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As ATP is hydrolyzed to ADP and P, the Myosin head returns to its prestroke high-energy or cocked position.

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After ATP attaches to Myosin, the link between Myosin and Actin weakens, and the Myosin head detaches.

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ADP and P are released and the Myosin head pivots and bends changing to its bent low-energy state. As a result it pulls the Actin filament towards the M line.

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Energized Myosin head attaches to an Actin myofilament, forming a cross bridge.

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Ca2+ combines with Troponin and removes the blocking of Tropomyosin by changing the Actin so that the Myosin binding sites are exposed. The Myosin then binds to Actin and forms cross bridges and contraction begins.

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Transmission of the action potential along the T-tubules cause the adjacent sarcoplasmic reticulum to release Ca+ which flows into the cytosol.

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The action potential moves down the sarcolemma and down the T-tubules.

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The brain sends a nerve impulse down to a neuromuscular junction. The nerve impulse causes voltage-gated Ca+ ion channels to open allowing Ca+ ions to enter the neuron. This increase releases Acetylcholine which is released into the cleft. Ach binds to an Ach receptor sight and activates voltage-gated Na+ ion channels which pumps more Na+ ions in and K+ ions out. This imbalance is called depolarization. The depolarization spreads opening voltage-gated Na+ ion channels and eventually initiating an action potential that moves along the lengths of the sarcolemma. Na+ concentrations caused by depolarization stimulate a change in membrane permeability by opening voltage-gated K+ ion pumps which allow K+ to diffuse across the sarcolemma out of the muscle fiber. This is known as repolarization.