Anatomy & Physiology Learning Centre
Muscle Contractions
Control of Skeletal Muscle Contractions
1. Muscle contraction begins when an
action potential reaches the synaptic
terminal of a motor neuron.
The neurotransmitter acetylcholine
(ACh) is then released into the synaptic
cleft of the neuromuscular junction.
ACh binds to ACh receptors on the
motor end plate of the skeletal muscle
fiber.
2. Binding of Ach causes the muscle cell’s
membrane (also known as the
sarcolemma) to become permeable to
Na+.
These ions rush into the sarcoplasm
(the cytoplasm of the muscle cell)
causing the entire surface of the cell to
depolarize (becomes more positively
charged). With the help of T tubules
(transverse tubules which run from the
surface of the muscle cell directly into
the cell), the depolarization reaches into the center of the cell as well.
3. The depolarization of T tubules causes the sarcoplasmic reticulum (similar to
an endoplasmic reticulum) to release Ca2+ into the sarcoplasm.
4. When Ca2+ binds to troponin, it alters the position of the tropomyosin on the
actin filament, exposing the myosin binding sites (see diagram on next page).
When the binding sites are exposed, “myosin heads” on the myosin filament can
then bind to the exposed sites on the actin filament.
5. As the myosin heads interact with actin, contraction begins. The sliding filament
model is used to describe how the contraction of the muscle cell occurs.
Authored by Katherine Cheung
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Myosin binding sites (yellow) are blocked Myosin binding sites (yellow) are exposed
by tropomyosin when muscle cells are when Ca2+ binds to troponin.
resting.
The Sliding Filament Model
1. Myosin heads are initially in an “activated” position with ADP and Pi bound to
them. When myosin heads bind to the myosin binding sites on actin, a cross-
bridge is formed.
2. ADP and Pi are then released and the myosin heads pivot (pulling inward and
pulling the actin filament along). This is called the power stroke and
contraction occurs.
Quick Analogy: The myosin head works like a mouse trap. When the myosin
heads are in an activated position, it is similar to setting a mouse trap. Energy is
stored in these positions. When the myosin head contacts the actin filament, the
release of ADP and Pi causes it to snap forward, like setting off the mouse trap.
3. ATP then binds to the myosin heads causing them to detach from the myosin
binding sites on actin.
4. The hydrolysis of ATP (into ADP and Pi) produces energy which is used to
move the myosin head back into an "activated" position.
Steps 1 to 4 are repeated as long as ATP is available and Ca2+ is present in the
sarcoplasm.
Helpful animation: [Link]
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Termination of muscle contraction
Muscle contraction stops when motor neurons no longer signal for a muscle
contraction. ACh is removed from the neuromuscular junction through
reabsorption at the synaptic terminal and digestion by acetylcholinesterase
(AChE). Without ACh at the motor end plate, there is no longer a depolarization
of the sarcolemma and T-tubules, and Ca2+ is actively pumped back into the
sarcoplasmic reticulum. Ca2+ releases from troponin and tropomyosin again
blocks the myosin binding sites. The myosin stops binding to the actin filament
and muscle contraction stops. Relaxation of the muscle occurs.
Practice questions:
1. Rigor mortis sets in a few hours after a person dies. Rigor mortis occurs when
the muscles stiffen. This is due to the fact that ATP can no longer be
generated by the muscle cells. How does the lack of ATP lead to rigor mortis?
Hint: in which step of the sliding filament model does lack of ATP affect most?
2. The green mamba snake produces venom containing an AChE inhibitor. An
AChE inhibitor prevents AChE from working. When bitten by a green mamba,
what are some of the effects you might see in your skeletal muscles?
3. Dantrolene is a drug used to treat muscle spasms (involuntary contractions of
skeletal muscles). It interferes with the release of Ca2+ from the sarcoplasmic
reticulum. Explain the mechanism of how this drug works to stop muscle
spasms.
Answers:
1. The lack of ATP affects step 3 of the sliding filament model. Without ATP, the
myosin heads remain attached to the actin filament. The muscles will stay
contracted leading to the stiffness seen in rigor mortis.
2. If AChE does not work, ACh cannot be broken down and remains attached to
the receptors on the motor end plate. This will lead to continuous
depolarization of the sarcolemma and Ca2+ remain in the sarcoplasm. This
will cause extended stimulation of skeletal muscles and they will continuously
contract. No relaxation occurs.
3. Without the release of Ca2+ from the sarcoplasmic reticulum, tropomyosin
continues to block the myosin binding sites on actin. Myosin heads cannot
interact with actin. This prevents muscle contractions from occurring and will
help treat muscle spasms.
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