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step 2: Power stroke. ATP and Pi are released and myosin head pivots and bends, changing its bent low energy state. Pulls actin filament to M line.

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Step 3: Cross bridge detachment. After ATP attaches to myosin, link between myosin and actin weakens, and the myosin head detaches.

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Step 4: Cocking of myosin head. As ATP is hydrolyzed to ATP and Pi, myosin head returns to prestroke high-energy, or "cocked position."

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step 1: Cross-bridge formation. Energized myosin head attaches to actin myofilament, forming cross-bridge.

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Step 3 and 4: Ca2+ combines with troponin and removes the blocking action of tropomyosin by changing shape of the actin so that the myosin binding site is exposed. Myosin and actin then form a cross-bridge and contraction begins.

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Step 2: Transmission of the action potential along the t-tubules cause the adjacent sarcoplasmic reticulum to release Ca2+ which flows into the cytosol.

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Step 1:  The action potential moves down the sarcolemma and t-tubules.

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The brain sends an action potential down to the Neuromuscular junction. The action potential causes voltage-gated calcium ion channels to open and calcium to enter the neuron which stimulates the release of ACh into the cleft. ACh binds to the receptor site and activates the voltage-gated sodium channel which pumps Na+ in and K+ out. This causes the cell interior to be depolarized. Inital depolarization then spreads to adjacent areas opening voltage-gated sodium channels and initiating an action potential that moves along the sarcolemma. Na+ concentration due to depolarization changes the membrane's permeability by opening K+ pumps that allow K+ to diffuse across the sarcolemma out the muscle fiber. This is known as repolarization.