20 30 40 50 60 70 80
tim e / s
(i) Calculate the mean tidal volume in the first 20 seconds. Express your answer to two decimal
places. Show your working
3
0.55 – 0.65dm
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When given a trace, describe how you can calculate the volume of oxygen absorbed in the lungs
in the first minute.
Measure the height difference between the 1st and the last peak within one minute.
Explain how you would use the trace from a spirometer to calculate tidal volume.
 Calibrate the vertical scale, Y axis (volume) so that one small box represents 0.1dm 3
 Calibrate the horizontal scale, X-axis (time) so that one small box represents 5 seconds
 Tidal volume is proportional to the height between the peak/crest and the trough.
 Tidal volume is calculated by multiplying the number of small boxes in this height by 0.1dm 3.
Explain how you would use the trace from a spirometer to calculate breathing rate.
 Breathing rate (breaths per minute) is calculated by counting the number of breaths (one breath is from trough
to trough) in 12 horizontal small boxes (one is 5 seconds).
Explain how you would use the trace from a spirometer to calculate vital capacity.
 Vital capacity is proportional to the height between the peak of IRV and the trough of ERV. To calculate vital
capacity, count the number of small boxes in this height and multiply by 0.1dm 3.
Explain how you would use the trace from a spirometer to calculate ventilation rate/ minute
volume/ minute ventilation
 Multiply tidal volume and breathing rate to get ventilation rate.
Explain how you would use the trace from a spirometer to compare the tidal volumes and
breathing rates of male and female human subjects.
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 Obtain 10 male and 10 female volunteers, all of the same age and same level of fitness.
 Make them rest for 30 minutes, then make them use the spirometer.
 Find each male individual’s tidal volume and breathing rate as above. Add up all the values for the males’ tidal
volumes and breathing rates and divide by 10 to obtain the mean tidal volume and the mean breathing rate,
respectively.
 Repeat the above for the 10 females.
 Compare the mean tidal volume and mean breathing rate for both males and females.
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a) From the figure, calculate the TV?
0.5 dm3
b) Calculate the breathing rate?
12 breaths per minute.
c) Calculate ventilation rate.
0.5 dm3 × 12 breaths per minute= 6 dm3min-1
d) Calculate the volume of O2 absorbed by the lungs.
0.375 dm3
e) If someone takes 11 breaths per minute with an average tidal volume of 0.45dm 3, calculate their ventilation
rate.
Ventilation Rate = 11 x 0.45
= 4.95 dm3 min -1
REGULATION OF VENTILATION RATE

The basic rhythm of breathing
- This is maintained by the medulla.
- In the medulla, found in hindbrain, there is a ventilation centre/ breathing centre/respiratory centre that consist of;
a) Inspiratory centre
- Increases the rate and depth of breathing.
b) Expiratory centre
- Inhibits inspiration.
- Stimulates expiration.
- The Ventilation Centre communicates with the intercostal (rib) muscles by the intercostal nerve and with the diaphragm
muscles by the phrenic nerve.
- There are also stretch receptors (pro-prio receptors) in the walls of the bronchi which communicate with the ventilation centre
by vagus nerve.
- During inhalation, impulses from the inspiratory centre travel along the sympathetic nerve (external intercostal nerve
and phrenic nerve) causing the external intercostal muscles and diaphragm muscles to contract, respectively. This
pushes the ribs upwards and outwards and the diaphragm flattens causing the air to enter the lungs. As the lungs
inflate, the stretch receptors in the walls of the bronchi are stimulated and send nerve impulses to the expiratory
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centre in the medulla via the vagus nerve. This automatically switches off the inspiratory centre, and it stops
stimulating the breathing muscles, hence no breathing in. As the muscles relax, it causes one to exhale. So the stretch
receptors are not stimulated, so the expiratory centre switches off (inactive) and the inspiratory centre switches on
(becomes active) and inspiration begins again.
Role of exercise in breathing rate and depth of breathing.
- Exercise causes increase in respiration that increases CO2 and lactic acid, both of which lower the pH in blood.
- Chemoreceptors in carotid arteries and aorta detect this low pH in blood and send nerve impulses to the inspiratory
centre in the ventilation centre that sends impulses to the external intercostal muscles and diaphragm muscles via
external intercostal nerve and phrenic nerve, respectively to increase the rate of contraction that increases rate and
depth of breathing which increases uptake of oxygen and removal of excess CO 2.
The diagram shows the ways in which the respiratory system and different parts of the brain interact with each
other to regulate breathing.
Cerebral hemisphere
Respiratory centres in
the pons and medulla
Intercostal muscles and Chemoreceptors

Diaphragm muscles
stretch receptors
and stretch receptors
a) Breathing can be controlled voluntarily and involuntarily. Name the part of the brain that controls involuntary breathing.
Medulla oblongata
b) Suggest one occasion when the depth of breathing is increased voluntarily.
a. Before diving
b. Before singing
c. Before sniffing
d. Before playing a musical instrument
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c) Using the information in the diagram, explain the roles of muscle spindles and nerves in the control of breathing during exercise.
- Baroreceptors / stretch receptors
- Detect degree of stretch in diaphragm and intercostal muscles
- Impulse sent to respiratory centre along sensory neurons
- Respiratory centre sends impulses along nerves to muscles (diaphragm and inter costal) to alter ventilation rate and depth of
breathing.
d) Ventilation of the lungs during breathing is essential in maintaining the concentration gradient of the respiratory gases. This ensures that gas
exchange is efficient. Explain why the chemoreceptors are particularly important during exercise.
- Exercise increases respiration that increases production of CO 2 and lactic acid that lower the PH in blood
- Chemoreceptors in carotid arteries and aorta detect this pH
- There chemoreceptors send impulses to medulla
- Resulting in increased impulses to intercostal and diaphragm muscles which increase rate and depth of breathing.
Explain how increase in minute volume and a cardiac output during exercise enable rapid delivery of oxygen to muscles.
As the minute volume increases, the tidal volume (volume of oxygen breathed in) increases; breathing rate increases to quickly delivery
large volume of oxygen to muscle; increase in cardiac output increases stroke volume; heart rate increases to shorten the time this large
volume of oxygen in the blood reaches muscles.
Cardiac output and resting heart rate of an athlete differs before and after completing training programme. Cardiac output in cm 3 before
and after remains the same e.g. 5000. However, resting heart rate/bpm is higher before training than after training e.g. 70 verses 55.
a) Calculate the athletes’ stroke volume after training. Show your working
Cardiac output= stroke volume x heart rate
5000/55 = 90.91cm3
b) Explain how training has caused the resting heart rate of the athlete to be lower
 Heart muscle is thicker (hypertrophy) and stronger than before
 Therefore each beat pumps out more blood (stroke volume)
 No need for many beats and so resting heart rate is lower.
Describe and explain the changes that you would expect to record in systolic and diastolic blood pressure while exercising before and after
the training programme.
 Due to training, the heart muscle thickens and strengthens, so that it contracts powerfully, increasing systolic pressure that in turn increases
stroke volume.
 Consequently, there is greater emptying of ventricles hence reducing diastolic pressure.
Describe how you would find the breathing rate of a person at rest
 Count breaths in a minute
 One breath is one upward and one downward movement of the chest
Summarize the effect of exercise on heart rate and breathing rate

 During exercise, respiration produces carbon dioxide and lactic acid that lower the pH of blood
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 Chemoreceptors in the wall of the aorta and walls of carotid arteries detect this blood and send impulses via
sensory neurons to the accelerator of CVCC in the medulla and Inspiratory Centre of the Breathing Centre
in the medulla. The accelerator of CVCC sends out impulses to the SAN via sympathetic neurone to
increase heart rate. The Inspiratory Centre sends out impulses to the diaphragm muscles and external
intercostal muscles via phrenic nerve and external intercostal nerve, respectively, to increase the rate and
depth of breathing.
ROLE OF ADRENALINE IN THE FIGHT OR FLIGHT RESPONSE

 Adrenaline hormone is a peptide/ protein hormone which is involved in the homeostatic response of the
heart and breathing system to exercise and stress.
 When you are stressed, the sympathetic nerve from the brain stimulates the adrenal medulla to release
the hormone adrenaline. It is carried around the body in the blood and binds to receptors in the target
organs including SAN, cardiovascular control center and breathing center.
 Adrenaline stimulates the cardiovascular control center in the brain increasing the impulses in the
sympathetic neurons which supplies the heart and this increases heart rate so that more glucose and
oxygen are supplied to the muscles and brain.
 It also has a direct effect on the SAN by increasing the frequency of excitation and so the heart rate
increases. This supplies extra oxygen and glucose for the muscles and brain in case one wants to run
away (flight) or stand and fight.
 Adrenaline is also responsible for the response of the body in stressful situations. In this case, the
sympathetic nerve from the brain sends impulses to the adrenal medulla so that adrenaline is released
and carried by the blood to the target organs.
N.B.
 Adrenaline is very similar to the noradrenaline released in the synapses of the sympathetic
nervous system which also increases heart rate.
 Stress is a state of mental or emotional strain caused by adverse circumstances or body’s
reaction to harmful situations. Increased heart rate and breathing rate are some of the
symptoms of stress.
HOMEOSTASIS
- This is the maintenance of a constant internal environment.
- The internal environment is made up of tissue fluid that supplies the cells with nutrients and remove wastes.
- Birds (aves) and mammals are endotherms
- Core body temperature, amount of water in the blood and blood glucose level are examples of processes that need to
be kept constant.
Importance of homeostasis
67
1. Due to constant temperature enzymes remain stable
2. Due to constant pH enzymes remain stable
3. Due to constant water potential of the blood and tissue fluids, the cells operate normally as they do not expand or
shrink
4. Due to constant blood glucose concentration, there is a reliable source of glucose for respiration by cells
5. Organisms with the ability to maintain a constant internal environment are more independent of the external
environment. They adapt well in different conditions
Negative feedback
- Many substances or systems in living organisms have a set concentration/set level /set point.
- Negative feedback refers to events that take place to normalize the deviated internal environment. This
process is important in homeostasis. It is the negative feedback that maintains homeostasis.
Negative feedback consists of:

(i) Set point – this is the desired level or norm at which the system operates. This is monitored by a receptor.
(ii) Receptor – this is a cell that detects any deviation from the set point and informs the controller.
(iii) Controller – co-ordinates/interprets information from various receptors and informs or sends instructions to
an Effector.
(iv) Effector – brings about the changes needed to return the system to the set point. This causes return to
normality through a feedback loop.
(v) Feedback loop – informs the receptor of the changes to the system brought about by the Effector.
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HOMEOSTASIS (THERMOREGULATION AND EXERCISE)
- Thermoregulation is the control of body temperature through negative feedback.
- Thermoregulation is carried out by the heat gain centre and heat loss centre in the thermoregulatory centre in the
hypothalamus in the brain.
- There are two types of temperature;
(i) Core (blood) temperature - monitored by thermoreceptors or temperature receptors in the thermoregulatory
centre.
(ii) Skin temperature (external temperature) it is detected or monitored by thermoreceptors in the skin which
deliver sensory input to the thermoregulatory centre via cutaneous nerves.
- Exercise releases a lot of heat which needs to be dispensed or removed from the body.
- When the temperature of the blood flowing through the thermoreceptors in the thermoregulatory centre increases due
to exercise, heat loss centre is activated. It sends out impulses along motor nerves to effectors.
- The heat loss centre;
(i) stimulates sweat glands to secrete sweat.
(ii) inhibits contraction of arterioles in the skin
(iii) inhibits hair erector muscles (relaxed hair lying flat).
(iv) liver (reduces metabolic rate).
(v) skeletal muscles (relax – no shivering).
- When the temperature of the blood flowing through the thermoreceptors in the thermoregulatory centre decreases,
heat gain centre is activated and sends out nerve impulses to;
1. Skin to constrict the arterioles.
2. Skin to contract hair erector muscles.
3. Skin to inhibit (relax) sweat glands.
4. Liver to raise metabolic rate.
5. Skeletal muscles to contract causing shivering (shivering thermoregulation)
6. Brown fat in skeletal muscle is metabolized to generate a lot of heat (non-shivering thermoregulation)
Suggest how the wood mouse maintains a constant body temperature when in a cold environment. (6)
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 Thermoreceptors in the skin and hypothalamus detect low temperature and send impulses to the heat gain centre in
the thermoregulatory center in the hypothalamus
 This heat gain centre sends out impulses to the muscles of skin arterioles to contract them and cause
vasoconstriction so that less blood reaches the skin capillaries/superficial capillaries causing less loss of heat. In
addition, the impulse causes muscles of shunt vessels to relax in order to dilate / widen the shunt vessel so that less
blood reaches the skin capillaries / superficial capillaries.
 Impulses reach hair erector muscles in the skin to cause contraction so that the hair stand upright to trap air that
acts as an insulator, so that less heat is lost by radiation and convection
 Heat is generated by shivering due to violent muscle contraction (shivering thermoregulation)
 Heat is generated by increasing metabolism of brown fat in skeletal muscles (non-shivering thermoregulation)
 Inhibition of sweat glands hence less sweating causing less heat loss by evaporation.
During the race, heat is generated and is lost from the body through the skin.
Describe how muscle, present in blood vessels in the skin, helps to increase heat loss from the body. (4)
 The muscles in the skin arterioles relax to cause vasodilation so that more blood reaches the superficial capillaries
so that more heat is lost through radiation and convection.
 The muscles in the shunts contract to cause vasoconstriction to redirect blood away from deeper skin arterioles
into surface arterioles and finally into superficial capillaries so that more heat is lost through radiation.
Two runners A and B were in a race. In the 1st 30 minutes the core temperature increased for both.
Suggest an explanation for the change in core temperatures of both runners in the first 30 minutes of the
race.
1. For muscles to contract, increased respiration takes place to produce a lot of ATP
2. Hydrolysis of these ATP molecules produces heat energy
3. more heat energy is produced than lost hence increase in core temperature
(b) Between 60 and 100 minutes of this race, the temperature of the two remained constant. Suggest an
explanation for the constant core temperatures of both runners 5)
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 negative feedback sets in to cool the body;
 temperature receptors in the hypothalamus detect this blood and sends impulses to heat loss centre
of the thermoregulatory centre that sends impulse to sweat glands to activate them to lose heat
through evaporation of water in the sweat; to skin arterioles to cause vasodilation so that more warm
blood reaches the superficial capillaries to lose heat through radiation; to shunt vessels to cause
vasoconstriction so more blood enter the skin arterioles and finally into superficial capillaries. Due to
this negative feedback, heat gained is equal to heat lost.
During this race, runner A lost 3.02 kg of water (and core temperature increased further) and runner B lost 2.43
kg of water (and core temp remained constant).
Using this information in the question and your own knowledge, suggest reasons for the change in core
temperature of runner A after 120 minutes (core temperature increased further for A but remained constant for
runner B ) (2)
 increase of pace that produces more heat than the body can lose
 Dehydration causes cooling mechanisms such sweating start to fail
WHEN HOMEOSTASIS FAILS

