UNIT 5

Exercise, energy and co-ordination

Topic 7: Run for your life!
Muscles and movement
By Mugo

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.
• 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.
◈ 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.
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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;

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 ▷ 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

- 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 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

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 • It involves the thick myosin filaments and the thin actin filaments sliding between each other. As a
result, 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

When action potential (nerve impulse) arrives at neuromuscular junction, sarcoplasmic reticulum is stimulated to release
Ca2+ that flood the sarcomere to trigger muscle contraction.

Muscle contraction.

- Action potential arrives at the neuromuscular junction and stimulates sarcoplasmic reticulum to release Ca2+ 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 450. 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, Pi and energy. This energy causes the myosin head to pull

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 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.

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

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.

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 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 Ca2+.

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)

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

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 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
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.
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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.

Connective tissue

Bones, cartilage, tendons & ligaments

Connective tissue connects/joins tissues, connects organs, supports other tissues and organs and transport
substances

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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.
• 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
• 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.

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 • 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
bone / skeleton is moved
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
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.

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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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 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.

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▷ Example of hydrolase is ATPase that catalyzes the hydrolysis of ATP to ADP, Pi and 34kJ of energy.

ATPase
ATP +H20 ADP + Pi +
34kJ

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. It is small hence easily enters or leaves the cell.
8. Soluble hence easily transported in blood.

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)

ATPas
ATP + H2O e ADP + Pi + 34kJ.

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 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
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

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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 ATP
phosphorylation/ETC membrane 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.

Enzymes during phosphorylation

Step 1

The enzyme hexokinase phosphorylates (adds a phosphate group) glucose in the cell's cytoplasm. In the process, a
phosphate group from ATP is transferred to glucose producing glucose 6-phosphate.

Glucose (C6H12O6) + hexokinase + ATP → ADP + Glucose 6-phosphate (C6H11O6P1) 

Step 2

The enzyme phosphoglucoisomerase converts glucose 6-phosphate into its isomer fructose 6-phosphate. Isomers
have the same molecular formula, but the atoms of each molecule are arranged differently.

Glucose 6-phosphate (C6H11O6P1) + Phosphoglucoisomerase → Fructose 6-phosphate (C6H11O6P1)

Step 3

The enzyme phosphofructokinase uses another ATP molecule to transfer a phosphate group to fructose 6-phosphate
to form fructose 1, 6-bisphosphate. 

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 Fructose 6-phosphate (C6H11O6P1) + phosphofructokinase + ATP → ADP + Fructose 1, 6-bisphosphate (C6H10O6P2) 

(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)
- 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.

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 - 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.

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(a) State which form of glucose is shown in the diagram. (1)
α / alpha
(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.

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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.
(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

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 (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 CO2; oxidation to
form reduced NAD & reduced FAD; and ATP formation (substrate level phosphorylation) to form ATP.
- In decarboxylation, CO2 is removed in two reactions
- In oxidation, hydrogen is removed in 4 reactions whereby in 3 of them NAD is the hydrogen
acceptor/coenzyme and in one, FAD is the hydrogen acceptor/coenzyme.
- This oxidation reaction releases energy that is stored by the hydrogen acceptors when they accept H. This
energy is later released in the Electron Transport Chain (ETC) and is used to synthesize ATP in oxidative
phosphorylation.
- In substrate level phosphorylation, ATP is produced directly in one reaction
- The products of Krebs cycle are:
a) CO2

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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:

(i) Reduced NAD and FAD move to the inner mitochondrial membrane where they release hydrogen atoms.
The H atoms split/ionize into electrons and protons (H+).
(ii) 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 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.
(iii) As the H+ flow through the ATP synthase, they release energy which combines ADP and Pi catalysed
ATP synthase, forming ATP. This is oxidative phosphorylation.
(iv) In the matrix, electrons combine with H+ to form H-atom that reduces oxygen to form water
(v) The products of oxidative phosphorylation are: ATP & Water

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NB
- Oxidative phosphorylation is the synthesis of ATP from ADP and Pi 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.

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 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.

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

31
 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
▷ 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

32
What happens to pyruvate in anaerobic respiration in yeast cells?
- Anaerobic respiration involves;
1. Glycolysis
2. Decarboxylation (pyruvate converted into ethanol/acetaldehyde)
3. Reduction of ethanol 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

33
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

(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.
34
 ▷ 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
- In fatty acid oxidation, the glycerol and fatty acids that make up triglyceride/fat are separated
- 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

35
 (i) Substrate-level phosphorylation
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+

36
- 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

- 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
38

Describe the reasons why aerobic respiration produces more ATP than anaerobic respiration from one

37
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
▷ 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.

38
- 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.

The diagram below shows the electron transport chain, which is part of aerobic
respiration.

39
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
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

40
 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.

• 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.

