MUSCLE

PHYSIOLOGY
 SYLLABUS

• Muscle physiology – comparison of

physiology of skeletal muscles, cardiac
muscles and smooth muscles.

• Physiology of muscle contraction

 INTRODUCTION
 Muscle is a soft tissue. Contain protein filaments
of actin and myosin that slide past one another,
producing a contraction – motor and motor nerves.

3 major groups of muscles

 Skeletal

 Cardiac

 Smooth
 SKELETAL MUSCLES
• Attached to bone via tendon or
aponeurosis.

• Contraction-locomotion

• Supplied by somatic nerves – neuro

muscular junction.

• Voluntary and involuntary.

• Striated, multinucleated cells.

SMOOTH MUSCLES

• Contraction-movement of food….etc

• Supplied by ANS.

• Controlled by pacemaker cells

(except eyes).

• Non-striated/ plain muscles, uni-

nucleated and not under volitional
control.
CARDIAC MUSCLES

• Contraction-movement of blood

• Supplied by ANS.

• Controlled by pacemakers.

• Striated, uni-nucleated and not

under volitional control.
COMPARATIVE PHYSIOLOGY
OF SKELETAL, SMOOTH &
CARDIAC MUSCLE FIBERS
Striated Muscle Smooth Muscle Cardiac Muscle
Cells Cells Cells

Voluntary Involuntary Involuntary

Line walls of most Found only in the

Attached to bones
internal organs Heart
Striated Muscle Smooth Muscle Cardiac Muscle
Cells Cells Cells

Very long, Branching chains of

Single, tapering,
cylindrical, cells, with single
cells with
multinucleate, nucleus and
a single nucleus
cells striations
 Striated Muscle Smooth Muscle Cardiac Muscle
Cells Cells Cells
Not self stimulating:
each fibre Self stimulating: Self stimulating:
innervated not individually impulse spreads
by branch of innervated, impulse from
somatic motor spreads from cell to cell
neuron as cell to cell
part of motor unit

Under control of Under control of

Under control of nervous, chemicals nervous, chemicals
nervous system and endocrine and endocrine
system system
Striated Muscle Smooth Muscle Cardiac Muscle
Cells Cells Cells

No rhythmic Rhythmic Rhythmic

contractions contractions contractions

Strength increases Stress - Relaxation Strength increases

with stretching Response with stretching
PHYSIOLOGY OF MUSCLE
CONTRACTION
Each myofibril contains myofilaments.
Thick filaments (DARK)-
 A bands contain thick filaments (primarily composed
of myosin).
Thin filaments (LIGHT)-
 I bands contain thin filaments (primarily composed
of actin).
 Center of each I band is Z disc.
Sarcomere -
 Z disc to Z disc.
 M lines :
Produced by protein filaments in a sarcomere.
Anchor myosin during contraction.
Titin -
 Elastic protein that runs through the myosin from M
line to Z disc.
 Contributes to elastic recoil of muscle.
 SLIDING FILAMENT THEORY
OF CONTRACTION
Sliding of filaments is produced by the actions of cross
bridges.
• Cross bridges are part of the myosin proteins that
extend out toward actin.
- Form arms that terminate in heads.
• Each myosin head contains an ATP-binding site.
- The myosin head functions as a myosin ATPase.
 CONTRACTION
 Myosin binding site splits ATP to ADP and Pi.
 ADP and Pi remain bound to myosin until myosin
heads attach to actin.
 Pi is released, causing the power stroke to occur.
 Power stroke pulls actin toward the center of the A
band.
 ADP is released, when myosin binds to a fresh ATP at
the end of the power stroke.
 Release of ADP upon binding to another ATP,
causes the cross bridge bond to break.
 Cross bridges detach, ready to bind again.
- Synchronous action
 MUSCLE RELAXATION

• APs must cease for the muscle to relax.

• ACh-esterase degrades ACh.
• Ca2+release channels close.
• Ca2+pumped back into SR through Ca2+- ATPase pumps.
• Choline recycled to make more ACh.
EXTRA CHUNKS
• Skeletal Muscles

Skeletal muscle attached to bone on each end by

tendons.