- Above or below certain temperatures, homeostasis fails (e.g. because the hypothalamus may be damaged).
- Instead, positive feedback may occur resulting in a high temperature continuing to rise or a low temperature falling
further. This can result in hyperthermia (above 38.30C) or hypothermia (below 350C) and may lead to death.
Temperature limits
- Core (blood) body temperature is 37.5oC.
- Oral temperature (under the tongue) is 370C.
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1. Low critical temperature (below 270C)
- The temperature at which the normal thermoregulatory mechanisms to conserve heat are no longer enough
and the metabolic rate increases to produce extra heat.
2. Low lethal temperature (below 250C)

- Temperature at which chemical reactions stop due to inactivity of enzymes and results to death.
NB
- Exercising hard in cold condition causes a lot of sweating after the exercise due to greater temperature gradient
between the body and environment, thus heat is lost very fast. This leads to hypothermia, low critical temperature
and eventually reaching low lethal temperature.
3. High critical temperature (about 41.70C)

- The temperatures at which the normal thermoregulatory mechanisms to release heat such as sweating are no
longer enough. Increase in external temperature causes increase in metabolic rate.
4. High lethal temperature

- Temperature at which chemical reactions stop due to denaturation of enzymes resulting to death. It is around
420C.
Questions
1. Explain what is meant by the term negative feedback?
Events that occur to normalize a deviated internal environment
2. Suggest what the consequences might be if you were unable to lose heat from the body during exercise.
- Core body temperature will rise above 370c
- Cause heat stroke
- Hypothalamus may become damaged
- Enzymes may be denatured
- Membrane proteins may be denatured
- Transport may be impaired
- Respiration may be impaired
- Coma and death may result
3. Describe the body’s likely responses to the core temperature dropping below 37 oC.
- Heat gain centre of thermoregulatory centre of hypothalamus stimulates effectors;
- Sweat production is inhibited
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- Reduced blood flow to the skin
- Shivering
- Metabolic rate of the liver may increase
- Hairs raised on skin
- Behavioral responses such as increased movement and putting on extra clothes.
STRUCTURE OF THE KIDNEY

 Humans have two bean shaped kidneys, found in the lower back
 Each kidney consist of about 1 million nephrons/kidney tubules.
 Each kidney receives blood from a renal artery that branches from aorta
 Each kidney returns blood via a renal vein that connects to vena cava.
 A pair of ureter carries urine from the kidney to the bladder.
 Urethra carries urine from the bladder to outside the body.
Urinary system
The structure of the Kidney

1. Renal capsule – this is a tough layer that covers the whole kidney.
2. Cortex – this has the Bowman’s capsule, PCT,DCT and small section of CD of the nephron.
3. Medulla – this has the loop of Henle of the nephron and large section of the Collecting Duct.
4. Renal Pelvis – This is the upper expanded section of ureter that receives urine from the collecting
ducts.
5. Ureter – this is the narrower region of
pelvis. There is a pair of ureter that
connects to bladder.
6. Renal vein
7. Renal artery
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 Each of the two kidneys has about 1 million nephrons.
TYPES OF NEPHRONS
1. Cortical nephrons: Found mainly in the renal cortex. They have a loop of Henle that just reaches into the
medulla. About 85% of human nephrons are cortical.
2. Juxtamedullary nephrons: Have long loops of Henle that penetrate right through the medulla. They are
efficient in producing concentrated urine e.g. in desert rats
STRUCTURE OF NEPHRON
 Bowman’s capsule: First part of the nephron where blood is initially filtered to form glomerular filtrate.
 Proximal convoluted tubule (PCT): Folded structure connected to the Bowman’s capsule where selective
reabsorption occurs.
 Loop of Henle: Selectively permeable loop that descends into the medulla and establishes a salt gradient.
 Distal convoluted tubule: Folded structure connected to the loop of Henle where further selective
reabsorption occurs
Each nephron connects to a collecting duct (CD) via DCT which drains the content into renal pelvis.
The CD is shared by nephrons and so not technically considered to be part of a single nephron
Blood vessels associated with nephron

1. Glomerulus (capillary knot/coiled capillaries). It is supplied with blood by afferent arteriole, a
branch of the renal artery; and removes blood by efferent arteriole that forms a network of
capillaries that surround the nephron and the blood in these capillaries flows into renal vein.
Bowman’s capsule together with glomerulus form renal corpuscle.
2. Peritubular capillaries that surround the PCT
3. Vasa recta capillaries that surround the Loop of Henle.
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Functions of Nephron.
 Nephrons filter blood and then selectively reabsorb useful materials from the filtrate before eliminating
the remainder as urine.
 There are four processes of forming urine;
1. Ultrafiltration – Blood is filtered out of the glomerulus at the Bowman’s capsule to form filtrate
2. Selective reabsorption – Usable materials are reabsorbed in convoluted tubules (PCT & DCT)
3. Secretion in the PCT and DCT
4. Osmoregulation – The loop of Henle establishes a salt gradient, that draws water out of CD
Ultrafiltration
 This is the filtration of small molecules such as glucose and urea out of the blood into the Bowman’s
capsule.
 The filtered out substances form glomerular filtrate in the lumen of Bowman’s capsule
 During filtration, the substances pass through three layers;
1) Capillary endothelium/Capillary wall, which has large gaps between endothelial cells.
2) Basement membrane, which acts as a filter (selective barrier).
3) Capsule wall, which is made of podocyte cells between which are large gaps called filtration
slits.
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How glomerular filtrate is formed in the Bowman’s capsule
 Wider afferent arteriole than efferent arteriole creates higher hydrostatic pressure in the glomerulus than
the pressure in the Bowman’s capsule.
 This causes ultrafiltration where blood components below 68,000 RMM such as urea, sodium ions,
chloride ions, potassium ions, uric acid, creatinine, water & glucose are filtered out through large gaps
between endothelial cells of the endothelium of blood capillaries/glomerulus, basement membrane that
acts as a filter/selective barrier and through the large gaps/filtration slits between podocytes of capsule
wall, forming glomerular filtrate.
 Components of blood above 68, 000 RMM such as proteins and blood cells cannot be filtered out
through basement membrane hence remain in the blood.
Selective Reabsorption
 This is the process of taking back any useful molecules from the fluid in the renal tubule (PCT, Loop of
Henle & DCT) in the nephron as it flows along.
Selective reabsorption in the PCT

 The lining of the PCT is made up of a single layer of cuboidal epithelial cells.
 These cuboidal epithelial cells of the PCT are adapted for their function of reabsorption as
follows;
1) The apical membrane of the cell, the membrane facing the lumen has microvilli to
increase the surface area for absorption.
2) There are tight junctions between adjacent cells so that fluid cannot pass between them
and instead go through the cells.
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3) Many mitochondria to produce ATP needed by Sodium-potassium pump proteins in the
in the basal membrane of the cells, membrane facing the capillaries
4) Sodium cotransport protein in the apical membrane
 Sodium ions are actively transported out of the cuboidal epithelial cells by Na-K pump. They then
diffuse into the blood. Sodium ions diffuse from lumen ubto cuboidal epithelial cells through:
1. Facilitated diffusion using sodium ion channels
2. Sodium cotransport protein where it passively diffuses from the lumen
into cuboidal epithelial cells.
 Glucose is actively transported from the lumen into the cuboidal epithelial cells using sodium cotransport protein.
The realization of the potential energy produced from passive movement of sodium is enough energy to
transport glucose across the membrane into the cuboidal epithelial cells. The energy technically comes from the
utilization of ATP by the sodium/potassium pump in the basal membrane which keeps sodium concentrations
within the cuboidal epithelial cells low thus giving the sodium in the lumen a high potential energy. In summary,
the passive movement of sodium ions down their concentration gradient provide energy to move the
glucose molecules against their concentration gradient. This is called Secondary Active Transport
because it does not directly use ATP but it is only possible because of active transport of sodium across
the basal membrane. Glucose is then passively transported through facilitated diffusion out of the epithelial
cells into the blood. 100% glucose is selectively reabsorbed in the PCT.
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 About 50% of urea diffuses from the lumen into cuboidal epithelial cells and then diffuse into the blood.
Urea creates osmotic gradient so that more water is reabsorbed.
 Negatively charged ions such as chloride and phosphates are reabsorbed down the electrochemical gradient
created by sodium ions.
 About 80% of water is reabsorbed by osmosis in the PCT as a result of osmotic gradient formed by
solutes.
 Uric acid is not reabsorbed
 Creatinine is not reabsorbed. Instead, creatinine is actively secreted by the cuboidal epithelial cells into
the lumen.
NB
100% of amino acids, vitamins and hormones are reabsorbed in the same way as glucose. They are co-
transported across the apical membrane with sodium.
Summary of selective reabsorption in the PCT

1. Sodium ions are actively transported out of the cuboidal epithelial cells by Na-K pump and then diffuse
into the blood. They diffuse from lumen to cuboidal epithelial cells through facilitated diffusion using
sodium ion channels and sodium cotransport protein where it passively diffuses from lumen into
cuboidal cells
2. Glucose (100%) is actively transported from the lumen into the cuboidal epithelial cells using sodium cotransport
protein. Glucose is then passively transported through facilitated diffusion out of the cuboidal epithelial cells into
the blood.
3. All amino acids, vitamins and hormones are co-transported across the apical membrane with sodium and
then diffuse into blood.
4. About 50% of urea diffuses from the lumen into cuboidal cells and then into the blood. Urea further
creates osmotic gradient so that more water is reabsorbed.
5. Negatively charged ions such as chloride and phosphates are reabsorbed through electrochemical gradient created
by sodium ions.
6. About 80% of water is reabsorbed through osmosis in the PCT due to osmotic gradient formed by solutes
7. Uric acid is not reabsorbed
8. Creatinine is not reabsorbed. Indeed, creatinine is actively secreted by the cells of the PCT into its
lumen.
NB. About 75 to 80% of filtrate is reabsorbed in the PCT.
LOOP OF HENLE
 Its role is to establish high solute concentration in the medulla of the kidney so that hypertonic urine
is produced (urine with more solutes and less water).
 It is divided into descending & ascending limb
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 The descending limb is permeable to water, but impermeable to sodium & chloride ions.
 The ascending limb is permeable to sodium & chloride ions but impermeable to water.
How the loop of Henle functions as a countercurrent multiplier system
1. Sodium ions and chloride ions are actively transported out of the upper part of the ascending
limb.
2. This raises the concentration of sodium and chloride ions in the medulla and this lowers the
water potential in the medulla.
3. This in turn causes loss of water from the descending limb and collecting duct by osmosis
into the medulla.
4. The loss of water concentrates sodium and chloride ions in the descending limb as it flows
towards the bottom of the medulla.
5. Sodium and chloride ions diffuse out in the lower part of ascending limb.
NB: In the upper part of the ascending limb not all sodium and chloride ions are pumped out and this will pass
to the DCT although it is less concentrated than before
DCT (DISTAL CONVOLUTED TUBULE)