41
 ▷ 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.
▷ 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

42
 ▷ 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
▷ State the time for the investigation
▷ Mass of woodlice and beads is stated
▷ Measuring volume and description of how to obtain volume (cross section area of manometer tube multiplied by
distance moved by the liquid)
▷ Calculation of rate of respiration/ rate of oxygen uptake (volume divided by time)
▷ Replicates (repeat two more times)
▷ Description of control e.g. no woodlice or use of beads

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.

b) Changes in temperature can cause large deficits in the volume of a gas. Explain how temperature
is controlled when using a respirometer.
43
 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
2
- Calculate the cross section area of the tube using π r
- 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)

2
Volume of oxygen absorbed=π r d

- 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.

44
 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.

45
3. Diastole (Complete cardiac diastole)
- 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 generates impulse.
- This impulse spreads over the atria walls, causing atrial systole that lasts for about 0.1 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 impulses pass into the bundle of His that carries the impulses to the Purkyne fibres.
- The Purkyne fibres carry impulses to the heart apex via the septum.
- The impulses spread over the ventricle walls causing contraction from the apex upwards.
- Blood is squeezed into the arteries (pulmonary artery and aorta). This is ventricular systole.

46
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

▷ 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.

47
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

48
 • Cardiac output could decrease if there was insufficient time to fill the ventricles (between contractions).

• 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.

49
INTRINSIC RHYTHM OF THE HEART AND EXERCISE
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 dm3 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 30dm3 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.
50
Discuss the importance of thick cardiac muscles.
• Lower heart rate (fewer contractions) is required to deliver enough oxygenated blood to the muscle.
• 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 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.

51
 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 Decelerator in the Cardiovascular

Control centre in the brain Control centre in the brain

Sympathetic (accelerator) Parasympathetic (Vagus)

nerve nerve

Sino atrial node (SAN)

Increase heart Decrease heart

rate rate

52
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.

53
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
54
 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 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
Decreased blood pH causes an increase in heart rate.
• A decrease in blood pH (caused by an increase in CO2) 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).
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 • 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
- 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 Effector of
nerve 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

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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
- 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)

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 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 3dm3.

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.

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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 (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 is measured.
2. This is safe for humans because it is harmful to breath in increased volume of CO2. 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.
- Breath normally through the mouth piece to get TV.
- Take a deep breath i.e. forced inhalation to get IRV
- Exhale deeply 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.

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 set time
- Number per 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.

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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
healthy 17-year-old student at rest.

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 Explain why the volume of air in the spirometer drops slowly over the first minute.
oxygen is absorbed by the bllod 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.

(i) Calculate the mean tidal volume in the first 20 seconds. Express your answer to two
decimal places. Show your working 0.55 – 0.65dm3
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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 0.1dm3
✓ Calibrate the horizontal scale, X-axis (time) so that one small box represents 5 seconds
✓ One breath is the height between the peak/crest and the trough.
✓ Tidal volume is calculated by multiplying the number of small boxes in this height by 0.1dm3.

Explain how you would use the trace from a spirometer to calculate breathing rate.
✓ Calibrate the vertical scale, Y axis (volume) so that one small box represents 0.1dm3
✓ Calibrate the horizontal scale, X-axis (time) so that one small box represents 5 seconds
✓ One breath is the height between the peak/crest and the trough.
✓ Tidal volume is calculated by multiplying the number of small boxes in this height by 0.1dm3.
✓ Breathing rate (breaths per minute) is calculated by counting the number of peaks (breaths) in 12
horizontal small boxes (one is 5 seconds).

Explain how you would use the trace from a spirometer to calculate vital capacity.
✓ Calibrate the vertical scale, Y axis (volume) so that one small box represents 0.1dm3
✓ Calibrate the horizontal scale, X-axis (time) so that one small box represents 5 seconds
✓ Vital capacity is 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 0.1dm3.

Explain how you would use the trace from a spirometer to calculate ventilation rate.
✓ Calibrate the vertical scale, Y axis (volume) so that one small box represents 0.1dm3
✓ Calibrate the horizontal scale, X-axis (time) so that one small box represents 5 seconds
✓ One breath is the height between the peak/crest and the trough.
✓ Tidal volume is calculated by multiplying the number of small boxes in this height by 0.1dm3.
✓ Breathing rate (breaths per minute) is calculated by counting the number of peaks (breaths) in 12
horizontal small boxes (one is 5 seconds).
✓ 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
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 breathing rates of male and female human subjects.
✓ Calibrate the vertical scale, Y axis (volume) so that one small box represents 0.1dm3
✓ Calibrate the horizontal scale, X-axis (time) so that one small box represents 5 seconds
✓ One breath is the height between the peak/crest and the trough.
✓ Tidal volume is calculated by multiplying the number of small boxes in this height by 0.1dm3.
✓ Breathing rate (breaths per minute) is calculated by counting the number of peaks (breaths) in 12
horizontal small boxes (one is 5 seconds).

✓ 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 0.45dm3, 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 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.

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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 CO2.

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 Chemoreceptors

Diaphragm muscles
and 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

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

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 - 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 CO2 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 cm3
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) 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, 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
• Chemoreceptors in the wall of the aorta and walls of carotid arteries detect this blood and send

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 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.

