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Step 4: Cocking of myosin head: energy from hydrolysis of ATP "cocks" myosin head into high-energy state.

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Step 3: Cross bridge detachment: ATP attaches to myosin head, causing bridge to detach.

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Step 2: Working (power) stroke: myosin head pivots and pulls actin filament toward M line.

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Step 1: Cross bridge formation: high-energy myosin head attaches to actin myofilaments forming a cross bridge.

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Step 3: Ca2+ combines with troponin and removes the blocking action of tropomyosin by changing the shape of the actin so that the myosin binding site are exposed.
Step 4: Myosin binds to actin forms cross bridges 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 down the T tubules.

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Step 1: The brain sends an action potential through the motor unit down to a neuromuscular junction.
Step 2: The action potential causes voltage gated calcium ion channels to open, which allow calcium ions to enter the neuron.  This increase in calcium stimulates the release of the neurotransmitter, ACh, which is released into the cleft.
Step 3: ACh binds to an ACh receptor sight and activates voltage gated sodium channel, which pumps Na+ in and K+ out. More Na+ is pumped into the muscle cell than K+ is pumped out causing the cell interior to become less negative.
Step 4: Initial depolarization spreads to adjacent areas, opening voltage gated Na+ channels and eventually initiating an action potential that moves along the lengths of the sarcolemma.
Step 5: Na+ concentrations, caused by depolarization, stimulate a change in membrane permeability by opening voltage-gated K+ pumps which allow K+ to diffuse across the sarcolemma out of the muscle fiber.  This is known as repolarization.