Physiology of

Muscle
 Acetylcholine

Motor end
plate (MEP)
Neuromuscular Transmission

Motor end plate potential

Properties of neuromuscular transmission:
1- Occurs in one direction (from nerve to muscle).
2- Delay 0.5 msec.
3- Easy fatigue.

4- Blocked by curare.

5- Stimulated by Ca++.
Inhibited by Mg++.
6- Stimulated by metacholine, pilocarpine, carbacol,
small dose of nicotine.

7- Stimulated by anticholinesterases (physostigmine,

neostigmine, DPF).
Miniature end plate potential

All-or none rule

Single muscle fiber

Motor unit
Motor Unit
Myasthenia Gravis:

Severe muscle weakness

Auto-immune disease:
Antibodies against Ach receptors

Treatment: anti-cholinesterase drugs

Molecular Theory for
Muscle Contraction
Ryanodine Ca2+ release
channel
 1- Type of muscle fiber.
Slow Red Fibers Fast Pale Fibers
Type I Fibers Type II Fibers
Small fibers Larger fibers

Innervated by small slowly conducting Innervated by large rapidly conducting

motor neurons motor neurons
Large amount of oxidative enzymes Large amount of glycolytic enzymes.
(many mitochondria)
Low ATPase activity High ATPase activity

Extensive capillaries: more blood Fewer capillaries: less blood supply

supply
High myoglobin content Low myoglobin content

More resistant to fatigue Less resistant to fatigue

Slow contraction Rapid contraction

 muscle twitch

Muscle
Tension

Muscle action potential

Muscle action potential
Clonus
Gradation of muscular contraction:
The force of muscle contraction in our bodies can be increased by:

- increasing the number of active motor units.

- increasing the frequency of discharge (number of nerve impulses per

unit time), in each motor nerve fibre to produce summation.
 Length-Tension relationship

Total length-tension relationship

Tension

Active length-tension relationship Passive length-tension relationship

Resting length

Sarcomere length 2.2 m

Length
Staircase phenomenon Treppe
 Creatine phosphate

10 sec
Creatine + Pi + E

Glycogen / Glucose

30-40 sec E + ADP + Pi ATP

Lactic acid + E 5-6 sec

Glucose / Fatty acid / amino acid

Unlimited O2

CO2 + H2O + E
Fate of Lactic acid formed during exercise:

1/5 of lactic acid is oxidized aerobically.

4/5 lactic acid will be converted to liver glycogen.

Functions of lactic acid produced during exercise:
1. 1/5 of lactic acid oxidized aerobically and produce energy to restore
ATP and CP in the muscle.
2. 4/5 lactic acid will be converted to liver glycogen which is a source of
blood glucose, needed for metabolism of heart, brain and muscles.
3. Lactic acid can be used as a fuel for cardiac muscle.
4. Locally, it dilates skeletal blood vessels to increase their blood
supply.
5. Lactic acid when passing to the general circulation, will produce
slight acidosis, which will stimulate the respiratory centres and
cardio-vascular centres, to increase respiration rate and heart rate.
Excess post-exercise O2 consumption: EPOC
Oxygen Debt:

Excess O2 consumed during post-exercise recovery

period in excess of resting consumption
5- Muscle Fatigue
-Decreased strength.
-Prolonged duration.
-Incomplete relaxation (contracture).

Causes:

1- Accumulation of metabolites (lactic acid).

2- Depletion of ATP, creatine phosphate & glycogen.
3- Interruption of blood supply.
4- Diminished neuromuscular transmission.
Muscle hypertrophy

Number of muscle fibers does not increase

Fiber content increases (myofibrils, ATP, CP, glycogen)

Reaction of muscle to denervation:
1- Paralysis & Atrophy.

2- Fasciculation.

3- Fibrillation.

Rigor Mortis
It is due depletion of muscle ATP leading to failure of
muscle relaxation (contracture).

It starts few hours and ends 15-25 hours after death.