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 and blood glucose level are examples of processes that need to be kept constant.

Importance of homeostasis
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

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 return to normality through a feedback loop.
(v)Feedback loop – informs the receptor of the changes to the system brought about by the Effector.

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 dispersed 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

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 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 to increase metabolism to generate heat (non shivering thermoregulation)

Suggest how the wood mouse maintains a constant body temperature when in a
cold environment. (6)
▷ 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 skin arterioles to cause vasoconstriction so that
less blood reaches the skin (superficial capillaries causing less loss of heat; or shunt vessels
dilate / widen so that less blood reaches the skin / 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.

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 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. more respiration to produce energy for muscle contraction
2. During respiration heat energy is released
3. more heat 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)

▷ 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 loss 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

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 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 or hypothermia and may lead to death.

Temperature limits
- Core (blood) body temperature is 37.5oC.
- Oral temperature (under the tongue) is 370C.

1. Low critical temperature

- 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

- Temperature at which chemical reactions top due to inactivity of enzymes and results to death.

NB
- Exercising hard in cold condition causes a lot of sweating after the exercise, losing heat very fast and
this can lead to hypothermia and eventually reaching low lethal temperature.

3. High critical temperature

- The temperatures at which the normal thermoregulatory mechanisms to release heat such as sweating
are no longer enough and the metabolic rate increases due to increase in external temperature.

4. High lethal temperature

- Temperature at which chemical reactions stop due to denaturation of enzymes resulting to death. It is
around 420C.

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Questions
1. Explain what is meant by the term negative feedback?
A change in a factor that brings about a response that counteracts the change so that the factor
returns to a norm value.
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 37oC.
- Heat gain centre of thermoregulatory centre of hypothalamus stimulates effectors;
- Sweat production is inhibited
- 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.

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 genes on
or off. They bind to promoter region on DNA adjacent to the gene to be regulated and control

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 the process of transcription.
- Depending on the transcription factor, the transcription of the adjacent gene is either up- or
down-regulated.
- 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.

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.

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 • 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.

• 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.

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 BENEFITS AND POTENTIAL DANGERS OF EXERCISE IN HUMANS
Doing too little exercise and too much exercise can lead to health problems. However, doing moderate and
regular exercise has health benefits.

BENEFITS OF MODERATE AND REGULAR EXERCISE

- Lowers resting blood pressure due to increased vasodilation of arterioles hence reduce the risk of CVD.
This is a benefit to the cardiovascular system
- Improves ratio of HDL to LDL hence reduces chances of CVD. This is a benefit to the cardiovascular
system
- Reduces risk of obesity as more glucose is respired and not converted to fat hence reducing risk of CVD.
This is a benefit to the cardiovascular system
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- Prevents development of type II diabetes as more glucose is respired. This is a benefit to the
cardiovascular system
- Ensures that joints are healthy.

HARMFUL EFFECTS OF TOO LITTLE EXERCISE

- Causes obesity which increases the risk for CVD
- Increases risk of type II diabetes because more glucose is not respired
- Damages joints due to overweight

Give two reasons why too little exercise may not be good for the health of a
person.

1. increased risk of obesity / overweight

2. (coronary) heart disease / CHD / build-up cholesterol in artery vessels
3. diabetes
4. high blood pressure / strokes ;
5. osteoporosis/decrease in bone density

HARMFUL EFFECTS OF TOO MUCH EXERCISE

- Suppression of the immune system. This is as a result of:
• When the body recovers after vigorous exercise the number and activity of T-killer cells decrease
increasing the chances of more infections such as cold and sore throats
• Due to damage of the muscles, there is inflammatory response in these muscles reducing
immune response elsewhere
• Too much exercise causes the release of stress hormones such as adrenaline and cortisol.
These hormones reduce the production of antibodies hence suppress the immune system and
also suppresses inflammation.

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 - Joint damages
There is increased wear and tear of joints.
Increased wear and tear of joints is as a result of:
• Articular cartilage wears away allowing bones to grind together
• Patellar tendinitis
Damage of the articular cartilage on the femur so that the patella (knee cap) grinds roughly
across the femur when the knee bends. It is also called jumper’s knee.
• Cruciate ligaments are damaged due to abrupt movements of joints or twisting of joints
• The bursae (fluid filled sacs) cushion the points of contact between bones, tendons and
ligaments. However they can swell up with excess fluid pressing against tissues in the joint
causing inflammation and tenderness. This is called bursitis of the knee also known as
housemaid’s knee.

Give two reasons why too much exercise may not be good for the health of a person.

▷ wear and tear on joints

▷ suppression of immune system / susceptibility to respiratory tract infections /reduced
numbers of WBCs

Gymnasts can damage their cruciate ligaments.

This is an injury that can be repaired using keyhole surgery.
(i) 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 and femur 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) movement .
3. this gives added stability ;

CONVENTIONAL METHOD OF TREATING SOFT TISSUE INJURY

RICE
R – Rest – this gives time for the recovery.
I – Ice reduces heat in the injured site.
C – Compression – reduces swelling.