 Sodium ions are actively pumped from the fluid in the tubule into the tissue fluid from where they diffuse
into the blood.
 Cells in the DCT actively secrete potassium ions, hydrogen ions and ammonia into the lumen of the
tubule. Here ammonia combine with hydrogen ions to form ammonium ions which are excreted in the
urine.
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Reabsorption and secretion of urea in the nephron
 About 50% of urea is reabsorbed in the PCT with the reabsorption of about 80% of water. Urea is dissolved in
water. So this little reabsorption of urea and high reabsorption of water increases the concentration of urea
going down to the loop of Henle.
 In the descending limb, a lot of water is further reabsorbed leaving behind high concentration of urea in the
lumen
 Urea is secreted into the lumen of the thin ascending limb from the medulla and this further increases the
concentration of urea.
 The thick ascending limb and DCT are impermeable to urea hence remain in the lumen. In addition DCT allows
for reabsorption of water further increasing concentration of urea in the lumen.
 ADH causes water channels/aquaporin and urea channels to open in the wall of the CD. This causes water and
urea to be reabsorbed and accumulate in the medulla. Urea is then secreted into the lumen of the thin ascending
limb of the Loop of Henle.
OSMOREGULATION/REGULATION OR CONTROL OF WATER

 Osmoregulation is the control of water in the blood.
 It is mainly carried out by the collecting duct that connects to several nephrons.
Explain how collecting ducts in the kidneys reduce the loss of water from the body.
 The Collecting Duct carries out osmoregulation by varying the volume of water reabsorbed.
 Concentrated blood is detected by osmoreceptors in the hypothalamus.
 The osmoreceptors produce an impulse that stimulates posterior pituitary gland to secrete
ADH/Vasopressin.
 ADH is transported by blood to the cells of collecting duct.
 It binds to the ADH receptors on membrane of cells of collecting duct.
 This activates enzyme-controlled reactions, ending with the production of an active phosphorylase
enzyme. This enzyme causes vesicles with water channels (aquaporins) to move & fuse with plasma
membrane and make it more permeable to water.
 This causes more water to flow out of lumen of the collecting duct through the water channels
(aquaporins), down the water potential gradient, into the blood.
 This causes the production of small volume of urine that is more concentrated.
 When there is an increase in water potential of the blood, the osmoreceptors in the hypothalamus are
no longer stimulated & ADH is not secreted.
 Lack of ADH causes aquaporins to move out of the CSM of the collecting duct cells, back into the
cytoplasm. This makes the CD cells impermeable to water, producing large volumes of urine that is more
dilute.
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DEAMINATION OF AMINO ACIDS
 The body cannot store excess protein.
 However, the excess amino acids should not be wasted as they provide useful energy.
 To make use of this energy, the liver removes the amino groups from amino acids in a process known as
deamination, where the amino group (NH2) of the amino acid together with the extra hydrogen atom,
combine to produce ammonia (NH3). The keto acid that remains may;
1) Enter the Krebs Cycle to be respired or
2) Converted to glucose or
3) Converted to glycogen for storage or
4) Converted to fat for storage
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 Ammonia is very soluble and very toxic compound
 In many aquatic animals such as fish that live in fresh water, Ammonia diffuses from the blood and
dissolves in the water around the animal.
 In terrestrial animals such as humans, ammonia rapidly build up in the blood and causes damage.
Damage is prevented by immediately converting ammonia to Urea which is less soluble and less toxic.
This takes place in Urea cycle where ammonia and CO2 combine to form Urea. Urea diffuses from the
liver cells into the blood plasma and taken to the kidney for excretion.
HOW GENES CAN BE SWITCHED ON BY TRANSCRIPTION FACTORS.

- Control of gene expression is another mechanism of body regulation.
- When a gene is expressed, a protein is made. This protein is involved in regulation.
- When a gene is not expressed a protein is not synthesized and this is also a form of regulation.
- Transcription factor is a protein that regulates/controls gene expression by switching on genes or by
switching them off. They bind to promoter region on DNA adjacent to the gene to be regulated and
control the process of transcription.
- Depending on the transcription factor, the gene either undergoes transcription or transcription is
inhibited
- A transcription factor that activates transcription (Activator) causes gene expression while the one that
stops transcription (repressor) stops gene expression.
HOW TRANSCRIPTION FACTOR CAUSES GENE EXPRESSION

 RNA polymerase binds to active transcription factor to form transcription initiation complex (TIC) which
binds to promoter region and causes transcription to form mRNA.
 Most transcription factors are synthesized in inactive form in cells and are then activated by signal proteins.
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HOW TRANSCRIPTION FACTOR STOPS GENE EXPRESSION
- A transcription factor that stops gene expression is also called repressor protein because it turns off the expression
of a gene by binding to promoter region in order to block the attachment of TIC hence no transcription.
Roles of hormones in regulation

 Peptide /protein hormones and steroid hormones affect their target cells in different ways:
Action of protein/peptide hormones e.g. insulin

 Protein/peptide hormone (1st messenger) binds to a receptor on the CSM of the target cell forming a hormone-
receptor complex.
 This complex activates an enzyme called Adenyl cyclase that catalyses the conversion of ATP into cyclic AMP
(cAMP).
 The cAMP acts as a second messenger which activates enzymes called transcription factors.
Action of steroid hormones e.g. testosterone.
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 The hormone, being lipid in nature, passes through the CSM of the target cell and binds directly to the receptor
molecule in the cytoplasm forming a hormone-receptor complex that enters the nucleus and acts as a transcription
factor to control transcription of a gene that synthesizes mRNA.
Topic 8: Coordination, Response and Gene Technology

Coordination
This is the way different organs efficiently work together to carry out a function.
The body is coordinated in two ways:
1. Nervous System
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2. Hormonal system/ endocrine system
NERVOUS SYSTEM
Nervous system is divided into 2 parts:
1. Central nervous system (CNS) - Brain and spinal cord
2. Peripheral nervous system (PNS) – Neurons/ Nerve cells
Neurones
- Neurones are specialized cells that carry nerves impulses /action potential.
- Neurones are also called nerve cells.
The features of all neurones

1. Cell body-with nucleus
2. Axon- this is the part of the nerve fibre that carries impulses away from the cell body.
3. Dendrites – these are finger like projections that conduct impulses to the cell body. One long dendrite is called
dendron. A dendron is found in sensory and relay neurone. A dendron therefore is part of the nerve fibre that
carries impulses towards the cell body.
4. Synaptic knobs-they pass on impulses to other neurones or to the muscle.
Neurones are able to carry impulses or action potential over a long distance because:
(i) Nerve fibres are long
(ii) Membranes are polarized (different charges on either side of the membrane).
Myelinated axon
 Most vertebrate neurones are associated with another specialized type of cell called the Schwann cell whose
membrane wraps itself repeatedly around the nerve fibre forming a fatty layer called myelin sheath.
 However, there are gaps between the myelin sheath called nodes of Ranvier.
Importance of myelin sheath
1. Protects the nerve cell from damage.
2. Speeds up the transmission of nerve impulses through saltatory conduction (jumping of impulses from node to
node). This is because myelin sheath (fatty in nature) is a poor conductor of nerve impulses or action potential.
3. Controls the movement of ions across the membranes, allowing the movement to take place only in the nodes of
Ranvier.
Functions of Schwann cells

1. They wrap around the neurone to nourish it.
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2. They wrap around the neurone to protect it.
3. They wrap around the neurone to produce myelin sheath.
A: Nucleus of Schwann cell

B: Cytoplasm of Schwann cell
C: Myelin Sheath
D: Axon
Types of neurones
 There are 3 types of neurones
(i) Sensory
(ii) Motor
(iii) Relay /connector /bipolar (because two fibres leave the same cell body).
Structures and functions of neurones

1. Sensory neurone
a) Structure
- Cell body is located along the nerve fibre of the neurone.
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- They have Schwann cells that produce myelin sheath hence it is myelinated.
- Between myelin sheaths there are nodes of Ranvier.
- The nerve fibre consists of dendron and axon.
b) Function
(i) Transmits sensory impulses from receptor cells to the CNS.
2. Motor Neurone (Effector neurone)

a) Structure
- Cell body is at the end of nerve fibre/axon which is surrounded by many Short dendrites
- Has Schwann cell hence they have myelin sheath and nodes of Ranvier.
- The whole nerve fibre is an axon and so there is no dendron.
b) Function
 Transmit motor impulses from the CNS to the effectors (muscles and glands).
3. Relay neurone
a) Structure
- Cell body is at the centre, between axon and dendron.
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- Nerve fibre consists of short axon and short dendron.
- They have no Schwann cell hence no myelin sheath and nodes of Ranvier.
- They are always found in the CNS e.g. in the grey matter of the spinal cord.
b) Function
They connect sensory to motor neurones and therefore transmit impulses from sensory to motor neurones. Lack of myelin
sheath slows down the transmission of impulses in the CNS to give enough time for its co-
ordination/interpretation/processing.
NB
 In all the 3 neurones, one end has dendrites which receive impulses e.g. dendrites of sensory neurone receive
impulses from receptors e.g. pressure receptors in the skin; dendrites of motor neurones receive impulses from
either synaptic knobs of sensory neurones or of relay neurones.
 On the other end of the neurones are the synaptic knobs which pass on impulses e.g. the sensory neurone passes on
impulses to the dendrites of relay or motor neurons. The synaptic knobs of the motor neurones pass on impulses to
the effectors e.g. muscles while the synaptic knobs of the relay neurone pass on impulses to the dendrites of motor
neurone.
Describe the differences in the structure of a myelinated sensory neurone and a myelinated motor neurone.
 Sensory has Dendron, motor does not have

 Sensory has shorter axon while motor has longer axon
 Sensory has no motor end plate, motor has
 Sensory has cell body along the nerve fibre while motor has cell body at the end of the nerve fibre
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NERVE IMPULSE
RESTING POTENTIAL
 A resting potential is the voltage (the difference in charge between two points) across the plasma membrane of a
neurone when it is not conducting an impulse, that is, it is at resting state.
 The resting potential is -70mV (on the inside of the neurone there are fewer positive ions: K + & Na+ than outside
by 70mV).
 The potential difference (pd) is therefore 70mV.
 The membrane is said to be polarized
 The following factors produce and maintain the resting potential:
1) Na-K pump in the membrane moves out 3Na+ for every 2K+ it moves inside hence the net effect is that outside
is more positive than inside.
2) The membrane is relatively impermeable to Na+ because few voltage dependent Na+ channels (sodium gates)
are open hence will allow little if any Na+ to diffuse back into the neurone but it is permeable to K+ because
many voltage dependent K+ channels (Potassium gates) are open hence freely diffuse from the inside to the
outside. The net effect is that there are more positive ions on the outside.
3) Cl- and the negatively charged large proteins remain inside the neurone hence inside is more negative than
outside.
ACTION POTENTIAL
 An action potential is depolarization and repolarization of a neuron, due to facilitated diffusion of ions across the
membrane through voltage-dependent ion channels.
 A resting sensory neurone receives a stimulus such as heat.
 This causes :
1) More voltage dependent Na+ channels to open,
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2) Na-K pump to be inactive
3) Voltage dependent K+ channels to close.
 This causes Na+ to diffuse into the neurone causing depolarization (reversing the potential across the membrane).
 Initially, the diffusion of Na+ is slow until the threshold stimulus (-50mV) is reached.
 After this threshold stimulus, there is sudden diffusion of Na + that quickly changes the inside to be more positive
than outside, causing action potential (+30mV).
 The +30mV is the action potential which means that on the inside of the membrane there are more positive ions
than the outside by 30mV.
 The potential difference is therefore 30 mV.
 The membrane is said to be depolarized.
 The following
graph shows the
movement of ions in an
out of the membrane
during action potential
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Resting potential 1
Stimulus 2
Voltage dependent Na+ channels open 2
Voltage dependent K+ channels close 2
Na-K pump inactivated 2
Depolarization 3
Threshold stimulus 4
Action potential 5
+
Voltage dependent Na channels close 5
Refractory period 5
Voltage dependent K+ channels open 5
Repolarization/recovery 6
Hyperpolarization 7
Voltage dependent potassium ion channels close 8
Restoration of resting potential 9
AFTER ACTION POTENTIAL

