An action potential emanating from the Central Nervous System (brain) causes the alpha motor neuron to send out an action potential over the axon it possesses. The action potential transmits by setting in motion the sodium dependent controls over the axiom to the synaptic cleft, hence reaching the motor neuron terminal. The calcium ion entry cases the neurotransmitter acetylcholine to mix with the plasma membrane. Acetylcholine is eventually released into the extracellular voids between the motor endplate of the leg muscle and the motor neuron terminal (Marieb & Katja, 2007).

Acetylcholine enters into the synapse, holds to and initiates the nicotinic acetylcholine receptors thus making the potassium and sodium muscles to seep in. the channel is highly permeable to sodium muscles thus ending up to be highly charged positively, hence initiating an action potential. The triggered action potential moves through the network of fiber muscles for instance the T- tubules. The eccentric contractions initiated acts as a braking force to stop further concentric contraction, thus preventing joint damage (Tassinary & Cacioppo, 2000). This also helps in keeping movement smooth. The depolarization initiates dihydropyridine receptors present in the T tubule membrane adjacent to the reticulum sarcoplasmic and ryanodine receptors. The whole process causes the release of calcium which the binds with the troponin C in the myofibrils; thus unblocking the sites for binding. The release of inorganic phosphate and ADP is tightly joined to the power stroke, thus releasing ATP (Colliander & Tesch, 1990).

Note: lack of ATP leads to a state of rigor mortis.

The ATP is then hydrolyzed by the myosin and the energy released is used to move each skeletal muscle. The united bending of several myosin heads, merge to move the muscle filaments comparative to myosin filaments; thus muscle contraction.