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E – Elevation - to straighten up a damaged joint.

MEDICAL TECHNOLOGY APPLIED TO SPORTS INJURY

1. Key hole surgery – to repair cruciate ligament
2. Prosthesis – knee joint replacement using prosthesis

Key Hole Surgery

- A small incision (4mm in diameter) is made in the joint.
- A tiny camera (endoscope) with a powerful light source at the end, delivered by fibre optics is inserted to project
the images inside the joint onto the TV monitor to identify the damage and find ways of fixing it. In the same or
different incision, miniature surgical instruments are inserted and the surgeon can operate the instruments from
outside the body while looking at the monitor.
- Damage to the cruciate ligaments in the knee can be handled effectively by key hole surgery
- Advantages of key hole surgery over conventional operation include:
1. Less damage to the joint
2. Less bleeding
3. Less risk of infection
4. Recovery is much quicker
5. Reduces likelihood of osteoarthritis that will cause knee joint replacement later
6. Less pain

Prosthesis
▷ It is an artificial body part such as prosthetic joint or artificial joint to replace hip or knee joint that has been
damaged by excessive exercise.
▷ This gives a degree of same function and same appearance hence eliminate pain and restore activity

The damaged knee joint can be replaced by prosthesis as follows;

- An incision is made into the joint.
- The patella is moved out of the way.
- The end of the tibia, patella and femur are trimmed.
- On the femur, a stainless steel or titanium prosthetic implant is attached using bone cement while on the patella
and tibia metal/plastic or ceramic is attached by bone cement.

PERFORMANCE ENHANCING SUBSTANCES AND TECHNIQUES

- The world anti-doping agency (WADA) is the body which oversees the battle against the use of performance
enhancing substances and techniques.
- There are three types of performance enhancing substances and techniques;
a) Substances and techniques are banned at all times in or out of competition unless there is a clear
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 medical reason for an athlete to take them.
b) Substances and techniques that are only banned for use during competition.
c) Substances and techniques that are banned only in particular sports.
- The following groups of substances and technique are completely banned;
(i) Anabolic steroids (drugs that resemble male hormones such testosterone) - they increase the mass and
strength of muscle to improve performance.
(ii) Hormones e.g. EPO which stimulates the formation of more red blood cells and growth hormones which
affect muscle growth.
(iii) Gene doping – to change genetic makeup of cell to enhance athletic performance.

ERYTHROPOEITIN (EPO)
- It is a peptide hormone
- It is naturally produced by the kidneys
- It stimulates the formation of new red blood cells in red bone marrow
- EPO can be produced using DNA technology and used to treat anaemia
- EPO occurs naturally in the body and the absence of this hormone can lead to serious health problems and death.
- An excess of red blood cells thickens the blood and can lead to CVDs. These are particularly common at night.
- EPO is a naturally occurring hormone hence very hard to find out whether the raised EPO level are natural or
synthetic.
- EPO is very popular with endurance athletes. Cycling is one sport where it is thought to be very commonly used.
- EPO binds to the receptor on the CSM of the target cell (stem cells in red bone marrow) to form hormone-receptor
complex. This complex activates Adenyl cyclase which converts ATP to cAMP which acts as a 2nd messenger and
its role is to trigger protein kinase cascade which gives a final product that enters the nucleus and acts as a
transcription factor.
- This transcription factor causes the expression of a gene to code for an enzyme that catalyses the formation of
more red blood cells in the bone marrow.
Questions
1. Explain how taking EPO would increase the performance and endurance
It increases the number of red blood cells hence increases haemoglobin. These red blood cells carry more oxygen to
muscles for aerobic respiration that produce more energy for these muscles for endurance and performance.

2. Suggest how EPO might stimulate the formation of new red blood cells
- Unspecialized stem cells in the red bone marrow divide and differentiate to form red blood cells .
- EPO binds to receptor on target cells (stem cells) in the bone marrow causing gene expression that will lead to
formation of an enzyme that catalyses the formation of more red blood cells.

3. Explain why EPO is not taken by sprint athletes

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Spring events rely on anaerobic respiration so performance is not dependent on the athlete’s aerobic capacity.

4. Explain why it is important to distinguish between natural (produced by kidney) and synthetic EPO
This will help to determine if athletes are taking EPO as performance enhancing drug

How EPO /how hormones affect target cells?

- EPO is a peptide hormone
- Peptide hormones such as EPO bind to receptors in the cell membrane and this hormone-receptor complex
activates adenyl-cyclase which converts ATP to cAMP which acts as a second messenger in the cytoplasm and
triggers protein kinase cascade whose final product enters the nucleus to act as a transcription factor.
- In case of EPO, the transcription factor switches on the genes to code for enzymes involved in the synthesis of
more red blood cells.

- Muscle atrophy
- Muscle atrophy is the wasting or loss of muscle tissue.

