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Nerve impulse arrives at the neuromuscular junction.
The motor neuron releases acetylcholine (ACh).
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End-plate potential and muscle action potential develop.
ACh binds nicotinic receptors on the motor end plate, causing Na⁺ influx. If threshold is reached, an action potential spreads across the sarcolemma.
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Action potential travels down T-tubules.
T-tubules conduct depolarization deep into the muscle fiber.
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Calcium is released from the sarcoplasmic reticulum (SR).
T-tubule depolarization activates dihydropyridine receptors, which open ryanodine receptors in the adjacent SR. This releases Ca²⁺ into the sarcoplasm. In skeletal muscle, extracellular Ca²⁺ entry is not required for this step.
Costanzo Physiology, 7th ed., p. 44.
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Ca²⁺ binds troponin C.
The troponin complex changes its shape.
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Tropomyosin moves away from actin’s myosin-binding sites.
This exposes the active sites on actin, permitting actin-myosin interaction.
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Cross-bridge cycle produces shortening.
- Energized myosin head, carrying ADP + Pi, binds actin.
- Pi, then ADP, are released.
- The myosin head pivots in the power stroke, pulling thin filaments toward the center of the sarcomere.
- A new ATP binds myosin, causing myosin to detach from actin.
- ATP is hydrolyzed to ADP + Pi, re-cocking the myosin head.
- The cycle repeats as long as Ca²⁺ and ATP are available.
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Sarcomere shortens.
Thin filaments slide past thick filaments. The I band and H zone decrease, while the A band remains constant. The filaments themselves do not shorten. The actomyosin cycle converts ATP’s chemical energy into force.
Histology: A Text and Atlas with Correlated Cell and Molecular Biology, pp. 816-818.
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Relaxation occurs.
ACh is broken down by acetylcholinesterase, action potentials stop, and SERCA pumps Ca²⁺ back into the SR. Ca²⁺ dissociates from troponin, tropomyosin again blocks actin binding sites, cross-bridge cycling stops, and the muscle relaxes.
This timing is consistent with the
NCBI physiology overview: the muscle action potential occurs first, followed by intracellular Ca²⁺ rise, then mechanical contraction.