 After achieving action potential/electrical impulse, the following events take place:
1) Voltage dependent Na+ channels close
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2) Refractory period sets in
3) Voltage dependent K+ channels open to start the process of re-polarization (the potential across the
membrane is restored).
REFRACTORY PERIOD
 This is a short recovery period that occurs immediately after the passage of a nerve impulse along the
nerve fibre of a nerve cell.
 During refractory period, voltage dependent Na + channels are closed and cannot open even with a much
bigger stimulus.
 So the membrane cannot be depolarized and a new action potential cannot be initiated.
 This has 2 important roles:
1) Separates nerve impulses from each other so they move as separate signals. This is because refractory
period takes from 1-10 milliseconds.
2) Nerve impulses move in one direction only along an axon. They go from an active region to a resting
region but not the other way because the membrane immediately behind the impulse is undergoing
recovery and cannot be depolarized.
REPOLARIZATION/RECOVERY
 Immediately after the passage of a nerve impulse along the axon/nerve fibre, that part of the axon
undergoes repolarization/recovery.
 The membrane is said to be repolarized
 During repolarization, more voltage dependent K + channels open so that K + diffuse out of the neurone to
make the outside more positive until resting potential is achieved (-70mV)
 Usually, even after achieving the resting potential, voltage dependent K + channels do not close causing
potassium-overshoot. This causes hyper-polarization.
HYPERPOLARIZATION
 This is an increase in the potential difference across the cell surface membrane of the neurone
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 Because the inside of the neurone is relatively more negatively charged at resting state, hyper-polarization
causes the inside of the neurone to be even more negative i.e. beyond -70mV
 The membrane is said to be hyper-polarized.
 However, voltage dependent K+ channels close. Potassium channels restore the resting potential by
causing the diffusion of potassium ions into the neurone.
ALL OR NOTHING NATURE OF ACTION POTENTIAL
 For depolarization to cause action potential, it must reach threshold stimulus. If not, there will be no action
potential.
 A bigger stimulus increases the frequency of the action potential (not the strength) and also increases the
number of nerve fibres to be stimulated.
 The speed of the impulse is only increased by:
1) Myelination that causes saltatory conduction.
2) Large diameter of the nerve fibre
PROPAGATION/TRANSMISSION OF NERVE IMPULSE ALONG
NON- MYELINATED NEURONE
 Na+ on the inside flow sideways to negative charges

 On the outside, the positive charges flow to negative charges, creating local circuits
 Impulses therefore, are transmitted along the membrane in form of local circuits
 Due to refractory period, impulse moves in one direction only from the active region (action potential) to the
resting region ahead and not behind the active region as this region is undergoing recovery/repolarization and
eventually hyper-polarization
 Due to lack of myelin sheath, the impulse is transmitted along the whole membrane hence transmission is slow
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PROPAGATION OF NERVE IMPULSE ALONG MYELINATED NEURONE
 Na+ on the inside of the membrane in the node of Ranvier flow sideways to negative charges in the node of
Ranvier.
 On the outside, the positive charges in the node of Ranvier flow to negative charges in the node of Ranvier,
creating local circuits.
 Impulses therefore, are transmitted along the membrane in form of local circuits from node to node
 Due to refractory period, impulse moves in one direction only from the active region (action potential) to the
resting region ahead and not behind the active region as this region is undergoing recovery/repolarization and
eventually hyper-polarization
 Due to presence of myelin sheath, there is saltatory conduction that causes faster conduction of impulses
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SYNAPSE
- A synapse is a junction where 2 neurones meet and consist of:
1. Part of the synaptic knob of the pre-synaptic neurone
2. Synaptic cleft/gap
3. Part of the post-synaptic neurone
- There are 2 types of synapses:

1) Electrical Synapse
 The synaptic cleft is about 2nm and the impulse can directly pass from neurone to neurone.
2) Chemical Synapse
 The synaptic cleft is about 20nm and the impulse cannot cross the gap and to do so a chemical or
Neurotransmitter is used. For example, a synapse whose neurotransmitter is acetylcholine is called
cholinergic synapse.
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FUNCTIONS OF SYNAPSE
1) Allows impulses to pass from one neurone to another

2) Ensures nerve impulse travels in one direction only. How?
- The synaptic vesicles containing neurotransmitter are only found in the pre-synaptic neurone. This
means that exocytosis of neurotransmitter can only happen in the pre-synaptic membrane
- The receptors for the neurotransmitter are only found in the post synaptic membrane. This means
that only the post synaptic membrane can be stimulated by the neurotransmitter causing
depolarization and action potential
3) Allows the next neurone to be either excited or inhibited
4) Information processing through summation and accommodation/fatigue;
a) Summation
 A process in the synapses that allows weak stimuli to generate post-synaptic action potential
by ensuring that enough neurotransmitter reach the receptor molecules on the post-synaptic
membrane
 This can happen in two different ways:
1) Spatial summation-
Each of the different synaptic knobs at synapses release small amount of
neurotransmitter at the same time so that enough is released at the synaptic cleft
to trigger post-synaptic action potential.
2) Temporal summation
Impulses from a single synaptic knob are received by the same synapse in quick succession.
This causes rapid and repeated release of enough neurotransmitters to trigger post-synaptic
action potential. These impulses, therefore facilitate/assist one another to be able to trigger
post-synaptic action potential
b) Synaptic fatigue
 The process by which a response is lost as all the neurotransmitter is discharged from the
vesicles of a synapse as a result of repeated stimulation. The response returns once vesicles
containing neurotransmitter are synthesized.
 This has two major roles:

1. Allows organisms to ignore repeated harmless stimuli so that the CNS does not
become overwhelmed with input.
2. Prevents the effectors from damage as a result of overstimulation due to constant
arrival of action potential in pre-synaptic knob.
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SYNAPTIC TRANSMISSION OF NERVE IMPULSE ACROSS CHEMICAL SYNAPSE
1) Action potential arrives in the synaptic knob of pre-synaptic neurone.

2) It causes the depolarization of the membrane causing Ca 2+ ion channels in the membrane to open.
3) Ca2+ ions enter the pre-synaptic knob.
4) Ca2+ ions cause synaptic vesicles containing the neurotransmitters to move and fuse with the pre-synaptic
membrane.
5) Neurotransmitters are released into the synaptic cleft by exocytosis and diffuse across the synaptic cleft.
6) Neurotransmitters bind with receptors on the post-synaptic membrane and cause Na + gates in the post-synaptic
membrane to open so that Na+ ions diffuse into the neurone.
7) The membrane depolarizes and if threshold stimulus is reached an action potential is initiated. This is called
excitatory post synaptic potential (EPSP).
8) After the action potential has been generated, the neurotransmitters are released from the receptors. They are taken
up across the pre- synaptic membrane either whole or after being broken down or they can diffuse away and be
broken down
NB:
In a cholinergic synapse the enzyme acetylcholinesterase breaks down acetylcholine into choline and acetate. In
the synaptic knob, choline combines with acetyl Co –A to form acetylcholine that are enclosed by vesicles in
readiness for another action potential.
POST-SYNAPTIC POTENTIALS
 Neurotransmitters can either cause excitatory post-synaptic potential (EPSP) or inhibitory post synaptic
potential (IPSP).
 Some neurotransmitters such as acetylcholine cause Excitatory post-synaptic potential (EPSP).
 Others are inhibitory, causing IPSP. Chloride ions flow into the neurone while K + ions diffuse outside i.e.
down their concentration gradients. In such a case more Na+ gates need to open to allow the diffusion of
more Na+ for depolarization to reach threshold stimulus in order to cause post-synaptic action potential.
EFFECTS OF DRUGS ON NERVE IMPULSE TRANSMISSION
Nicotine
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 Nicotinic acetylcholine receptors (cholinergic receptors) are receptors that respond to the neurotransmitter
acetylcholine and nicotine drug.
 Part of the nicotine molecule is similar in shape to acetylcholine (ACh) molecule and will fit into
nicotinic acetylcholine receptors on post synaptic membranes. The binding of nicotine molecules produces
similar effects to that of ACh molecules, initiating action potentials in the postsynaptic neurones or
muscle fibre.
 However nicotine has the following effects;
1. Nicotine is not broken down by enzymes and so remains in the receptors for longer than Ach and
this unnecessarily overwhelms the CNS.
2. A large dose of nicotine blocks the synaptic cleft and this can be can be fatal.
3. Nicotine stimulates many cholinergic neurons in the brain to increase the release of acetylcholine
that increases post synaptic action potentials that activate regions of the brain that deal with
cognition and attention and so, the two are enhanced.
4. Nicotine stimulates cholinergic neurons to increase the release of acetylcholine that increases post
synaptic action potentials that activate neurones in limbic system to release dopamine. This
dopamine generates post synaptic action potential that activates reward centers in the brain. This
reinforces the desire to use them again because it feels good and this is the basis of addiction.
NB
1. Nicotine is an agonist for acetylcholine, so amplifies the effect of acetylcholine, causing neurons
to fire more rapidly.
2. Unlike ACh, nicotine is not regulated by the body. While neurons typically release small amounts
of acetylcholine in a regulated manner, nicotine is not.
3. Not all ACh receptors are equally responsive to nicotine; those at neuromuscular junctions have
only a low affinity for nicotine.
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Lidocaine
 Lidocaine is an anesthetic drug, commonly used by dentists before drilling or removing a tooth
 Lidocaine molecules block voltage gated-sodium channels/sodium gates, preventing production of an

action potential in sensory neurons hence no feeling of pain.
Question
Pain is felt when nerve impulses travel along neurones to the pain centre in the brain.
Dentists inject an anaesthetic drug such as lidocaine into a patient’s gum to provide pain relief. This
anaesthetic drug works by binding to channel proteins in the axons of neurones. These neurones
normally transmit impulses that the brain interprets as pain. Explain how this anaesthetic drug prevents
the patient feeling pain (4)
 Most sodium gates are blocked.

 There is less diffusion of sodium ions into neurone
 There is less depolarisation that does not reach threshold stimulus
 Action potential is not generated ;
 No impulses reaches the pain centre in the brain.
Cobra Venom
 Cobra venom is a mixture of neurotoxins, one of which is α-cobratoxin.
 This toxin is a nicotinic acetylcholine receptor antagonist.
 It binds (blocks) reversibly to ACh receptors in post synaptic membranes and neuromuscular junctions
and prevents transmission of impulses across synapses including neuromuscular junctions between
motor neurons and muscles. Consequently muscles are not stimulated to contract and gradually the
person affected becomes paralyzed.
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 When the toxin reaches the muscles involved in breathing it causes death. However, in very low
concentrations it can relax the muscles of the trachea and bronchi in severe asthma attacks and so saves
lives.
The Nervous System
 The nervous system is divided into two systems:

1. The Central Nervous System (CNS) consists of the:
 Brain: The brain processes information and issues instructions to ensure full coordinated
responses.
 Spinal cord: Carries the neurones into and out of the brain and also coordinates many
reflex actions/ reflexes.
2. The Peripheral Nervous System (PNS) consists of:
 12 cranial nerves,
 31 pairs of spinal nerves.