STEROID HORMONES
- These are hormones that are lipid in nature.
- Steroid hormones are divided into two;
a) Natural anabolic steroid: Testosterone
b) Synthetic anabolic steroid : Nandrolone
- Testosterone hormone is a natural anabolic steroid hormone.
- It is made from cholesterol produced in the testis by males and in small amounts by adrenal glands in both males
and females.
- Testosterone increases anabolic reactions such as protein synthesis in muscles, increasing the size and strength
of the muscle.
- Athletes and body builders use injections of testosterone to increase muscle development. However, this is not
very effective as natural testosterone is quickly broken down in the body.
- To overcome this problem, synthetic anabolic steroid called Nandrolone has been developed which survives
longer in the body.

- Athletes and body builders have been overusing the synthetic anabolic steroid, but they have several side effects;
(i) Decrease in sperm production which can lead to impotence
(ii) Changes in menstrual cycle in women
(iii) High blood pressure
(iv) Liver damage
(v) Heart attacks

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 (vi) Kidney failure
(vii) Raised level of aggression particularly in young men

How anabolic steroids affect target cells?

The steroid hormone passes through the CSM of the target cell e.g. muscle and binds to the receptor in the cytoplasm
forming a hormone-receptor complex. This complex enters the nucleus and acts as a transcription factor that switches
on a gene, that is expressed to form proteins that make the muscles bigger and stronger.

Muscle hypertrophy
▷ Is an increase in the cross-sectional area of individual muscle fibres, due to an increase in

contractile proteins.
The protein is used to build muscle

To detect anabolic steroids and their by products

They can be detected in urine samples by the technique of Mass Spectrometry. However, as these substances occur
naturally it is difficult to set a level above which the athlete can confidently be said to be doping.

However, there is a solution to this; testosterone and a related compound called epitestosterone are both found in urine.
When an athlete takes an anabolic steroid the ratio of testosterone to epitestosterone (the T:E ratio) increases . The World
Anti-Doping Code states that an athlete with a T:E ratio about 4:1 is guilty of doping. ‘

Are outstanding athletes born, made or both?

(i) Both : Phenotype (athletism) is as a result of interaction between genotype (genes) and the environment
(training).
(ii) Born: a) inheritance of fast or slow twitch muscle fibers or sprint genes
b) Inheritance of genes that influence muscle development
(iii) Made: muscle development can be improved by;
- Diet
- Drugs
- Training

Before being used by humans drugs are tested on animals. However, there are ethical issues supporting or opposing the
use of animals for research. Comment on this.
1. Absolutists: fight for animal rights and believe that we should never keep animals or use them for any purpose

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 including medical research.
2. Relativists: they fight for animal welfare and they believe that animals should be treated well, minimizing harm
and suffering as much as possible. They believe that animals can be used for medical research.
3. Utilitarians: They believe that as long as the overall expected benefits are greater than the overall harm then
animals may be used for medical research.

How a biologist might justify the use of animals in experiments

(i) Expected benefits are greater than expected harm – utilitarian philosophy.
(ii) It reduces the chances of harm when being tested on people having been tested on animals.
(iii) Animal experiments give greater understanding of the human and animal body.

Comment on the ethical viewpoints for and against the use of performance enhancing
drugs by athletes.
The absolutist’s view would be that they should never be used because:
1) of the health risks,
2) of possibility of death,
3) it is illegal
4) of Possibility of uninformed decision taking that may have far reaching health and legal consequences.
5) athletes should compete using their innate {anatomical / physiological} abilities so that fair competition
is promoted

The rationalist’s view would be that their use is acceptable if there is a justifiable reason such as:
1) it is a personal choice.
2) It helps to overcome inequalities in training resources, medical support and altitude.
3) There is a pressure from coaches, sponsors and public.
4) Financial rewards for best performance.

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 GREY MATTER
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.
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 and far red light.

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 - 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.

- 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 darkens and light and therefore based on this ratio plants can be;
1) Long day plants (LDPs)
2) Short day plants (SDPs)

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 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 darkens, 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.
- 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.

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 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)
- 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.

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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.

HOW HUMANS RESPOND TO LIGHT:

PUPIL REFLEX

• The iris in the eye contains a pair of antagonistic muscles called circular and radial muscles. These
muscles are the effectors.
• These muscles control the size of the pupil.
1. In high light intensity, photoreceptors in the retina generate more nerve impulses that are
transmitted by the optic nerve to the brain for co-ordination. The brain then initiates motor
impulse that is transmitted by parasympathetic motor neurone to the circular muscles 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.
2. In low light intensity, photoreceptors in the retina generate fewer nerve impulses that are
transmitted by optic nerve to the brain for co-ordination. The brain then initiates motor
impulse that is transmitted by sympathetic motor neurone to radial muscles 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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 3.

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.
NERVOUS SYSTEM
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 towards the cell body. One long
dendrite is called dendron. A dendron is found in sensory and relay neurone. So, a Dendron is the 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

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 • 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.
2. They wrap around the neurone to protect it.
3. They wrap around the neurone to produce myelin sheath.

