regulation of skeletal muscle contraction by regulation of release of sequestered calcium ion

Definition

Target type: biologicalprocess

Any process that modulates the frequency, rate or extent of skeletal muscle contraction via the regulation of the release of sequestered calcium ion by sarcoplasmic reticulum into cytosol. The sarcoplasmic reticulum is the endoplasmic reticulum of striated muscle, specialised for the sequestration of calcium ions that are released upon receipt of a signal relayed by the T tubules from the neuromuscular junction. [GOC:mtg_muscle]

Skeletal muscle contraction is a complex process that is tightly regulated by the release of sequestered calcium ions. The process begins with a nerve impulse arriving at the neuromuscular junction, where it triggers the release of acetylcholine (ACh) from the motor neuron. ACh diffuses across the synaptic cleft and binds to receptors on the sarcolemma, the plasma membrane of the muscle fiber. This binding initiates a cascade of events that lead to the depolarization of the sarcolemma and the propagation of an action potential down the T-tubules, invaginations of the sarcolemma that run deep into the muscle fiber.

The action potential then travels to the sarcoplasmic reticulum (SR), a specialized organelle within the muscle fiber that stores calcium ions. The SR is closely associated with the T-tubules, and the action potential triggers the opening of calcium release channels in the SR membrane. This allows calcium ions to flood out of the SR and into the sarcoplasm, the cytoplasm of the muscle fiber.

Calcium ions bind to troponin, a protein that is part of the thin filaments of the sarcomere, the basic contractile unit of muscle. This binding causes a conformational change in troponin, which in turn causes tropomyosin, another protein associated with the thin filaments, to move away from the myosin-binding sites on actin.

With the myosin-binding sites on actin exposed, myosin heads, which are the globular heads of the myosin protein, can bind to actin and initiate the power stroke, a cyclical process of binding, pulling, and detaching that causes the thin filaments to slide past the thick filaments. This sliding movement, which is powered by the hydrolysis of ATP, shortens the sarcomere and ultimately leads to muscle contraction.

As the action potential subsides, calcium release channels in the SR membrane close, and calcium ions are actively pumped back into the SR by calcium ATPase pumps. This removal of calcium ions from the sarcoplasm causes troponin to revert to its original conformation, allowing tropomyosin to block the myosin-binding sites on actin again. Without calcium ions bound to troponin, myosin can no longer bind to actin, and the muscle relaxes.

The regulation of skeletal muscle contraction by calcium ion release is a highly efficient and precise process. It allows for the rapid and coordinated contraction of muscle fibers, enabling movement and maintaining posture. Any disruption to this process, such as in diseases like muscular dystrophy, can lead to significant impairments in muscle function.'
"

Proteins (2)

Compounds (12)