 The PNS acts as the system of electrical wires that allows for communication between the
CNS and the body’s muscles and sensory receptors. They also control the automatic functions
of the bowel, bladder, respiratory (breathing), and heart function.
Spinal cord
 Impulses from sensory receptors travel along sensory neurons into the spinal cord through the dorsal
roots and then travel along sensory neurones up the spinal cord to the brain. Instructions from the brain
travel as impulses down motor neurones in the spinal cord and out in motor neurones through the ventral
roots to the effector organs.
 Spinal cord is also a coordination Centre for reflex responses
Reflexes
 A reflex is a rapid, involuntary response to a stimulus / rapid responses that occur without conscious
thought/ quick automatic response to a stimulus.
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 A reflex arc is the pathway traveled by the nerve impulses during a reflex.
 Most reflexes are spinal reflexes with pathways that traverse only the spinal cord. During a spinal reflex,
information may be transmitted to the brain, but it is the spinal cord, not the brain, that is responsible for
the integration of sensory information and a response transmitted to motor neurons. An example of
spinal reflex is hand withdrawal from a hot object.
 Some reflexes are cranial reflexes with pathways through cranial nerves and the brainstem. An example
of cranial reflex is pupil reflex
 Both reflexes involve parts of the CNS.
 Sensory neurons also transfer information to the conscious areas of the brain so that you know what has
happened.
NB:
- Reflex or reflex action is a quick and automatic response to stimulus. It passes along a reflex arc. Reflex
provides survival value to organisms through escape response to avoid further damage.
Spinal nerves
 A spinal nerve is a mixed nerve, which carries motor and sensory neurones between the spinal cord and the
body.
 In the human body there are 31 pairs of spinal nerves, one on each side of the vertebral column/ backbone/ spine.
 The spinal nerves are part of the peripheral nervous system.
 Near the spinal cord each spinal nerve branches into two roots:
1. Dorsal root: Carries sensory neurone that enters the spinal cord. The cell body of this sensory neurone lies
in a spinal ganglion that is outside the spinal cord.
2. Ventral root: Carries motor neurone out of spinal cord. The cell body of the motor neurone lies in the grey
matter of the spinal cord.
Cranial nerves
 Cranial nerves are the nerves that emerge directly from the brain (including the brainstem).
 There are 12 pairs of cranial nerves.
 Cranial nerves relay information between the brain and parts of the body
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SPINAL REFLEX
➢ A stimulus such as heat is received by a sensory receptor; for example, heat receptors in the skin.
➢ The sensory receptor such as the heat receptor produces an impulse.
➢ An impulse travels along the sensory neuron, the spinal nerve, the dorsal root that consists of
dorsal root ganglion into the white matter and then grey matter of the spinal cord. It synapses with
a relay neurone which then synapses with a motor neuron within the grey matter.
➢ The impulse passes along the motor neurone, leaving the spinal cord through the ventral root. It
then travels to an effector organ, which is often a muscle.
➢ The motor end plate in the muscle transfers the stimulus to the muscle which then contracts,
moving the body part away from danger e.g. heat. This is response.
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N.B. Not all reflex arcs have relay neurons. For example, knee-jerk reflex that involves contraction of quadriceps does not
have relay neuron but the ones involving contraction of the hamstring have the relay neuron.
Pupil reflex (How pupils dilate and contract to control the amount of light entering the eye)
The basic principle of the pupil reflex involves the following stages:
Bright light.
➢ Bright light falls on the sensory cells of the retina and produce more nerve impulses.
➢ The impulse travels along sensory neurons in the optic nerve to the control centre in the midbrain.
➢ The impulse then travels along two neurons to further control centres (visual cortex).
➢ In the visual cortex, the brain then initiates motor impulse that is transmitted by parasympathetic motor
neurone/ the oculomotor to the circular muscles in the iris which respond by contracting while the radial
muscles relax. This reduces the size of the pupil so that less light is admitted into the eye to prevent the
damage to the retina.
Dim Light.
➢ Dim light falls on the sensory cells of the retina and produce fewer nerve impulses.
➢ The impulse travels along sensory neurons in the optic nerve to the control centre in the midbrain.
➢ The impulse then travels along two neurons to further control centres (visual cortex).
➢ In the visual cortex, the brain initiates motor impulse that is transmitted by sympathetic motor neurone/
the oculomotor to the radial muscles in the iris which respond by contracting while the circular muscles
relax. This increases the size of the pupil so that more light is admitted into the eye to see in dim light.
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Vision
- Receptors are specialized cells that are able to detect stimuli.
- Receptors are usually grouped together in sense organs.
Human photoreceptors
- Human eyes have 2 types of photoreceptor cells found in the retina at the back of the eye.
- Cones allow colour vision in bright light and are clustered in the fovea (yellow spot) of the retina.
- Rods provide black and white vision but are much more sensitive than cones and can work in dim light conditions.
Rods are spread throughout the retina.
- Blind spot neither has cones nor rods.
The eye has 3 layers. These are;
a) Sclera
- outer most
- tough membrane
b) Choroid
- Prevents internal reflection of light
c) Retina
- Layer of rods and cones hence it is called photosensitive layer.
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THE RETINA
 Has 3 layers;
1. Outermost layer (photosensitive layer)
i. Consists of rods and cones.
ii. It is partly embedded in the choroid.
2. Middle layer
i. With bipolar neurones.
3. Inner layer
i. Ganglion cells whose axons form optic nerve.
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Structure of Rod cells
- These are cells in the outermost layer of the retina that are rod shaped.
- They are distributed throughout the retina but are absent from fovea (yellow spot) and blind spot.
- The rod cell is divided into 3 parts;
a) Outer segment
- Contains lamella that contains a visual pigment known as rhodopsin.
b) The narrow region (constriction)

- Connects outer segment with inner segment and contains;
(i) Cytoplasm
(ii) A pair of cilia
c) The inner segment
- Contains;
(i) Nucleus that controls activity of rod cell.
(ii) Mitochondria that provides energy for re-synthesis of rhodopsin
(iii) Polysomes – centre for synthesis of protein that is needed for production of rhodopsin and lamella.
(iv) Sodium pumps in the membrane that move out Na+.
Rhodopsin
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- This is a visual pigment in the lamellae of the outer segment of the rod cells.
- It is also called ‘visual purple’.
- Rhodopsin consist of two compounds;
a) Opsin – A protein
b) Retinal – a light absorbing compound derivative of vitamin A.
- Retinal exists in isomers i.e. cis and trans isomers.
- When exposed to light cis isomer is converted to trans isomer.
Differences between rod cells and other neurones

(i) At resting state, the outer segment is highly permeable to Na +, unlike other neurones. Na + flow into the cell
and the resting potential is -40mV and not -70mV.
(ii) When resting, they secrete a neurotransmitter called glutamate that diffuses across the synaptic cleft between
the rod cell and a bipolar cell neurone. This neurotransmitter inhibits the bipolar neurone from becoming
depolarized.
Summary
- In the dark, rod cells remain slightly depolarized because Na gates are open and continuously release the inhibitory
neurotransmitter called glutamate.
- Rod cell consist of lamella in its outer segment. These lamellae contain a pigment called rhodopsin.
- Rhodopsin consists of opsin (protein) and cis-retinal.
- When rhodopsin is exposed to light it breaks down or bleaches into opsin (protein) and trans-retinal.
- Photoreceptors in mammals are specialized cells (rods and cones) while in plants are chemicals like phytochrome.
Question
Describe how rhodopsin generates nerve impulse?
- Rhodopsin is made up of cis retinal and the protein opsin.
- When rhodopsin absorbs light energy, it bleaches/splits into trans retinal and opsin.
- The protein interacts with the other proteins in the CSM of the outer segment, closing the Na + gates. At the same time
sodium pump in the inner segment continuously and excessively pumps out Na + leading to hyperpolarization
(generator potential) in the rod cell which stops the release of glutamate so that there is depolarization in the bipolar
cell and action potential (impulse) in the ganglion cells. The action potential/impulse is carried to the brain by the optic
nerve/sensory neurone for interpretation.
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Due to hyperpolarization, there is inhibition of glutamate to the bipolar cells. This causes more Na ions to flow into the
bipolar cells and causes depolarization. However, this depolarization only reaches -55mV which is graded potential. This
is lower than the threshold stimulus hence action potential cannot be generated in the bipolar cells. The graded potential
produced from the bipolar cells causes it to release neurotransmitters that bind to the receptors on the ganglion cells. This
causes more Na gates to open in the ganglion that causes depolarization, threshold stimulus and action potential/ nerve
impulse.
NB
- Rhodopsin is very sensitive to bright light and so rods are mainly used in dim light for white and black vision.
- In bright light, rhodopsin is broken down quicker than it can be reformed.
- In dim light, production of rhodopsin is able to keep pace with the slow rate of breakdown.
- So, the overall function of rods is vision in poor light.
Light adaptation of the eye

 In normal daylight, almost all rods are bleached and cannot respond to low level or intensity of light and the eye is
said to be light –adapted.
Dark adaption of the eye
If one moves from bright light into a dark room the following takes place;
 Opsin uncouples from the cell surface membrane of the outer segment of the rod cell
 Trans retinal converts to cis retinal
 Reformation of rhodopsin from opsin and cis retinal takes place
 After about 30 minutes in the dark, almost all rhodopsin are entirely reformed form the
opsin and cis retinal and the eye is fully sensitive to light of low intensity and the eye is
said to be dark adapted
 Permeability of the cell surface membrane to Na+ increases/partial depolarisation
 Hyperpolarization of cell decreases
 More neurotransmitter (glutamate) is released hence bipolar neurone is not depolarized.
- If one moves from bright light into a dark room, it takes time before one can see what is in the room.
- This is the time when the re-synthesis of rhodopsin (that is normally broken down in bright light) takes place.
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Visual acuity
- It is the ability of the eye to see 2 points as separate points (resolution) i.e. the ability to see fine details.
- Cone cells have greater visual acuity than rod cells because each cone synapses with one bipolar cell and the
information is sent separately to the brain giving more accurate images and other details. This means that there is no
convergence of information or pooling of information carried by cones.
- However, several rods synapse with one bipolar cell (diffused bipolar cell) or neurone giving rise to synaptic
convergence (pooling of information) at the diffused bipolar cells. The brain receives a mixture of information and
therefore the brain gives less accurate images and other details.
Question;
Draw the structure of the retina and using arrows indicate;
1) Movement of light: from ganglion cell towards rods and cones
2) Movement of impulse: from rods and cones towards ganglion cells
3) Position of rhodopsin: in the lamella in the outer segment of rod cell.
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Detection of light by plants
Plants respond to:
(i) Direction from which light comes – phototropism.
(ii) Intensity of light.
(iii) Ratio of light to dark over a 24 hour period (photoperiodism)
(iv) Wavelength of light
Light affects plants as follows;

(i) Growth of plants
(ii) Direction of growth of plants
(iii) Reproduction of plants
(iv) Flowering of plants
(v) Germination of seeds
Photoperiodism
- Photoperiod is the ratio of light to dark over a 24 hour period.
- Plants respond to photoperiodism through flowering and seed germination.
- So, flowering and seed germination are photoperiodic responses.
- The photoreceptor (sensory receptor) which responds to photoperiodism is a pigment called phytochrome.
- Phytochrome is mainly found in the leaves, seeds, buds among others.
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Phytochrome
- Is a small conjugated protein.
- It is mainly found in the leaves, seeds and buds.
- It enables plants to respond to the ratio of light to dark over a 24 hour period (photoperiodism).
- It exists in 2 interconvertible forms;
(i) Phytochrome red /Pr / P660 - blue in colour
(ii) Phytochrome far red /Pfr / P730 - blue green in colour
- The conversion from one form to another is due to absorption of red light, far red light, and the presence of
darkness.
- Phytochrome, when produced is blue in colour.
- This blue phytochrome is able to absorb red light at 660nm hence it is called Pr/P660. When it absorbs red light, it
is immediately converted to blue-green pigment (phytochrome). This blue-green phytochrome is able to absorb far
red light at 730nm hence it is called Pfr/P730. When it absorbs far red light, it is immediately converted to blue
pigment (phytochrome).
The speed of conversion of Pr to Pfr or Pfr to Pr depends on:

(i) Light intensity
 In lower light intensity the conversion is slow where it takes minutes but in higher light intensity
the conversion is faster where it takes seconds.
(ii) Darkness
 In the dark, there is slow conversion of Pfr to Pr.
- Pr (blue pigment containing far red light) is more stable but not biologically active as it has a lot of far red.
- Pfr (blue-green pigment containing red light) is less stable and that is why in the dark, it is slowly converted to Pr
and when exposed to far red light, it is immediately converted to Pr. However, it is biologically active as it has a
lot of red light (which is biologically active).
- Red light and far red light are antagonistic in their actions.
- As normal sunlight contains more red light than far red light, then most pigments in the day are Pfr (blue-green).
- In the night /dark, before sunrise, there is more Pr because there is slow conversion of Pfr to Pr in the dark. In
addition, enzymes break down the Pfr in the dark.
How photoperiodism controls flowering.

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- Critical period /threshold is the minimum length of darkness needed to stimulate flowering. If critical period is not
reached, there will be no flowering.
- Phytochrome and florigen (a hormone that controls flowering) are found in leaf cells.
- Florigen is made in response to the ratio of Pfr to Pr in leaf cells. It travels to the flower buds (cells in shoot apex)
to stimulate flowering (to open the flower buds).
- Plants flower as a result of ratio of darkness and light and therefore based on this ratio plants can be;
1) Long day plants (LDPs)
2) Short day plants (SDPs)
3) Day neutral Plants (DNPs)
Long day plants (LDPs)
- They flower when the period of uninterrupted darkness is less than 12 hours.
- Due to short hours of darkness, only few Pfr are converted to Pr. This great ratio of Pfr to Pr triggers leaf cells to
produce florigen which travels to flower buds to cause flowering in LDPs. Hence they successfully flower in
summer. A flash of red light in the middle of the dark period triggers flowering even if it is a long night. Examples
include barley, spinach and wheat.
Short day plants (SDPs)

- They flower when the period of uninterrupted darkness is more than 12 hours.
- Due to long hours of darkness most Pfr are converted Pr. This great ratio of Pr to Pfr triggers leaf cells to produce
florigen that travels to flower buds to cause flowering in SDPs. Hence they successfully flower in autumn and
spring. A flash of red light in the middle of the dark period negates the effect of the dark period and reduces or
stops flowering. Examples include tobacco plants.
Day neutral plants (DNPs)

- Flowering is not controlled by photoperiodism (phytochrome).
How photoperiodism controls seed germination.