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.
- They have Schwann cells that produce myelin sheath hence it is myelinated and so it has nodes of
Ranvier.
- The nerve fibre consists of dendron and axon.
b) Function
(i) Transmits sensory impulses from receptor cells to the CNS.

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2. Motor Neurone (Effector neurone)
a) Structure
- Cell body is at the end of nerve fibre/axon.
- Has Schwann cell hence they have myelin sheath and nodes of Ranvier.
- The whole nerve fibre is an axon i.e. no dendron.
- Short and many dendrites around the cell body.

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.
- Nerve fibre consists of short axon and short dendron.
- They have no Schwann cell hence no myelin sheath and nodes of Ranvier.

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 - 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 speed of transmission of impulses in the CNS to give enough time for its
co-ordination.

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 longer Dendron than axon
▷ Sensory has shorter axon while motor has longer axon

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 ▷ Sensory has no motor end plate, motor has

NERVE IMPULSE

Membrane potential is the difference in electrical potential between the inside and outside the cell.
The action potential is the brief electrical impulse that is responsible for the propagation of
information down the axon of a neuron. The action potential is approximately +30 mV. An action
potential is an all or nothing phenomenon. It either reaches the threshold and produces an action
potential or it doesn’t.

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 The resting potential is the membrane potential of a neuron when the neuron is at rest and not
receiving any excitatory or inhibitory signals. The resting potential is approximately –70 mV.
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,
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).

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• 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
• 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

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 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 does not increase the value of the potential but it 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

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• Due to presence of myelin sheath, there is saltatory conduction that causes faster conduction of
impulses

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:

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 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.

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) Can filter out low level stimuli
5) 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

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 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.

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 Ca2+ 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+ channels 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 synoptic knob, choline combines with acetyl Co –A to form acetylcholine that are
enclosed by vesicles in readiness for another action potential.

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 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+ channels need to open to
allow the diffusion of more Na+ for depolarization to reach threshold stimulus in order to cause
post-synaptic action potential.

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.
NB:
- 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;
a) Outermost layer (photosensitive layer)
▪ Consists of rods and cones.
▪ It is partly embedded in the choroid.
b) Middle layer
▪ With bipolar neurones.
c) Inner layer
▪ Ganglion cells and axons of the 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).
- 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.

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 (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+.
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 of the opened Na gates 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.

Rhodopsin
- 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 derived of vitamin A.
- Retinal exists in isomers i.e. cis and trans isomers.
- When exposed to light cis isomer is converted to trans isomer.

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.

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- 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.

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.

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

▷ trans retinal converts to cis retinal

▷ rhodopsin is reformed from opsin and cis retinal

▷ this results in dark adaptation

▷ permeability of the cell surface membrane to Na+ increases/partial depolarisation

▷ hyperpolarisation 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.

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

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 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.

Cones
▷ They are cone shaped
▷ Found in the outer layer of the retina
▷ They are located in fovea/yellow spot
▷ There are 3 types of cones;
1. responds to red (Primary colour)
2. responds to green (Secondary colour)
3. responds to blue (Primary colour)
▷ So, cones are involved in trichromatic vision in humans
▷ The pigment in the cones is called iodopsin
▷ The pigment is in the lamella in the outer segment of the cone cell
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.
4) Position of iodopsin: in the lamella in the outer segment of cone cell.

CRITICAL WINDOW/CRITICAL PERIOD FOR DEVELOPMENT

• This is the period after birth where the nervous system needs specific stimulus in order to fully and properly
develop.

Critical window for visual development

• Critical window for visual development is the period after birth where exposure to light stimulus is
needed for normal visual development.
• This exposure to light allows the growth of neurones from the retina to the thalamus and then to the
visual cortex that contains columns of cells.
• Failure to receive light (specific stimulus) during critical window for visual development, the following

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 are the consequences:

1. Narrower
columns of cells in visual cortex, or none develops at all
2. Shorter sensory neurones, or do not develop at all
3. Fewer synapses, or none develop at all
4. Fewer and shorter synaptic connections, or none at all.

• Visual cortex is made up of columns of cells.

• Adjacent columns of cells receive stimulation from right and left eye at the same time.
• At birth, axons compete for columns of cells in visual cortex. When both eyes receive enough light
(specific stimulus) during critical window for visual development, the sensory neurones from the retina
of the two eyes fire equally in the columns of cells and these neurones remain strong and active.

NB:

Even with visual impairment due to the fact that sensory information does not reach visual cortex, pupil
reflex takes place as the neurones between retina and mid-brain are fully grown.

Visual Deprivation Studies

• These studies give evidence of a critical period in visual development in mammals.

Evidence for critical window for visual development in humans (Medical observations).

• Cataract present at birth if not diagnosed and removed early within 10 yrs after birth will lead to
permanent visual impairment. The critical window for visual development in human is the first 10 yrs.
Even with the removal of the cataract later the eye is visually impaired.

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 • Bandaging of an eye due to minor eye infection for just 2 weeks within the first 10 yrs lead to the eye
being visually impaired.

