Calcium is an essential element within the process of muscle contraction due to its direct involvement in the interaction between muscle fiber proteins, such as actin, troponin, and myosin. Myofibrils have the ability to interact with ATP and contract only in the presence of certain concentrations of calcium ions in the medium. In the resting muscle, the concentration of calcium ions is maintained below the threshold value with the participation of Ca2+-dependent ATPase. At rest, this active transport system accumulates calcium in the cisterns of the sarcoplasmic reticulum and the tubules of the T-system.
Before the stimulus, calcium is stored in the sarcoplasmic reticulum within the muscle cells. After the action potential reaches the T-tubules and the sarcoplasmic reticulum, calcium ions are released from it into the sarcoplasm (Kuo & Ehrlich, 2015). At rest, the tropomyosin molecules are above the active centers of the actin protein and prevent the attachment of the head section of myosin. After the release of calcium from the sarcoplasmic reticulum, they attach to troponin. Troponin changes its configuration and lifts tropomyosin molecules from the actin’s active sites. As soon as the active areas of actin are opened, the myosin heads are attached to them and the process of contraction of the muscle fiber begins (Kuo & Ehrlich, 2015). After the contraction is completed, calcium ions are reabsorbed into the sarcoplasmic reticulum through Ca2+ pumps on the membrane of the organelle.
In conclusion, calcium plays a vital role in the muscle contraction process, where it deactivates one of the contractions inhibiting muscle proteins. Specifically, the ions are released from the sarcoplasmic reticulum organelle. They bind to troponin, which blocks myosin and actin interaction. Calcium hinders the troponin’s capability to be aligned with actin, which allows myosin head to move along the actin fiber. Therefore, the contraction movement is possible, after which the ions are reabsorbed. Ca2+ acts as switching element that transfers the neuronal signal into a mechanical force through troponin removal from the active fibers.
Kuo, I. Y., & Ehrlich, B. E. (2015). Signaling in muscle contraction. Cold Spring Harbor Perspectives in Biology, 7(2), 1-15. Web.