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Step 4: Cocking of myosin head. As ATP is hydrolyzed to ADP and P, the myosin head returns to its pre stroke high energy.

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Step 3:

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step 2: ADP and P are released and the myosin head pivots and bends, changing to it's bent low energy state. As a result it pulls the actin filament toward the M line

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step 1: energized myosin head attaches to an actin myofilament, forming a cross bridge

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Step 3 and 4: 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
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 (protrusion of the sarcolemma that protrude deep into muscle cell

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Event 1:
The brain sends nerve impulses through the motor unit down to a nuro transmuscular junction where the end of the nerve cell meets a muscle cell motor unit- consist + ap the motor neuron and all muscles it supplies. Nerve impulses causes voltage gated calcium ion channels to open which allow calcium ions to enter the neuron. This increase in Ca stimulates the release of the neurotransmitter, acetylcholine, which is released into the cleft. Ach binds to a Ach receptor sight and activates voltage gated sodium channel which pumps Na+ in and K+ out. More Na+ is pumped out causing the cell interior to become less negative or depolarized. Initial depolarization spreads to adjacent areas, opening voltage gated sodium channels and eventually initiating an action potential that moves along the lengths of the sarcolemma (muscle cell membrane). Na+ concentrates caused by depolarization, stimulates 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.