Molecular mechanism:
Muscle contraction mechanism is described by sliding filament theory. This theory described by Andrew F Huxle, Rolf Niedergerke, Hugh Huxley and Jean Hanson in 1954. Muscle contraction is a cyclic repetitive process. In which, actin filament slide over myosin and generate tension in the muscle.
Action potential from CNS reaches neuromuscular junction and release the acetylcholine near to muscle fibre. Acetylcholine diffuse the synapse where it binds to the nicotinic acetylcholine receptors. After binding, receptors get activated on neuromuscular junction and it lead to the opening of the sodium/potassium channel. It results in sodium influx and potassium outflow from the cell. Sodium/potassium movement from the muscle cell generate an action potential which leads to the depolarization of the inner muscle fibre.
Depolarization in the inner muscle fibre activates L-type voltage dependent calcium channels (Ex. Dihydropyridinereceptors) in the sarcoplasmic reticulum. This channels are closely resembles the calcium release channels such as ryanodine receptors. Activation of voltage gated calcium channels presence in the sarcoplasmic reticulum start to release the calcium.
The released calcium binds to the troponin C which present in the myosin fibril and modulates the tropomyosin allosterically. In normal condition tropomyosin do not allow the myosin to bind on thin fibres. But in presence of calcium, troponin (troponin T), it undergoes the allosteric modification and troponin loose the affinity over thin filament. It results in tropomyosin migration from the thin filament. Immediately, myosin binds strongly with the freed area of thin filament. This process is an energy coupled process, so myosin utilizes the ATP energy by cleaving into ADP and inorganic phosphate. Actin also involve in this process, here it helps to release the inorganic phosphate from the myosin. The overall results in sarcomere shortening. In this state, the distance in between the Z band shortens. The movement of myosin was observed around 10 to 12 nm per power stroke. The availability of ATP increases the power stroke cycles (energy generation by lysing the ATP).

Meanwhile, sarcoplasmic reticulum actively collect the calcium present in the sarcoplasm. This results in the decrease in sarcoplasmic calcium level. So, the calcium start to migrate from the thin filaments which results in tropomysin remodelling to the native form. The native form of tropomyosin replaces the myosin and bind with the thin filament (Figure 16.2).