In order for skeletal muscle to develop force, a muscle cell must be able to con

An action potential is generated at the motor end plate by the binding of acetylcholine to the nicotinic receptor. That action potential travels along the sarcolemma and down the transverse tubules. Located within the membrane of the transverse tubules are dihydropyridine receptors that are voltage sensitive. These receptors are usually activated by depolarization. The membrane of the transverse tubule comes into contact with the sarcoplasmic reticulum, allowing the dihydropyridine receptor to directly interact with the ryanodine receptor on the sarcoplasmic reticulum. When the dihydropyridine receptor is activated by membrane depolarization from the action potential, the ryanodine receptor is stimulated to release calcium from the sarcoplasmic reticulum. As intracellular calcium increases, the release of calcium is enhanced by the binding of calcium to another calcium channel on the sarcoplasmic reticulum. In addition to their proximity to the transverse tubule, the sarcoplasmic reticulum is positioned near contractile proteins of the sarcomere to facilitate the delivery of calcium to those contractile proteins. As calcium increases within the cell, it binds to a subunit of the troponin molecule. This binding causes a conformational change in the other two troponin subunits that move the filamentous tropomyosin. At rest, tropomyosin blocks the myosin binding site on the actin molecules. Thus, the movement of tropomyosin exposes the binding site that would allow the energized myosin to interact with actin.