SKELETAL MUSCLE
PHYSIOLOGY
BY
REV DR CHARLESANTWI-
BOASIAKO
(PHYSIOLOGIST)
UGMS KORLE-BU
Specific leaning objectives
Branching cells
One or two nuclei per cell
Striated
Involuntary
Medium speed contractions
Fusiform cells
One nucleus per cell
Non-striated
Involuntary
Slow, wave-like contractions
Channel
41 REV. A.B.C. PHYSIOLOGIST
The influx of sodium will create an action potential in
the sarcolemma.
Note: This is the same mechanism for generating
action potentials for the nerve impulse.
The action potential travels down a T tubule.
As the action potential passes through the
sarcoplamic reticulum it stimulates the release of
calcium ions.
Calcium binds with troponin to move tropomyosin
and expose the binding sites.
Myosin heads attach to the binding sites of the actin
filament and create a power stroke.
ATP detaches the myosin heads and energizes them
for another contraction.
The process will continue until the action potentials
cease. Without action potentials the calcium ions will
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return to the sarcoplasmic reticulum. REV. A.B.C. PHYSIOLOGIST
Excitation-Contraction
Excitation- refers to the process by which
an action potential in the cell membrane
(sarcolemma) excites the muscle cell to
produce a muscle contraction.
The action potential that was generated at
the neuromuscular junction will spread out
over the sarcolemma and down the T-
tubules into the core of the muscle cell.
This action potential travels very close to the
sarcoplasmic reticulum (SR) and will open
Ca2+ channels, causing the release of Ca2+
from the terminal cisternae of the SR.
The Ca2+ will bind to troponin C on the thin
myofilaments, causing tropomyosin to
uncover the myosin binding sites found on
actin. Myosin will now be able to attach to the
actin and a power stroke will occur.
Relaxation of Muscle
Once action potentials stop, Ca2+ will no
longer diffuse out of the sarcoplasmic
reticulum (SR).
Special calcium pumps rapidly pump Ca2+
back into the SR, up its concentration
gradient; this requires ATP.
Without the calcium present in the cytoplasm
of the muscle cell, the tropomyosin will cover
the myosin binding sites once again.
Myosin will be unable to bind to actin and
power strokes will not occur. The muscle will
relax.
Muscle Contraction
Summary
Nerve impulse reaches myoneural junction
Acetylcholine is released from motor
neuron
Ach binds with receptors in the muscle
membrane to allow sodium to enter
Sodium influx will generate an action
potential in the sarcolemma
Motor unite
One motor neuron plus all the muscle
fibers it enervates (causes to contract).
Motor unit recruitment
Motor Unit
All the muscle cells controlled by
one nerve cell
Summation
Tetanization
Complete
Incomplete
Relationship of velocity of contraction and load
Length tension relationship
Energetics muscle contraction.
The energy is required to:
Formthe cross bridges
Pump Ca2+ from the sarcoplasm to SR
Pump Na+ and K+ across the membrane.
ATP (rephosphorelation)
Phosphocreatine
Glycogen
Oxidative metabolism
Types of fibers
Type I (slow,oxidative,red)
Smaller fiber
Slow ATPase activity of myosin head
More extensive blood supply
More capillaries
High number of mitochondria
Large number of aerobic respiratory
enzymes
Fiber contains large amount of myoglobin.
Type II (Fast, glycolytic, white)
Much larger fibers for great strength of
contraction
Fast ATPase activity of myosin head
Extensive sarcoplasmic reticulum for rapid
release of Ca++ for contraction.
Large amount of glycolytic enzyme for
glycolysis
Less extensive blood supply
Less capillaries
Few mitochondria
Muscle Fatigue
Muscle fatigue is often due to a lack of
oxygen that causes ATP deficit.
Lactic acid builds up from anaerobic
respiration.
Lactic acid fatigues the muscle.