An impulse travels down the axon and enters the muscle at the neurpmuscular junction causing voltage regulated calcium channels in the axon membrane to open. Calcium ions from the extracellular fluid flow in to the axon terminal. this causes synaptic vesicles to fuse with the presynaptic membrane and realease the transmitter substance, Acetylcholine into the synaptic cleft.
Acetylcholine (ACh) diffuses across the gap and attached to receptors on the sarcolemma. This causes an action potential (impulse wave) to be sent along the sarcolemma, spreading along the muscle fibre.
Impulse spreads along the sarcolemma.
Once generated the action potential spreads along the sarcolemma and goes deep inside the muscle fibre by going down the T tubules. At this point the action potential triggers teh release of Calxium ions from the sarcoplasmic reticulum.
Calcium is released from the SR: actin sites are activated. The released Calcium ions bind to Troponin. The troponin changes shape, removing the blocking action of Tropomyosin. The actin active sites are now exposed (the black spot) allowing the myosin heads to attach to the site.
Myosin head performs powerstroke and pulls actin filament. ADP and Pi are released.
Crossbrides detach whilst new ATP molecules attach to myosin head.
ATP is broken down to provide energy for new corss bridge formation.
Ca++ is removed from the cytoplasm, tropomyosin blocks the actin site.
A drop in the stimulus causes Calcium concentration to decrease and muscle to relax.