- Some seeds such as lettuce seeds germinate if exposed to a flash of red light.
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- If exposed to a flash of red light followed by a flash of far red light, they will not germinate.
- With a series of flashes of light, it is the colour (wavelength) of the final flash which determines whether or not the
seeds will germinate.
- It is the phytochrome that reacts with red and far red light to either cause or inhibit germination.
- It is the biologically active Pfr (with red light) which causes germination and Pr (far red) that inhibits germination.
Question-
Describe the mechanism that prevents lettuce seeds from germinating in the dark.
In the dark there is no red light to be absorbed to form Pfr that would stimulate germination. Any Pfr present is
converted back to Pr which inhibits germination.
PHOTOTROPISM
- This is the growth movement of parts of plants in response to unilateral light.
- Light is the stimulus.
- In presence of unilateral light, the shoot of plant bends towards the light (positive phototropism) and the roots if
exposed, will grow away from light (negative phototropism).
- Shoots are said to be positively phototropic and roots negatively phototropic.
- Positive phototropism by shoots enables;
(i) Photosynthesis to take place.
(ii) Pollination to take place.
- Negative phototropism by roots enables;

(i) The plant to anchor firmly in the soil.
(ii) The plant to absorb water.
(iii) The plant to absorb minerals.
To describe the role of auxins in positive phototropism

- Auxins are plant growth regulators.
- The first auxin to be discovered was indoleacetic acid (IAA)
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- Auxins are synthesized in the meristem cells in the tip of the shoot i.e. zone of cell division and diffuse back to the
zone of cell elongation, where they cause the cells to elongate hence growth.
- With illumination (light) from all sides auxins move down from the shoot tip and cause elongation of cells across
the zone of elongation, causing plant to grow upwards.
- With illumination from one side (unilateral light), auxins laterally diffuse from the lighted side to the shaded/dark
side of the zone of cell elongation of the shoot. This causes those cells in the dark side to elongate, hence more
growth in the dark side than lighted side. This causes the shoot to bend towards the light i.e. positive phototropism.
NB.
Light does not destroy auxins. Instead, it causes redistribution of auxins from lighted side to shaded side of region
of cell elongation.
TO EXPLAIN THE ROLE OF IAA IN POSITIVE PHOTOTROPISM
 Unilateral light causes IAA in the region of cell elongation to diffuse laterally from the lighted side to the
darker/shaded side of the region of cell elongation.
 IAA molecules bind to their receptors in CSM of cells in this region of cell elongation .This activates the proton
pump in the CSM so that it moves H+ into the cell wall, lowering the pH in the cell wall. This low pH activates
enzymes that break down the hydrogen bonds between adjacent cellulose microfibrils making the cell wall
flexible or soft.
 The cell absorbs water by osmosis causing the cell to elongate.
 As the cells mature, the enzymes destroy IAA, raising the pH in the cell wall. This pH causes the reformation
of hydrogen bonds. This causes the cell wall to become more rigid and the cell cannot expand any more.
 Due to more IAA in the shaded/darker side, there is more cell elongation hence more growth and the shoot bends
towards light. This is positive phototropism.
Describe the role of gibberellins in stem elongation.
 It is present in high concentrations in young leaves, stems and seeds although it is in most parts of the
plant.
 The height of some plants is partly controlled by their genes.
 The dominant allele of the gene (Le) codes for the synthesis of an enzyme that catalyzes the
synthesis of an active form of gibberellin, GA (gibberellic acid) that stimulates cell division & cell
elongation in the stem, so causing the plant to grow tall. This is stem elongation. The recessive allele,
le, codes for a non-functional enzyme.
Describe the role of gibberellins in the germination of barley seeds.
 Barley seed is dormant / metabolically inactive

 Seed absorbs water
 Water stimulates embryo to produce gibberellin
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 Gibberellin diffuses to aleurone layer to stimulate it to carryout protein synthesis to produce amylase. Gibberellin
do this by triggering transcription of a gene to get mRNA that codes for amylase
 Amylase hydrolyses starch in endosperm to maltose
 Maltose diffuses into embryo and is hydrolyzed to glucose by maltase for respiration to get energy used for
germination of the seed.
Questions
1. List 2 similarities between chemical and electrical co-ordination.

 Have receptors
 Involve chemical: neurotransmitters and plant growth regulators such as auxins and hormones in animals.
2. List differences between chemical (hormone) and nervous (electrical) co-ordination
Nervous Hormones
- Involves electricals/impulses - Involves chemicals, called hormones
- Transported along neurones - Transported in blood
- Has short term effect - Has long term effect e.g. growth hormone
- Affects a smaller area - Affects many parts e.g. adrenaline
- Its transport is faster - Its transport is slower
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Compare photoreception in mammals with that in plants
1. Both involve light sensitive pigments: rods and cones in mammals and phytochromes in flowering plants.
2. Both involve conversion of pigment from one type/form to another. Phytochromes are converted from blue to
blue-green and vice versa. Rhodopsin to opsin and trans-retinal.
3. In plants, activation of phytochrome leads to production of chemical signal/hormone e.g. florigen; while activation
of rhodopsin and iodopsin (Pigment in the cone) leads to production of electrical signal/nerve impulse.
Give three similarities between IAA and animal hormones.
Both are
1. chemicals
2. produced in cells
3. move away from site of production
Auxins can be used to kill unwanted plants such as weeds growing in grass.
The auxin stimulates the weeds to grow rapidly. Suggest an explanation for how auxins
stimulate the weeds to grow rapidly but not the grass.
Weeds take up more auxins; auxin/IAA causes cell elongation, a form of growth ;
The response of the coleoptile occurs because IAA (auxin) binds to membrane
receptors. This promotes the active transport of hydrogen ions out of the cell
cytoplasm.
(i) Explain what is meant by the term active transport. (2)
movement of molecules against a
concentration gradient ; using ATP
(ii) Hydrogen ions provide the optimum pH for enzymes that break the bonds
between adjacent cellulose microfibrils. Name the bonds that are broken by these enzymes.
Hydrogen
(iii) Suggest what happens to cells in the coleoptile, after the breaking of these
bonds, that allows the response to light from one direction. (2)
Cell wall becomes flexible and soft; cells absorb water; by osmosis; cells elongate
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The Human Brain
 The human brain has the following functions:

1) Receives impulses or information from the receptors in the sense organs via the sensory
neurones.
2) Interprets or co-ordinates that information.
3) Initiates the impulses that are transmitted to the effectors i.e. muscles and glands via motor
neurones.
 The major parts of the brain are:
a) Cerebrum/cerebral hemispheres/cerebral cortex – in the fore brain
b) Hypothalamus – in the fore brain
c) Cerebellum – in the hind brain
d) Medulla Oblongata – in the hind brain
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W cerebrum/cerebral cortex
X hypothalamus
Y medulla
Z Cerebellum
a) THE CEREBRUM
- It is located at the fore brain (at the front of the brain).
- It is the largest part of the brain in the mammal.
- It is divided into 2 cerebral hemispheres connected by a structure called the corpus callosum (a band like
structure that connects the left and right part of the brain).
- The major functions of cerebrum are:
 Ability to see
 Ability to think
 Ability to learn
 Feel emotions
 Memory
 Intelligence
 Personality
 Language
 Speech
 Imagination
 Reasoning ability
 Acquired skills
 Initiates muscle contraction
- Cerebrum is divided into 4 major parts:

a) Frontal Lobe (higher centers of the brain)=
Co-ordinates thinking among other things.
b) Parietal Lobe=
Co-ordinates calculations among other things.
c) Occipital Lobe (Visual Cortex)=
Coordinates visual information from the eye.
d) Temporal lobe=
Coordinates auditory information from ears.
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b) HYPOTHALAMUS
- It is located at the forebrain, above the pituitary gland.
- It has the following functions:

 Co-ordinates thermoregulation i.e. controls body temperature.
 Co-ordinates Osmoregulation i.e. controls water balance.
 Controls pituitary gland
 Controls drinking and feeding
 Controls aggression
 Controls awakeness and sleepiness.
c) PITUITARY GLAND
- It is located at the forebrain, below hypothalamus
- Pituitary gland has anterior lobe and posterior lobe.
- It is mainly under the control of hypothalamus. Hypothalamus contains nerve cells called neurosecretory
cells. There are two types of neurosecretory cells:
1. Neurosecretory cells 1: They produce two types of substances:
(a) Releasing factors that stimulate the release of hormones from anterior
pituitary.
(b) Release-inhibiting factors that inhibit the release of hormones from
anterior pituitary.
2. Neurosecretory cells 2: They produce secretions that are stored in the posterior pituitary and
released later as hormones
- Under the control of hypothalamus the pituitary gland produces 6 hormones from the anterior lobe such
as LH and FSH and 2 from posterior lobe and these are ADH and oxytocin
d) CEREBELLUM
- It is located at the hind brain (back of the brain).
- It is leaf shaped
- It has the following functions:

 Co-ordinates fine movements (co-ordinates muscle movement)
 Co-ordinates balance
 Co-ordinates posture
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e) MEDULLA OBLONGATA
- It is located at the hind brain (back of the brain) – at the top of spinal cord.
- It controls or co-ordinates:
 Heart rate = In the cardiovascular control centre (CVCC)
 Breathing rate = In the breathing centre
 Blood pressure
 Sneezing
 Vomiting
 Coughing
EFFECTS OF IMBALANCES IN BRAIN CHEMICALS
- These brain chemicals include the following neurotransmitters:

1) Dopamine
2) Serotonin
3) Noradrenaline
- 2 major conditions that are as a result of imbalances in these brain chemicals are:
1) Parkinson’s disease
2) Clinical depression
PARKINSON’S DISEASE
- This is a disorder of the CNS that causes lack of control of skeletal muscles by the motor cortex in the brain.
Motor cortex controls muscular movement.
- This is because of the death of dopamine-secreting neurones in the basal ganglia or substantia nigra in the
mid-brain.
- These neurones usually release dopamine in the motor cortex in the forebrain that generates impulse that is
transmitted to the skeletal muscles via motor neurone.
- Due to reduction in the production of dopamine, motor cortex gradually loses motor control of the skeletal
muscles.
- Dopamine is associated with:
1) Control of movement
2) Emotional responses
- The symptoms of Parkinson’s disease are :
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1) Stiffness of muscle movement
2) Tremors of muscles
3) Slowness of movement
4) Poor balance
5) Walking problems
6) Difficulties in speech
7) Difficulties in breathing
8) Depression: This is because of 3 reasons:
 Dopamine is active in part of the brain that deals with emotions
 The symptoms of the disease cause depression
 The knowledge that it is terminal: no cure
TREATMENTS FOR PARKINSON’S DISEASE
- The drugs involved in treatment include:

1) Levodopa (L-dopa)
 Dopamine itself cannot be used to treat Parkinson’s disease because it cannot cross into the brain from
the bloodstream (blood-brain barrier). So, a precursor of dopamine called L-dopa is taken instead.
 L-dopa is a precursor in the manufacture of dopamine. L-Dopa crosses the blood-brain barrier and
enters the brain. It is converted into dopamine and binds to dopamine receptors in the post-synaptic
neuron and generates impulse that restores motor control of the skeletal muscles and also control
emotions.
2) Dopamine Agonists
 They mimic the role of dopamine in the brain and therefore bind to dopamine receptors on the post-
synaptic membrane in the synapse to trigger post-synaptic potential.
3) Monoamine Oxidase B inhibitors (MAOB Inhibitors)
 MAOB breaks down dopamine in the brain synapse.
 So, MAOB inhibitors are drugs that inhibit this enzyme so that dopamine is not destroyed.
 Selegiline is a MAOB inhibitor.
CLINICAL DEPRESSION
- This is the prolonged feeling of sadness, anxiety, hopelessness, loss of interest, restlessness, helplessness and
insomnia.
- A lack of serotonin has been linked to clinical depression.
- Serotonin plays an important role in determining a person’s mood.
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- Neurones that secrete serotonin are situated in the brain stem (Mid-brain, pons and Medulla and is continuous
with spinal cord) whose axons spread to cerebrum, cerebellum and spinal cord.
- In addition to serotonin, noradrenaline and dopamine also play part in depression.
- Sometimes depression is triggered by external factors e.g.