Use of animals to provide evidence for critical window for visual development (Hubel and Wiesel
experiments)-Monocular deprivation of Light.

In monocular deprivation of light, one eye is bandaged so that only one eye allows light to enter.

1. Critical window for visual development in kittens is 4th week. Even lack of light for few hours in the 4th
week, vision in that eye is impaired. Deprivation under 3 weeks has no effect as they are born blind.
Deprivation after 3 months had no effect as all the neurones for vision had fully grown
2. Critical window for visual development in monkeys is the first 6 months after birth. One week
deprivation of light in one eye causes visual impairment.

COMPARISON OF MECHANISM OF COORDINATION IN PLANTS AND ANIMALS.

Questions
1. Suggest why chemical co-ordination alone works for plants while most animals use both chemical and
electrical means of co-ordinations
▷ Due to mobility of animals, fast responses are required and this is provided for by electrical
co-ordination. Plants are usually immobile hence survive with chemical coordination only.
▷ Chemical co-ordination depends on diffusion and movement in mass flow systems such as blood
and phloem and so speed is limited. It usually involves growth as the mechanism for response. It is
sufficient for plant responses.
2. 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.
3. List differences between chemical (hormone) and nervous (electrical) co-ordination
Nervous Hormones
- Involves electricals - Involves chemicals

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 - Transported along neurones - Transported in blood
- Has short term effect - Has long term effect
- Affects a smaller area - Affects many parts
- Its transport is faster - Its transport is slower

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 tras-retinal.
3. In plants, activation of phytochrome leads to production of chemical signal/hormone e.g. florigen; while
activation of rhodopsin and iodopsin 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
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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

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.

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 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

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

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 • 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.

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) 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

d) 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)

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 • Breathing rate = In the breathing centre
• Blood pressure
• Sneezing
• Vomiting
• Coughing

BRAIN DEVELOPMENT

- Humans are born with a range of innate behaviours (behavioural responses that do not need to
be learnt).
- These innate behaviours are:
• Crying
• Grasping
• Sucking
- However the brain still needs much growth and development after birth through the formation of
synapses and growth of axons.

THE ROLE OF NATURE AND NURTURE IN BRAIN DEVELOPMENT

1) Nature
▷ Involves genes
▷ Genes have major influence in the development of our characteristics while environment or learning has little
influence.

2) Nurture

▷ This involves characteristics that are learnt or are heavily influenced by the environment.
▷ Most of our characteristics are determined by nature and not nurture.
▷ We are the result of a mixture of genetic (nature) and environmental factors (nurture).

EVIDENCE FOR THE RELATIVE ROLES OF NATURE AND NURTURE IN BRAIN

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DEVELOPMENT COME FROM A VARIETY OF SOURCES:

1. THE ABILITIES OF NEWBORN BABIES

• Newborn babies have some innate capacities, i.e. grasping, sucking, and crying.
• This suggest that genes help to form the brain and some behaviours before the baby is born. This is nature.
2. STUDIES OF INDIVIDUALS WITH DAMAGED BRAIN AREAS
• Neorones that control voluntary movement, speech and reasoning are located in the cerebral cortex.
• It is now evident that in case of brain damage that touches on any of the above functions new neurons
are made at different part of the brain taking over the job that was being carried out by the damaged
area, hence the ability to recover some of the brain functions.
• This demonstrates that some neurones have the ability to change due to nature and nurture.
3. ANIMAL EXPERIMENTS
• E.g. Hubel and Weisel's experiments on critical window for sight, suggest that external stimulation e.g.
light is important in brain development. This is nurture.
4. TWIN STUDIES
• Identical twins are genetically identical.
• Twin studies can help to estimate the relative contribution of genes and the environment. Any differences
between identical twins must be due to the effects of the environment.
• Identical twins raised apart show greater difference than those raised together suggesting some
environmental influence.
• However, twins raised together may develop different personalities due to a desire to be different and this
is environmental.

A number of investigations have been carried out to study the effect of nature and
nurture on human development. (a) Explain how twin studies could be used to compare the
effects of nature and nurture on human development. (4)

▷ Identical / monozygotic twins are genetically identical derived from one zygote
▷ So any phenotypic difference is due to nurture /environmental
▷ Non-identical twins / dizygotic twins are genetically different ; any phenotype that is
different when the environment is the same is likely to be nature / genetic

5. CROSS-CULTURAL STUDIES
Investigations into the visual perception of groups from different cultural backgrounds support the idea that visual
clues for depth perception are at least partially learnt hence role of nurture.

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 Facial expressions can show different emotions. Explain how a cross‑cultural study could be used to investigate
whether recognising different emotions through facial expression is due to nature or nurture. (2)

▷ Study groups from different cultures:

a. If outcome is the same then it is likely to be nature.
b. If outcome is different in the groups then it is likely to be nurture

Suggest how this cross‑cultural study could be carried out to make sure that the results are valid.(2)
▷ Large sample size
▷ Standardized sampling technique e.g. age, gender ;same range of emotions used

EFFECTS OF IMBALANCES IN BRAIN CHEMICALS

- These brain chemicals include the following neurotransmitters:

1) Dopamine

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 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 :
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:

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 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.
- 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

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 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.

