User:Pumwi23/Muscle contraction

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Picture showing the different interactions within the ECC pathway

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Excitation–contraction coupling (ECC) is the process by which a muscular action potential in the muscle fiber causes myofibrils to contract. In skeletal muscle, excitation–contraction coupling relies on a direct coupling between two key proteins, the sarcoplasmic reticulum (SR) calcium release channel identified as the ryanodine receptor 1 (RYR1) and the voltage-gated L-type calcium channel 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 (usually through neural innervation) results in a muscle action potential, which spreads across the muscle's surface and into the muscle fiber's network of T-tubules, 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 ryanodine receptors open, Ca²⁺ is released from the sarcoplasmic reticulum into the local junctional space and diffuses into the bulk cytoplasm to cause a calcium spark. 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 Ca²⁺ released into the cytosol binds to Troponin C by the actin filaments, to allow cross-bridge cycling, producing force and, in some situations, motion.

When the desired motion is accomplished, relaxation can be achieved quickly through numerous pathways. Relaxation is quickly achieved through a Ca²⁺ buffer with various cytoplasmic proteins binding to Ca²⁺ with very high affinity. These cytoplasmic proteins allow for quick relaxation in fast twitch muscles. Although slower, the sarco/endoplasmic reticulum calcium-ATPase (SERCA) actively pumps Ca²⁺ back into the sarcoplasmic reticulum, resulting in a permanent relaxation until the next action potential arrives.

Mitochondria also participate in Ca²⁺ reuptake, ultimately delivering their gathered Ca²⁺ to SERCA for storage in the sarcoplasmic reticulum. A few of the relaxation mechanisms (NCX, Ca2+ pumps and Ca2+ leak channels) move Ca2+ completely out of the cells as well. As Ca²⁺ concentration declines to resting levels, Ca2+ releases from Troponin C, disallowing cross bridge-cycling, causing the force to decline and relaxation to occur. Once relaxation has fully occured, the muscle is able to contract again, thus resetting the cycle.