Before a muscle cells can act, it must receive an action potential from a motor neuron. After the sarcolemma of the muscle cell receives the action potential, the electrical impulse travels inward through the transverse tubules and sarcoplasmic reticulum. This electrical charge causes the sarcoplasmic reticulum to quickly release calcium ions into the sarcoplasm. While in a resting state, the tropomyosin protein strands are covering the binding sites on the actin filaments, thus preventing any action-myosin interaction. However, once the calcium ions are released from the sarcoplasmic reticulum they bind with troponin, which has a strong affinity for calcium ions. Troponin, which lies on top of the tropomyosin, then initiates a molecular process of shifting the tropomyosin molecules off the binding sites (on the actin). The myosin cross-bridges can now attach to the binding sites on the actin filaments. …show more content…
This causes the actin filaments to slide over (or be pulled over) the myosin protein and muscle shortening to occur. Present on the globular heads of the myosin cross-bridges is the enzyme ATPase, which speeds up the splitting of ATP to yield adenosine diphosphate (ADP), inorganic phosphate (P), and energy. Adenosine triphosphate is the energy molecule for all muscle actions. Immediately after the power stroke, the myosin cross-bridges detach from their receptor site and rotate back to their original positions. Adenosine triphosphate provides the energy required for the dissociation of actin and myosin. Following this detachment of the cross-bridges, hydrolysis (or splitting) of ATP can reoccur,