MECHANISM OF

MUSCLE
CONTRACTION
Ginus Partadiredja
The Department of Physiology
UGM, Yogyakarta

 Muscle = neuron excited chemically, electrically,

mechanically to produce action potentials
Muscle neuron contractile mechanism activated by
action potentials

Skeletal muscle:
cross-striations
does not contract without innervation
lacks anatomic & functional connections between fibers
voluntary control
Cardiac muscle:
cross-striations
functionally syncytial
contracts rhythmically in the absence of external innervation
contains pacemaker
Smooth muscle:
Lacks cross-striations
functionally syncytial
contains pacemaker

 Skeletal muscle muscle fibers myofibrils

Muscle fiber: multinucleated, long, cylindrical, single cell
surrounded by sarcolemma (cell membrane)

 Skeletal muscle muscle fibers myofibrils filaments

Hexagonal pattern

 Filaments = contractile proteins:

Myosin II (thick filament)
Actin
Tropomyosin
Troponin: - Troponin I
thin filament
- Troponin T
- Troponin C

Thick filaments A bands

Thin filaments I bands

 Myosin 2 globular heads & long tail

Head of myosin contains actin-binding site & catalytic site
that hydrolize ATP

 Thin filaments two chains of actin

Tropomyosin in the groove of actin
Troponin: T binds other troponin to tropomyosin
I inhibits the interaction of myosin & actin
C contains the binding sites for Ca+2

 Sarcotubular system = T system + sarcoplasmic reticulum

T system of tubules + adjacent terminal cisternae = triad
T system rapid transmission of action potentials from
the cell membrane to the fibrils

 The resting membrane potential of muscle = -90 mV

The action potential = 2 4 ms
The speed along the muscle = 5 m/s
The absolute refractory period = 1 3 ms

The distribution of ions nerve cells

Depolarization = Na+ influx
Repolarization = K+ efflux
Depolarization starts at motor end plate transmitted
along the fiber contractile response

Sequence of events during transmission from the motor

nerve the muscles = transmission in synapses between
neurons

Sequence of Events in Contraction and Relaxation of

Skeletal Muscle
Steps in Contraction:
1. Discharge of motor neuron end of motor neuron Ca+2
enters the endings

2. Release of transmitter (acetylcholine) at motor end-plate

3. Binding of acetylcholine to nicotinic acetylcholine
receptors (concentrated at the tops of the junctional folds)

Junctional folds

4. Increased Na+ and K+ conductance in end-plate membrane

5. Generation of end-plate potential
6. Generation of action potential in muscle fibers

7. Inward spread of depolarization along T tubules

excitation contraction coupling
8. Release of Ca+2 from terminal cisterns of sarcoplasmic
reticulum and diffusion to thick and thin filaments

9. Binding of Ca+2 to troponin C, uncovering myosin-binding

sites on actin (at resting, troponin I is tightly bound to actin
and tropomyosin covers the sites where myosin heads bind
to actin)
ATP is then split ADP + Pi contraction

10. Formation of cross-linkages between actin and myosin

and sliding of thin on thick filaments, producing movement

Steps in Relaxation:
1. Ca+2 pumped back into sarcoplasmic reticulum
diffuses into the terminal cisterns, ready to be released
by next action potential
2. Release of Ca+2 from troponin
3. Cessation of interaction between actin and myosin

Muscular Contraction
The width of A bands is constant
Z lines move closer

Production of ATP in Muscle Fibers (Tortora & Derrickson,

2006)

3 ways of ATP production:

1. From creatine phosphate
2. Anaerobic cellular respiration (ATP-producing reactions
not requiring oxygen)
3. Aerobic cellular respiration (ATP-producing reactions
requiring oxygen, in mitochondria)

