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step 2: ADP and P are released, and the myosin head is changed to its bent low-energy state when it pivots and bends.

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Step 4: ATP is hydrolyzed to ADP and P, and the myosin head returns to its high energy "cocked" position.

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Step 3: Myosin attaches to ATP, and this causes the link between myosin and actin to weaken, causing the myosin head to detach and the cross bridge to break

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step 1: Myosin, now energized, attaches to an actin myofilament, forming a cross bridge.

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Step 3 and 4: The CA2+ combines with troponin and changes the shape of the actin, removing the blocking actin of the tropomyosin. This exposes the binding site of the myosin. Myosin binds with the actin, forming a cross bridge, and starting muscle contraction.

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Step 2: As the action potential moves down the T tubules, the Sarcoplasmic Reticulum releases CA2+, which flows into cytoplasm.

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Step 1:  The action potential moves down the sarcolemma and down the T tubules (protrusion of sarcolemma).

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The brain sends an action potential down to a neuromuscular junction (gap between axon terminal and motor cell). This causes voltage gated Ca ions to enter the neuron, which stimulates the release of acetylcholine. When ACh binds to ACh receptor sites, voltage gated Na+ ion channels are activated, and Na+ ions are pumped into the cell while K+ ions ions are pumped out. More Na+ is pumped out than K+is pumped in, causing depolarization. This depolarization spreads down the sarcolemma, opening NA+ channels, and causing an action potential down it. Na concentrations stimulate the opening of voltage gated K+ ion channels, allowing K+ to diffuse across the sarcolemma, in an event called repolarization