calcium is stored in sarcoplasmic reticulum ( sr ) in a muscle cell.
calcium is stored in sarcoplasmic reticulum ( sr ) in a muscle cell.
where is calcium stored in a muscle cell?
sarcoplasmic reticulum ( sr )
excitation–contraction coupling is the process by which a muscular action potential in the muscle fiber causes the myofibrils to contract. in skeletal muscle, excitation–contraction coupling relies on a direct coupling between key proteins, the sarcoplasmic reticulum (sr) calcium release channel (identified as the ryanodine receptor, ryr) and voltage-gated l-type calcium channels (identified as dihydropyridine receptors, dhprs). dhprs are located on the sarcolemma (which includes the surface sarcolemma and the transverse tubules), while the ryrs reside across the sr membrane. the close apposition of a transverse tubule and two sr regions containing ryrs is described as a triad and is predominantly where excitation–contraction coupling takes place. excitation–contraction coupling occurs when depolarization of skeletal muscle cell results in a muscle action potential, which spreads across the cell surface and into the muscle fiber's network of t-tubules, thereby depolarizing the inner portion of the muscle fiber. depolarization of the inner portions activates dihydropyridine receptors in the terminal cisternae, which are in close proximity to ryanodine receptors in the adjacent sarcoplasmic reticulum. the activated dihydropyridine receptors physically interact with ryanodine receptors to activate them via foot processes (involving conformational changes that allosterically activates the ryanodine receptors). as the ryanodine receptors open, is released from the sarcoplasmic reticulum into the local junctional space, which then diffuses into the bulk cytoplasm to cause a calcium spark. note that the sarcoplasmic reticulum has a large calcium buffering capacity partially due to a calcium-binding protein called calsequestrin. the near synchronous activation of thousands of calcium sparks by the action potential causes a cell-wide increase in calcium giving rise to the upstroke of the calcium transient. the released into the cytosol binds to troponin c by the actin filaments, to allow crossbridge cycling, producing force and, in some situations, motion. the sarco/endoplasmic reticulum calcium-atpase (serca) actively pumps back into the sarcoplasmic reticulum. as declines back to resting levels, the force declines and relaxation occurs.
muscle contraction
exertional rhabdomyolysis results from damage to the intercellular proteins inside the sarcolemma. myosin and actin break down in the sarcomeres when atp is no longer available due to injury to the sarcoplasmic reticulum. damage to the sarcolemma and sarcoplasmic reticulum from direct trauma or high force production causes a high influx of calcium into the muscle fibers increasing calcium permeability. calcium ions build up in the mitochondria, impairing cellular respiration. the mitochondria are unable to produce enough atp to power the cell properly. reduction in atp production impairs the cells ability to extract calcium from the muscle cell. the ion imbalance causes calcium-dependent enzymes to activate which break down muscle proteins even further. a high concentration of calcium activates muscle cells, causing the muscle to contract while inhibiting its ability to relax. the increase of sustained muscle contraction leads to oxygen and atp depletion with prolonged exposure to calcium. the muscle cell membrane pump may become damaged allowing free form myoglobin to leak into the bloodstream.
exertional rhabdomyolysis