1. Creatine Phosphate
Creatine: small amino acid-like molecule formed in liver,
kidneys, pancreas transported to muscles
Relaxed muscles creatine phosphate 3-4x > ATP
Relaxation: ATP + creatine creatine phosphate + ADP
(by creatine kinase)
Contraction: creatine phosphate + ADP ATP + creatine
(by creatine kinase)
For 15 seconds contraction (100-m dash)

2. Anaerobic Cellular Respiration

Creatine phosphate is depleted then:
Glucose (from blood or from the breakdown of glycogen in
muscles) glycolysis 2 pyruvic acid + 2 ATP (produces
4 ATP but net gain of 2 ATP)
Pyruvic acid mitochondria, aerobic respiration ATP
No oxygen (anaerobic) in cytosol: 80% Pyruvic acid
lactic acid blood (becomes acid) liver convert back
into glucose
For 30 - 40 seconds activity (400-m race)

3. Aerobic Cellular Respiration

Sources of ATP: pyruvic acid, fatty acid (breakdown of
triglycerides; yields > 100 ATP), amino acids (breakdown
of proteins)
Sufficient oxygen: Pyruvic acid mitochondria
oxydized ATP + CO2 + H2O + heat
Slower than glycolysis, but yields 36 ATP
Sources of oxygen: hemoglobin & myoglobin
For > 10 minutes activity (marathon race)

Energy Sources (Ganong, 2005)

ATP + H2O ADP + H3PO4 + 7.3 kcal
Phosphorylcreatine + ADP Creatine + ATP
Rest & light exercise:
FFA CO2 + H2O + ATP
Increased intensity of exercise
Glucose + 2 ATP (or glycogen + 1 ATP) 2 Lactic acid + 4 ATP
(anaerobic)
Glucose + 2 ATP (or glycogen + 1 ATP) 6CO2 + 6H2O + 40ATP
(aerobic)

 100-m dash (10 seconds) 85% of energy is derived

anaerobically
2-mile race (10 minutes) 20% of energy is derived
anaerobically
long-distance race (60 minutes) 5% of energy is derived
anaerobically

 Muscle fatigue: The inability of muscle to maintain force

of contraction after prolonged activity, caused by:
Inadequate release of Ca+2 from sarcoplasmic
reticulum
Depletion of creatine phosphate
ATP levels = resting levels
Insufficient oxygen
Depletion of glycogen
Buildup of lactic acid & ADP
Failure of action potentials in releasing ACh

Oxygen Consumption after Exercise

Oxygen debt added oxygen, over and above the

resting oxygen consumption, taken into the body after
exercise
1. Convert lactic acid glycogen stores in liver (small
amount)
2. Resynthesize creatine phosphate & ATP
3. Replace the oxygen removed from myoglobin

Much of lactic acid pyruvic acid for ATP production

(heart, liver, kidneys, skeletal muscles)
Better term: recovery oxygen uptake (

chemical

reactions, heart & muscles still working, recovery

processes)

Types of Contraction

Isotonic (A) and isometric (B) contraction

Types of Contraction
Isometric (same length) contraction: Contraction occurs
without an appreciable decrease in the length of the whole
muscle do not work (work = force x distance)

 Isotonic (same tension) contraction: Contraction against

a constant load do work

Isotonic contraction

Cause more damage

Muscle twitch: brief contraction followed by relaxation of all

muscle fibers in a motor unit caused by a single action
potential in its motor neuron
Fast muscle fibers: fine movements (7.5 ms)
Slow muscle fibers: gross movements (100 ms)

Summation of Contractions
No refractory period such as in neurons in muscle fibers
Repeated stimulation summation of contractions
Tetanus (tetanic contraction) continuous contraction:
Fused (complete) tetanus
Unfused (incomplete) tetanus

Types of Muscle Fibers

Type I
Other names

Slow, oxidative,
red muscles

Type II
Fast;
glycolytic;
white muscles

Myosin isoenzyme ATPase rate Slow

Fast

Ca+2 pumping capacity of

sarcoplasmic reticulum

Moderate

High

Diameter

Moderate

Large

Glycolytic capacity

Moderate

High

Oxidative capacity (content of

mitochondria, capillary
density, myoglobin content)