X-ray
• X-ray imaging uses broad beam X-rays.
• These broad beam X-rays cannot be used for imaging soft tissues as they are only absorbed by dense
materials such as bone.
• When they are used to identify fractures in bones, x-rays are directed at the affected part, and behind
this part is a white sheet of photographic film. Bones absorb X-rays so these X-rays do not penetrate to
the film hence the film remains white (when no fracture).
• The X-rays that are not absorbed (due to fracture) pass through and turn the film black.
• Radiologists take care to avoid unnecessary exposure to X-rays because they damage DNA causing
mutation. However, some forms of cancer are treated with radiotherapy. In this process, X-rays are used
to kill cancer cells.

Disadvantages of X-ray
1. Harmful as it can causes mutation.
2. Cannot be used in soft tissues as they do not absorb standard broad beam x –rays.
3. Hairline fractures may not be detected.
4. Give only still pictures.

Computerized Axial Tomography (CT and CAT) Scan

• Was developed to overcome the limitations of X-rays.

• 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.

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 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:
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.

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Functional MRI (fMRI)

• It is a modified MRI scan that uses radiowaves and magnetic field.

• The fMRI allows the brain activity to be seen/studied in real action during live tasks such as eating
chocolate.
• The fMRI imaging measures the changes in blood flow as follows:
1) There is increased supply of oxygenated blood 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.
2) The area does not absorb fMRI signals/radiowaves hence reflect them.
3) The area is seen as white (or 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:
1. No use of X-rays hence no mutations.
2. Greater resolution than CT scan.
3. It looks at the brain functions/activities.
• The disadvantage of fMRI;
Very expensive.

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 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

• 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.

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
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 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.
• It causes the depolarization of the membrane and Ca2+ 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 onh 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.

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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.
▷ 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.
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 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.

USES OF GENETIC MODIFICATION

The human Genome Project (HGP) and the development of new drugs

- HGP was launched to identify the genes and their roles in an organism.
- Human genome is all the genes of the human species. A gene pool is all the alleles in a population.
- The HGP was officially started in 1996 and it was a multinational project.
- It is estimated that our genome contains 20,000 to 25,000 genes.
- The average human gene has about 3000 bases.

- Of late, HGP has made the following developments:

1. Identified new genes
2. Identified genes responsible for inherited diseases.
3. Identified new drug targets (specific molecules that drugs interact with to have their effects, e.g.
enzymes)

- The identification of disease genes and their products is allowing biologists to find new drug targets.
This allows biologists to develop drugs that can work best with the genome/genotype of individual or
certain ethnic groups. This is Pharmacogenomics. Pharmacogenomics is the development of drugs that

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 can work best with the genome/genotype of individual or certain ethnic groups.

The following are the advantages of information about patient’s genome:

a) Doctors will prescribe the correct drug
b) The drug will be at the correct dose
c) Drugs will have fewer side effects
d) Doctors will make more accurate diagnosis of diseases
e) If one understands which genes they carry, they may understand what disease they are likely to be at
risk from and take control of their health.
f) HGP makes it easier to rapidly identify the patient’s specific drug
g) We might be able to change our genetic inheritance by eliminating the genes that code for inherited
diseases or replacing the faulty genes.

Social, economic and ethical issues about possible developments from the HGP

1) Ownership of the information: Some scientists may apply for patents on genetic sequences so
that they have ownership, or have to be paid for any treatments developed by the use of the
knowledge of that sequence-ethical issue
2) Confidentiality of one’s genome is a concern because the information can reach the insurance
companies or employers who may finally deny them services- social issue
3) Can lead to eugenics (the genetic selection of humans) and designer babies-ethical issue
4) Identification of genome is very expensive hence benefit the rich few-ethical issue

Describe one ethical implication associated with the use of information obtained from the analysis of
the human genome.
▷ discrimination e.g. insurers might have access to a person’s DNA
▷ who decides whether a person is tested
▷ need for confidentiality
▷ expensive medical treatments might be restricted

HOW DRUGS CAN BE PRODUCED USING GENETICALLY MODIFIED ORGANISMS (GMOs)

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 • A GMO is an organism with foreign DNA. This DNA is introduced in the organism through gene
technology/genetic engineering.
• Transgenic is the transfer of a gene from one species to another.
• Gene technology 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.
• 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
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 (artificial gene).

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
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 catalyses the formation of cDNA double strand molecule, 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
• 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)

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 - 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
- Bacterial cells are common host cells

DIRECT INTRODUCTION OF GENES INTO PLANT CELLS

- Genes can be inserted into plant cells using particle gun.

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

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 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)

- 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

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 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.
- 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
- 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.

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- Potential hazards such as allergies.
- Unethical due to use of animals such as sheep.

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