1) Work
2) Relationship
3) Bereavement (death of family member)
- A gene 5-HTT codes for re-uptake protein (monoamine transporter protein) that transports serotonin from the
synaptic cleft to the presynaptic neuron.
DRUG TREATMENTS FOR DEPRESSION

1) Selective Serotonin Re-uptake Inhibitor (SSRI)
 It inhibits the re-uptake protein so that serotonin remains in the synaptic cleft to trigger post synaptic potential
that lifts the mood.
An example of SSRI is Prozac. It gradually restores serotonin to the normal level and maintains it.
NB:
A drug called ecstasy (MDMA) 3,4-methylenedioxy-N-methylamphetamine)) works like
prozac. However, it is not medically recommended because it gives a sudden excess of
serotonin which gives an elevated mood which lasts for several hours.
2) Tricyclic antidepressants (TCAs)
They increase levels of serotonin and noradrenaline in the brain.
3) MAOB Inhibitors
They inhibit the enzymes that break down serotonin (also dopamine) in the synapse of the brain.
Cocaine is a drug that inhibits the uptake of dopamine by the presynaptic neurone. Suggest how cocaine can
help a person to have an increased sense of pleasure. (3)
 Cocaine binds to the re-uptake channel / re-uptake protein

 Dopamine remains in synaptic cleft
 Dopamine binds to receptors in postsynaptic membrane causing depolarization, and if
threshold stimulus is achieved, action potentials / impulses in postsynaptic neurone are
generated that enter the pleasure centre
Brain Imaging
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Brain imaging are methods that allow neuroscientists to see inside the living brain. These methods help neuroscientists:
Understand the relationships between specific areas of the brain and what function they serve.
Locate the areas of the brain that are affected by neurological disorders.
Develop new strategies to treat brain disorders.
 Several imaging techniques are useful for medical diagnosis and investigating brain structure and function.
Computerized Axial Tomography (CT and CAT) Scan
 Was developed to overcome the limitations of X-rays (X-rays was using broad beam X-rays on bones only)
 CAT can be used in soft tissues.
 CT scans use narrow beam X-rays rotated around the patient to pass through the tissues from different angles.
 The narrow beam X-rays are detected by the brain tissue which sends out information to the computer which analysis
this information and produce an image of different soft tissues in the brain on the computer screen.
 CT scan is used to:
a) Detect brain disease.
b) Monitor the progress of illness of the tissues of the brain.
 The advantages of CT scan over X-ray are:

1. Can image soft tissues.
2. Greater resolution than X-ray.
 The disadvantages of CT scan are:

i. Use of x-rays that are harmful as they can cause mutations.
ii. Limited resolution as compared to MRI and fMRI hence small structures cannot be distinguished.
iii. CT scans give only still pictures hence are used to look at damaged structures in the brain and not the functions
of those parts of the brain.
Magnetic Resonance Imaging (MRI) Scans
 This imaging technique uses magnetic field and radio waves to detect soft tissues.
 Radio waves are put in a strong magnetic field
 It is based on the absorption of radio waves by water molecules in tissues and these water molecules transmit the radio
waves to the computer to be analyzed and produce an image on the computer screen.
 MRI Scans can be used as follows:
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a) In the diagnosis of tumours, strokes, brain injuries and infections.
b) To track/monitor degenerative diseases like Alzheeimers by comparing scans over a period of time.
 A brain image from MRI e.g. a tumour gives 5 pieces of information;
a) Locality of tumour
b) Size of tumour
c) Type of tumour
d) The brain function that has been affected by that tumour
e) The blood vessel supplying the tumour
 The advantages of MRI scans are:

1. No use of X-ray hence no mutations.
2. Greater resolution than CT scan.
 The disadvantage of MRI scans is:
MRI scans give only still pictures hence are used to look at damaged brain structures and not at functions.
Functional MRI (fMRI)

 It is a modified MRI scan that uses radio waves and magnetic field.
 The fMRI allows one to observe different areas of the brain in action while people perform different
tasks such as eating chocolate.
 The basis of fMRI scanning is monitoring the absorption of oxygen (movement of oxygenated blood)
in different brain areas.
 How fMRI is used in brain imaging:
(i) There is an increased supply of oxygenated blood (oxygen) to the active areas. This increased
activity could be due to a tumour or the part is involved in a task such when eating chocolate.
(ii) The area does not absorb fMRI signals/radio waves hence reflect them.
(iii) The area is seen as white (or the area lights up or it shows a different colour) hence can compare
with other areas.
 The fMRI can produce up to 4 images per second, so the technique can be used to follow the sequence of
events over quite short time periods.
 The advantages of fMRI scans are:
(i) No use of X-rays hence no mutations.
(ii) Greater resolution than CT scan.
(iii) It looks at the brain functions/activities.
 The disadvantage of fMRI; Very expensive.
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Positron Emission Tomography (PET) scans
 PET scans are produced by detecting the radiation given off by a radiotracer (radioactive isotope)
injected into a patient.
 Computer analysis shows areas in which the radiotracer builds up forming a detailed 3D images of the
inside of the body, including the brain.
Radiotracer is any radioactive isotope (isotope is an atom of the same element with the same number of protons but
a different number of neutrons; radioactive substance is a substance that emits radiation) introduced into the body
to study metabolic processes.
 PET scans have two major roles:
1. Reveal abnormal areas in the body
2. Show how different areas of the brain are actually working.
 The greatest advantage of PET scans is that they can show how parts of your brain are actually working.
 To produce a PET scan;
 The patient is injected with a radiotracer (radioactive isotope) which is similar to glucose so
that it is treated like glucose by the body and so just like glucose it is carried to all the cells.
 The scanner detects the radiation which the radiotracer gives off and the computer system
analyses where it accumulates and where it does not. For example, cancer cells absorb more
radiotracers than normal cells and therefore PET scan clearly shows cancerous cells. In
addition, areas of the brain that are less active than normal e.g. areas that have died as a result
of diseases such as Alzheimers, which causes dementia, absorb less radiotracer than expected.
Learning and habituation

 Learning is a process that causes behavioral change as a result of experience of new situations.
 For learning to be effective, you must remember what you have learnt.
 Memories are formed by changing or making new synapses in the nervous system.
 Several types of learned behaviour are recognised, including habituation.
Habituation
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 Habituation is a type of learning that involves reduced response to a repeated harmless stimulus.
 It allows animals to ignore unimportant stimuli so that they can concentrate on more rewarding or threatening
stimuli.
 Habituation becomes effective if:
1. The stimulus is repeated.
2. The repeated stimulus is the same and done at regular intervals.
Understanding habituation using sea slugs (Aplysia)
 Aplysia breathes using a gill found in a cavity on the upper side of the body
 In this cavity, water passes through and is expelled through a siphon tube at one end.
 If the siphon is touched by water, the whole gill is withdrawn into the body cavity as a defense mechanism.
 However, because the sea slug lives in the sea, the movement of the water constantly stimulates the siphon and
therefore the animal learns by habituation not to withdraw its gill every time a wave touches it.
Description of habituation in sea slugs
With repeated waves (stimulus) on the siphon, the time period the gills remain withdrawn keep reducing and
eventually the gills will not withdraw even if there is a stimulus.
Explanation of habituation in sea slugs.
 With repeated stimulation of the siphon, Ca2+ channels in the membrane of pre-synaptic knob of the pre-
synaptic neurone become less responsive, so that less Ca2+ enter the pre-synaptic knob.
 This causes little neurotransmitter to be released into synaptic cleft
 Only few neurotransmitters bind to receptors on post synaptic membrane, so that less sodium ions diffuse
into the neurone.
 This causes depolarisation that does not reach threshold stimulus hence action potential is not triggered in the
post-synaptic neurone (motor neurone).
 The gill muscles do not receive the impulse hence they do not withdraw.
EXPERIMENT USING SEA SLUG TO EXPLAIN HOW HABITUATION OCCURS

A. Sea slugs used in habituation experiment need to have been reared in captivity rather than in the sea. This is
because sea slugs raised in the sea have already habituated due to water currents and tidal changes in the sea.
B. Gill withdraws when siphon is stimulated by water jet. Jet of water is a stimulus. Siphon has pressure receptors
which generate impulse that is carried by sensory neurone to the CNS and then carried by the motor neurone to
the gill muscle that contracts and the gill withdraws. Withdraw of gills is the response. After several minutes of
repeated stimulation of the siphon, the gill no longer withdraws. This is habituation.
Description of habituation in sea slugs in the laborary

With repeated water jet (stimulus) directed on the siphon, the time period the gills remain withdrawn keep
reducing and eventually the gills will not withdraw even if there is a stimulus.
What causes the withdraw of gills.

 Stimulus (currents, tidal waves or water jet) causes pressure receptors in the siphon tube to generate
impulse (action potential)
 Action potential arrives in the pre-synaptic knob of pre-synaptic neurone.
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 It causes the depolarization of the membrane and Ca 2+ ion channels open in the membrane. Ca2+ ions
enter the neurone.
 Ca2+ ions cause synaptic vesicles containing the neurotransmitter to move and fuse with the pre-synaptic
membrane.
 Neurotransmitter is released into the synaptic cleft by exocytosis and diffuses across the synaptic cleft.
 Neurotransmitter binds on to receptors on the post-synaptic membrane and causes Na + channels to open.
This causes Na+ ion to flow in or diffuse into the neurone.
 The membrane depolarizes and if threshold stimulus is reached an action potential is initiated –
excitatory post synaptic potential (E.P.S.P)
 After action potential the neurotransmitter are released from the receptors and will be taken up across the
pre- synaptic membrane (whole or after being broken down) or it can diffuse away and be broken down
How habituation is achieved.

 With repeated stimulation, Ca2+ channels in the pre-synaptic knob become less responsive so that less
Ca2+ crosses the pre-synaptic membrane.
 Less neurotransmitter is released.
 There is less depolarization of the postsynaptic membrane so no action potential triggered in the motor
neurone.
Description of habituation in sea slugs
With repeated water jet (stimulus) directed on the siphon, the time period the gills remain withdrawn keep
reducing and eventually the gills will not withdraw even if there is a stimulus.
Explanation of habituation in sea slugs.
 With repeated stimulation of the siphon, Ca2+ channels in the membrane of pre-synaptic knob of the pre-
synaptic neurone becomes less responsive, so that less Ca2+ enter the pre-synaptic knob.
 This causes little neurotransmitter to be released into synaptic cleft
 Only few neurotransmitters bind to receptors on post synaptic membrane, so that less sodium ions diffuse
into the neurone.
 This causes depolarisation that does not reach threshold stimulus hence action potential is not triggered in the
post-synaptic neurone (motor neurone).
 The gill muscles do not receive the impulse hence they do not withdraw.
Investigating habituation using land snails

 It measures the time a snail remains withdrawn into its shell when you tap the surface it is moving on at a regular
time interval or gently touch the snail’s head.
 Initially the snail tends to remain into its shell for a significant period of time after each tap.
 As tapping continues the snail stays in its shell for a shorter duration as it becomes habituated to the taping.
Lab Experiment on habituation using snails
Purpose:
 To investigate habituation of snails to a stimulus
Touching snails
 Lots of people, at some time of their childhood, will have touched a snail in the garden and noticed that it
withdraws its eye stalks into its body.
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 For such a slow moving animal this seems very quick response, this suggests it is an important response for
protection and survival.
 A snail only withdraws into its shell when it is either inactive or threatened.
 When touched, it withdraws to avoid danger.
 Do snails become habituated to a stimulus, ceasing to withdraw with repeated stimulation?
 In this investigation you will collect data to find out if habituation to a touch stimulus does occur in these
organisms.
Safety
 Wash your hands thoroughly after touching the snails.
 All the equipment used must be disinfected.
 Take care that the stimulus causes no harm to the snails.
You will need:

 One giant African land snail (or a garden snail if not available)
 One dampened cotton wool bud
 Suitable clean, firm surface for the snails (e.g. a plastic chopping board)
 Stopwatch.
Procedure:
1. Collect one giant African land snail, and place it on a clean, firm surface.
2. Allow the snail to get used to (acclimatize) its new surroundings for a few minutes until it has fully emerged from
its shell.
3. Use a wet cotton wool bud
4. Using the wet cotton wool bud firmly touch the snail between eye stalks and immediately start the stopwatch.
5. Measure the length of time between the touch and the snail being fully emerged from its shell once again, with its
eye stalks fully extended. This is the time it remains withdrawn.
6. Repeat the procedure in Step 3 for a total of 10 touches, timing how long the snail takes to re-emerge each time
7. Record your results in a suitable table.
Touch No. Time withdrawn/minutes.
10
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8. Present your results in an appropriate graph.
The appropriate graph is scatter which is associated with correlation. This is negative correlation.
Questions:
1. Write your hypothesis, which this experiment will test.

2. Using your graph, state if you think there is a positive, negative, or no, correlation between the number of
stimulations and the time for eye stalk withdrawal.
3. Explain any patterns or trends in your data, supporting your ideas with evidence from the data and your biological
knowledge of habituation. Relate your findings to your hypothesis.
4. Suggest a reason why snails may become habituated to a prodding stimulus in the wild.
5. Evaluate the procedure used for this experiment.
6. This experiment has been shown to be less successful if the snails are handled regularly prior to the experiment.
Suggest why this handling prior to the experiment could affect the results of the experiment.
GENE TECHNOLOGY
HOW DRUGS CAN BE PRODUCED USING GENETICALLY MODIFIED ORGANISMS (GMOs)
 A GMO is an organism with foreign DNA. This DNA is introduced in the organism through genetic
modification/genetic engineering/ gene editing.
 Genetic engineering/genetic modification/gene editing is the insertion of genes from one organism into the genetic
material of another organism or changing the genetic material of an organism. In other words, genetic modification
is when a gene is cut from a DNA of a donor organism, inserted into a vector to form recombinant DNA (rDNA)
which is introduced into another organism to form a GMO.
 Transgenic is the transfer of a gene from one species to another.
 The requirements of transfer of genes from one organism to another are:
a) Donor organism-From which the required gene is cut from its DNA
b) Enzymes: restriction, ligase, DNA polymerase and reverse transcriptase.
c) Vectors: plasmids, viruses and liposomes
d) Host cell such as bacteria and yeast to carry rDNA into recipient organism/cell
130
e) Recipient organism-This receives the required gene in form of rDNA
ENZYMES IN GENETIC ENGINEERING
1) Restriction Endonucleases/restriction enzymes

