the plama membrane or cell membrane in the skeletal muscle cell is called sarcolemma.
the plama membrane or cell membrane in the skeletal muscle cell is called sarcolemma.
the plama membrane or cell membrane in the skeletal muscle cell is called?
sarcolemma
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
based upon animal studies, hmb appears to be metabolized within skeletal muscle into cholesterol, which may then be incorporated into the muscle cell membrane, thereby enhancing membrane integrity and function. the effects of hmb on muscle protein metabolism may help stabilize muscle cell structure. one review suggested that the observed hmb-induced reduction in the plasma concentration of muscle damage biomarkers (i.e., muscle enzymes such as creatine kinase and lactate dehydrogenase) in humans following intense exercise may be due to a cholesterol-mediated improvement in muscle cell membrane function.
beta-hydroxy beta-methylbutyric acid