• Agonist muscle:

Prime mover of any skeletal muscle movement.

• Antagonist muscle:

Flexors and extensors that act on the same joint

to produce opposite actions.
Functions of Muscle Tissue

• Excitability capable of response to chemical signals,

stretch or other signals & responding with electrical
changes across the plasma membrane

• Conductivity local electrical change triggers a wave of

excitation that travels along the muscle fiber
Contractility -- shortens when stimulated Extensibility -
- capable of being stretched Elasticity -- returns to its
original resting length after being stretched
 MOTOR UNIT
When somatic neuron is activated, all the muscle fibers it
innervates contract with all or none contractions.
Innervation ratio -
• Ratio of motor neuron: muscle fibers.
• Fine neural control over the strength occurs when many
small motor units are involved.
Recruitment -
• Larger and larger motor units are activated to
produce greater strength.
 Each somatic neuron together
with all the muscle fibers it
innervates.
 Each muscle fiber receives a
single axon terminal from a
somatic neuron.
 Each axon can have collateral
branches to innervate an equal #
of fibers.
 SLIDING FILAMENT THEORY
OF CONTRACTION

Muscle contraction-
• Occurs because of sliding of thin filaments over and
between thick filaments towards center.
• Shortening the distance from Z disc to Z disc.
A bands:

• Contain actin.

• Move closer together.

• Do not shorten.

I bands:

• Distance between A bands of successive sarcomeres.

• Decrease in length.

H bands shorten.

• Contain only myosin.

• Shorten during contraction.

REGULATION OF CONTRACTION

• Regulation of cross bridge attachment to actin due to:

Tropomyosin - Lies within grove between double row of G-
actin.
Troponin - Attached to tropomyosin.
• Serves as a switch for muscle contraction and relaxation.
In relaxed muscle - Tropomyosin blocks binding sites on
actin.
 ROLE OF CA2+ IN MUSCLE
CONTRACTION
Muscle Relaxation:
[Ca2+] in sarcoplasm low when tropomyosin blocks
attachment.
• Prevents muscle contraction.
• Ca2+ is pumped back into the SR in the terminal
cisternae.
• Muscle relaxes.
 EXCITATION-CONTRACTION
COUPLING
• Na+ diffusion produces end-
plate potential
(depolarization). positive
ions are attracted to
negative plasma membrane.
• If depolarization sufficient,
threshold occurs, producing
APs.
• APs travel down
sarcolema and T tubules.
• SR terminal cisternae releases
Ca2+from chemical release
channels:
• Electromechanical release
mechanism.
• Ca2+ is also released through a
Ca2+- induced Ca2+ release.
• Ca2+attaches to troponin.
• Tropomyosin- troponin
complex configuration
change occurs.
• Cross bridges attach to
actin.
SEQUENCE - MUSCLE CONTRACTION
1. An action potential travels along a motor nerve to its
endings on muscle fibers.

2. The nerve secretes a small amount of the

neurotransmitter substance – acetylcholine at each
ending.

3. The acetylcholine acts on a local area of the muscle

fibre membrane to open multiple “acetylcholine –gated”
cation channels through protein molecules floating in
the membrane.
4. The acetylcholine acts on a local area of the muscle
fibre membrane to open multiple “acetylcholine –
gated” cation channels through protein molecules
floating in the membrane.

5. The action potential travels along the muscle fibre

membrane in the same way that action potentials
travel along nerve fibre membranes.
6. The action potential depolarizes the muscle
membrane, and much of the action potential
electricity flows through the centre of the muscle
fibre. Here it causes the sarcoplasmic reticulum to
release large quantities of calcium ions that have
been stored within this reticulum.

7. The calcium ions initiate attractive forces between

the actin and myosin filaments, causing them to
slide alongside each other, which is the contractile
process.
8. After a fraction of a second, the calcium ion are
pumped back into the sarcoplasmic reticulum until a
new muscle action potential comes along; this
removal of calcium ions from the myofibrils causes
the muscle contraction to cease.