 They recognize specific site or specific base sequence on the DNA that constitute a gene and cut it out
in a staggered manner, leaving sticky ends that will join with sticky ends of the vector with
complementary bases.
 They also cut vector at specific site or at specific base sequence in a staggered manner leaving sticky
ends that will join with sticky ends of the gene with complementary bases. Examples of restriction
enzymes are Hind (III) or EcoRI
2) Reverse Transcriptase
- This catalyses the formation of an artificial gene
- From a protein, it is possible to know the amino acids and the corresponding mRNA responsible for that protein.
This mRNA is obtained from the donor organisms.
- Reverse transcriptase catalyses the synthesis of a complimentary (cDNA) single strand from mRNA. The mRNA
acts as a template to synthesize the cDNA single strand.
Suggest why isolating the mRNA coding for a polypeptide is easier than isolating the gene for that
polypeptide from the DNA.
 DNA has all the genes and so restriction enzymes are needed to cut out the genes.
 However, mRNA has been transcribed from only from gene hence no need for restriction enzyme.
3) DNA polymerase
 When a cDNA single strand has been obtained from reverse transcriptase, the DNA polymerase catalyses the
formation of cDNA double strand molecule (artificial gene), by catalyzing the formation of
phoshphodiester bonds between the newly aligned nucleotides.
4) DNA Ligase
- It catalysis the formation of phosphodiester bonds between the vector and the gene to form rDNA
ROLES OF VECTORS IN GENETIC ENGINEERING

- Vectors are molecular carriers which carry the genes into the cells
- Genes are short segments of DNA which code for specific polypeptides
- Due to their small size, genes cannot be introduced into the host cell using physical introduction methods. So one
needs molecular carriers or vectors which carry these genes into cells
- There are 3 types of vectors;
1) Plasmids
131
 These are small, circular DNA found in some bacteria.
 They are separate from the bacterial DNA and replicate independently and easily.
 A plasmid carries resistant genes.
 A plasmid can be transferred from one bacterium to another without any harm.
 Plasmids have 5 main features which make them ideal vectors to carry genes into host cells;
I. They are small hence easy to handle
II. Ability to replicate within the bacterial cell/any other cell
III. They are double/stranded DNA molecules hence easy to join a gene into a plasmid as the genes are double
stranded portions of the DNA
IV. They readily move into and out of the bacterial cell wall. Therefore, after the gene has been inserted into the
plasmid forming rDNA, the rDNA will enter the host cell through natural cell invasion process. However, the
calcium ions can be used to soften the bacterial cell wall for the easier absorption of the rDNA
V. Plasmids carry genes for resistance for specific antibiotics and therefore it is easier to use these plasmids to
identify the transformed cells (cells that have taken up the rDNA). In other words, some plasmids are used as
marker genes to identify the transformed cells (cells that have successfully absorbed the rDNA).
- Plasmids are the most suitable vectors to carry genes into bacteria and plant cells.
2) Virus (Viral DNA)

- Most viruses are capable of having their DNA incorporated into the DNA of the host cell
- Therefore a gene can be inserted into the disharmed viral DNA to be carried into the host cell.
NB:
Viruses are mainly used to carry genes into the animal and yeast cells.
However, they cause side effects in the organism as follows:
1. Raised heart rate
2. Immune reaction
3. Fatigue
4. Headache
5. Fever.
So, they are not used and instead plasmids together with liposomes are used.
3) Liposomes
These are vesicles made up of phospholipid bilayers that together with plasmids transfer genes into animal cells.
HOST CELLS
- Host cells carry genes in form of rDNA
132
- Bacterial cells are common host cells
Use of microarrays to identify active genes
1. Microarray/chip is a collection of microscopic DNA spots (DNA probes or oligos) containing known
genes (known DNA base sequences) attached to a solid surface.
2. Obtain mRNA that expresses a protein/enzyme in a cell.
3. Using reverse transcriptase, mRNA is converted to cDNA/ssDNA.
4. Add fluorescent dye to this cDNA.
5. Add the fluorescent cDNA to DNA probes.
6. Any complementary sequences present will hybridize/bind.
7. Wash off excess cDNA after hybridization.
8. The microarray is exposed to laser light that causes fluorescence where there is hybridisation
9. The brighter the light emitted, the higher the level of expression of particular gene in the cell from
which the original mRNA was obtained.
133
Analysis of a simple microarray
A DNA microarray might be used to investigate the level of gene expression in a cancerous cell
compared to that in healthy (control) cell, for example. The steps to such an investigation are:
1. The mRNA is extracted from the cancerous cells and the control cells.
2. The cDNA is created from both samples of mRNA using reverse transcriptase.
3. The cDNA from the cancer cell is tagged with a red fluorescent dye, whilst that from the control cell is
tagged with green fluorescent dye.
4. The two samples are then mixed together and added to microarray and complementary sequences
hybridize
5. At each probe location the red-and green-labelled cDNA compete to bind to the gene-specific probe.
6. The microarray is subjected to laser light.
7. A dot will fluoresce red if that particular gene is expressed more strongly in the cancerous cell/ tissue
compared to the normal cell/tissue.
8. A dot will fluoresce green if that particular gene is expressed more strongly in the control tissue
compared to the cancerous cell/tissue.
9. Yellow dots indicate equal amounts of red and green cDNA have bound to that spot – Meaning the level
of expression is the same in both tissue. Then the cDNA is in both cells and so does not cause mutation hence
insignificant. If grey, no complementary DNA probe
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BIOINFORMATICS
 This is a branch of Biology that combines computer science, statistics and mathematics to collect,
process, analyse, store and retrieve biological information and data. This create a database.
 A database is a collection of information that is organized so that it can be easily accessed, managed and
updated. Examples of data bases used to collect relevant biological information include;
1. Genbank – Genetic sequence database
2. RCSB – Protein database
3. EBI – Molecular biology database (genes, proteins and chemicals)
 An application of bioinformatics is when human genes for insulin were identified and this led to genetic
engineering to produce a lot of human insulin.
GENETICALLY MODIFIED PLANTS (GMP)
- Genetically modified crops such as bananas, potatoes, maize or soya have potential to produce medicines and
other chemicals cheaply and efficiently.
- Plants have been genetically engineered to manufacture proteins for treating conditions such as cirrhosis of liver,
CF and anemia
QUESTION
Describe how it might be possible to transform a banana crop into a GM plant to produce edible drug such
as vaccine
1) The gene that codes for the edible drug (vaccine) is identified through base sequencing.
2) The restriction enzyme cuts out this gene in a staggered manner to make sticky ends.
3) The same enzyme is used to cut open the plasmid.
4) Gene is inserted into the plasmid using DNA ligase to form rDNA.
5) This rDNA is introduced into bacteria to form transformed bacteria.
6) The transformed bacteria are identified by gene markers.
7) The transformed bacteria are co-cultured with banana cells and the plasmid inserts the gene into the plant DNA.
8) The plant cells grow into a mass of undifferentiated cells (callus) and the plantlets from this callus will have acquired the
gene of interest that will be expressed later to synthesize the required vaccine and the banana plant becomes GM plant.
GENETICALLY MODIFIED ANIMALS (GMA)
135
- Liposome – rDNA (plasmid and gene) complexes introduce genes into animal cells
- In addition, genes can be introduced directly into the nucleus of a fertilized egg.
- This egg is implanted into a surrogate female.
- Viruses (retroviruses) can also introduce new genes into fertilized eggs. Retroviruses incorporates its DNA into the
host DNA
- It is much more difficult to introduce genes into eukaryotes as the cells contain a membrane bound nucleus unlike
prokaryotes such as bacteria.
1) Production of alpha – 1 – antitrypsin (AAT) enzyme

- This enzyme prevents the development of emphysema disease, (collapsing of lungs)
- Emphysema could be a genetic disorder or could be as a result of smoking
- Emphysema is caused by elastase enzyme/protease produced by WBCs in the lungs. The enzyme then digests the
lung tissue
- Alpha -1-antitrypsin enzyme inhibits the activity of elastase hence no emphysema
- This alpha-1-antitrypsin enzyme is secreted by liver cells into the blood stream. However, some people have a
genetic disorder which prevents them from producing the enzyme
- Gene for the production of the enzyme is identified and isolated from the liver cells and inserted into fertilized eggs
of sheep. These surrogate sheep will give birth to transgenic sheep that will produce milk with the enzyme which is
purified and given to people with emphysema
2) Production of blood clotting factors

- Human cells have gene for this factor that is transferred into fertilized egg in sheep
- It is given to people suffering from hemophilia
3) Production of human growth hormone-
- The gene is isolated from the pituitary gland and introduced in E. coli bacteria.
- It is given to people suffering from pituitary dwarfism
GENETICALLY MODIFIED MICRO-ORGANISMS E.G. Bacterial production of insulin to treat type (II)
diabetes
- Identify the mRNA for the production of insulin from the beta cells in the islets of Langerhans in the pancreas.
- This mRNA is isolated.
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- The mRNA acts as a template to synthesize cDNA single strand using reverse transcriptase. The cDNA single stand acts as a template to
synthesize cDNA double stand catalyzed by DNA polymerase. The sticky ends are made by adding extra G nucleotides to the ends of the
gene.
- Plasmids are cut open using restriction enzymes. The sticky ends are made by adding extra C nucleotides to the ends of the cut plasmid.
- Gene of interest is inserted into the vector to form recombinant DNA (rDNA). The two are joined by DNA ligase that catalyzes the formation
of phosphodiester bonds
- The rDNA is introduced in the micro-organism such as E-coli forming transformed E-coli cells, which are identified by gene markers.
- These transformed E-coli are cloned in fermenters (continuous fermenters)
- The gene will express itself in the bacteria through protein synthesis to produce insulin that is secreted into the medium
- Insulin is isolated and purified
SOME POSSIBLE CONCERNS OVER THE DEVELOPMENT & USE OF GENETICALLY MODIFIED
ORGANISMS (GMOs).
 Genetic pollution (transfer of the unwanted genes to natural wild species).

 Antibiotic resistance genes that are used to identify GM bacteria (used as marker genes) could lead to antibiotic
resistance developing in these bacteria.
 GM crops could become super-crops that out-compete other plants. This can lead to extinction of other species
hence disrupting the food chains.
 GM crops produce infertile seeds that cannot be replanted. This forces farmers to keep buying new seeds from
seed companies and this is expensive.
 Potential hazards such as allergies.
 Unethical due to use of animals such as sheep.
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UNIT 5

Unit 5: Respiration, Internal Environment, Coordination and Gene Technology

Topic 7 – Respiration, Muscles and the Internal Environment

Enzymes in metabolic pathway

Structure of ATP molecule

Uses of energy from hydrolysis of ATP in cells

Types of cellular respiration

Net gain of ATP during glycolysis

(c) State the final products of glycolysis. (3)

What happens to products of glycolysis in aerobic respiration?

- The process of oxidative phosphorylation is as follows:

- Accumulation of lactic acid in the human muscle causes cramps.

What happens to pyruvate in anaerobic respiration in yeast cells?

- The products of anaerobic respiration in yeast cells are;

 They have fast twitch muscle fibres

 lactate build up causing a drop in pH (more acidic)

 Lactate diffuses in the blood and is transported to the liver

FATTY ACID OXIDATION

b) Calculate efficiency of anaerobic respiration;

In aerobic respiration, describe two processes that synthesize ATP

(i) Substrate-level phosphorylation

(ii) Oxidative phosphorylation

What happens to the electrons released at the end of ETC

What happens to H atom released from substrate during aerobic respiration

Describe the role of the mitochondrion in aerobic respiration

List the substances that diffuse into the mitochondrion

List the processes in anaerobic respiration in human muscle.

Name structure X and explain its role in aerobic respiration. (3)

(ii) Name substance X and w

 RQ = volume of carbon dioxide given out in unit time

For the aerobic respiration of palmitic acid:

C18H36O2 + 26O2  18CO2 + 18H2O

Describe the term respirometer

 It is an apparatus that measures the oxygen uptake by an organism

Explain the purpose of the syringe in the set up.

 reset / move the coloured oil

 Carbon dioxide is produced in respiration

 Mass of organism may differ; so, use same mass

Describe the function of the clip

a) Explain how a respirometer is designed to overcome this problem

c) What would happen if KOH is not added

Volume of oxygen absorbed=π r 2d

- To calculate the rate of oxygen uptake: the volume is divided by time

SKELETAL MUSCLE FIBRES OF THE SKELETAL MUSCLE

 They are also called striated or voluntary muscle.

 These are pairs of muscles which pull in opposite direction.

The extensor muscle is relaxed and the flexor muscle is contracted

(c) Explain why muscles occur in antagonistic pairs. (2)

 muscles cannot extend themselves

 Extensor muscles (quadriceps) contract / shorten / and the leg is straightened

 Flexor muscle (hamstring) relaxes and is stretched

 Tendons attach muscles to bones

Triceps Extend the arm at the elbow Press-up, throwing a javelin

 This is the basic unit of contraction of skeletal muscle fibre.

- Fibrous protein around the actin filament.

Contraction of skeletal muscles

Evidence of the sliding –filament mechanism

- Activates calcium pump to move Ca2+ to sarcoplasmic reticulum during relaxation.

- ATP for synthesis of neurotransmitter

- Sarcoplasmic reticulum contain calcium ions

TYPES OF SKELETAL MUSCLE FIBRES

4. More capillaries; to deliver a lot of oxygen for aerobic respiration

5. Less (stored) glycogen, as fat is used as fuel