High

Low

Examples

Long muscles of
the back

Estraocular

Charateristics

Functions
Examples

Type I
(Red muscles)
Slow response;
long latency;
adapted for
long, slow
contractions

Type II
(White muscles)
Short twitch
durations

Posture
maintenance
Long muscles in
the back

Fine, skilled
movements
Extraocular
muscles, hand
muscles

Slow
Oxidative
Fibers

Fast
OxidativeGlycolytic
Fibers

Fast
Glycolytic
Fibers

Fiber
diameter
Myoglobin
content
Mitochondria

Smallest

Intermediate

Largest

Large
amount
Many

Large
amount
Many

Small
amount
Few

Capillaries
Color

Many
Red

Many
Red-pink

Few
White
(pale)

Structural
Characteristi
c

Slow
Oxidative
Fibers

Fast
OxidativeGlycolytic
Fibers

Fast
Glycolytic
Fibers

Capacity of
generating
ATP

High;
aerobic
respiration

Intermediate; Low;
aerobic &
anaerobic
anaerobic
(glycolysis)
(glycolysis)

Rate of ATP
hydrolysis
Contraction
velocity
Fatigue

Slow

Fast

Fast

Slow

Fast

Fast

High

Intermediate

Low

Functional
Characteristi
c

Slow
Oxidative
Fibers

Fast
OxidativeGlycolytic
Fibers

Fast
Glycolytic
Fibers

Creatine
kinase

Lowest
amount

Intermediate
amount

Highest
amount

Glycogen
stores

Low

Intermediate

High

Order of
recruitment

First

Second

Third

Location

Postural
muscles
(e.g. neck)

Lower limb

Upper limb

Slow
Oxidative
Fibers
Primary Maintaining
function posture;
s
aerobic
endurance
(running a
marathon)

Fast
OxidativeGlycolytic
Fibers

Fast Glycolytic
Fibers

Walking,
sprinting

Rapid, intense
movement of
short duration
(weight lifting;
throwing a ball)

Disorders and Abnormalities

Myasthenia gravis: skeletal muscles are weak and tire
easily; caused by autoantibodies destroying nicotinic
acetylcholine receptors
Lambert-Eaton syndrome: muscle weakness; caused by
antibodies against Ca+2 channels in the nerve endings
Denervation hypersensitivity
Contracture: No relaxation due to the inhibition of Ca+2
transport into the reticulum

Disorders and Abnormalities

Hypotonia: decreased or lost muscle tone
Flaccid paralysis loss of muscle tone, loss/ reduction
of tendon reflexes, atrophy, degeneration of muscles
(disorders of nervous system; electrolytes imbalances
(Na+, Ca+2, Mg+2)
Hypertonia: increased muscle tone
Spastic paralysis increased muscle tone, tendon
reflexes, pathological reflexes (Babinski sign)
Rigidity increased muscle tone, not reflexes
(tetanus)

Disorders and Abnormalities

Muscular dystrophy: progressive weakness of skeletal
muscle caused by mutations in genes for muscle proteins
Duchenes muscular dystrophy dystrophin protein is
absent from muscle; X-linked; fatal by 30 y/o
Metabolic myopathies (e.g. McArdles syndrome)
mutations in genes of enzymes involved in carbohydrates,
fats, and proteins, metabolism
Myotonia muscle relaxation is prolonged after
contraction; abnormal genes in chromosomes 7, 17, or 19,
which produce abnormalities of Na+ or Cl- channels

References
1. Ganong WF (2005). Review of Medical Physiology, 22nd
ed. Chapter 3, Pages: 65-78; Chapter 4, Pages: 116-120
2. Tortora GJ & Derrickson B (2006). Principles of Anatomy
and Physiology, 11th ed. Chapter 10, Pages: 290-314.