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Mechanism and Contraction Events of Cardiac Muscle Fibers
Cardiomyocytes are capable of coordinated contraction, controlled through intercalated discs. The IDs spread action potentials to support the synchronized contraction of the myocardium. In cardiac, skeletal, and some smooth muscle tissue, contraction occurs through a phenomenon known as excitation contraction coupling (ECC). ECC describes the process of converting an electrical stimulus from the neurons into a mechanical response. In muscle tissue, the electrical stimulus is an action potential and the desired mechanical response is contraction.
In cardiac muscle, ECC is dependent on a phenomenon called calcium-induced calcium release (CICR), which involves the conduction of calcium ions into the cell triggering further release of ions into the cytoplasm. Like skeletal muscle, the initiation and upshoot of the action potential in ventricular muscle cells is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, in cardiac muscle, an inward flux of extracellular calcium ions through calcium channels on the T-tubules sustains the depolarization of cardiac muscle cells for a longer duration. Contraction in cardiac muscle occurs via the sliding filament model of contraction . In the sliding filament model, myosin filaments slide along actin filaments to shorten or lengthen the muscle fiber for contraction and relaxation. The pathway of contraction can be described in five steps:
An action potential, induced by pacemaker cells, is conducted to contractile cardiomyocytes through IDs, specifically gap junctions.
As the action potential travels between sarcomeres, it activates the calcium channels in the T-tubules, resulting in an influx of calcium ions into the cell.
Calcium in the cytoplasm then binds to cardiac troponin-C, which moves the troponin complex away from the actin binding site. This removal of the troponin complex frees the actin to be bound by myosin and initiates contraction.
The myosin head pulls the actin filament toward the center of the sarcomere, contracting the muscle.
Intracellular calcium is then removed by the sarcoplasmic reticulum, dropping intracellular calcium concentration, returning the troponin complex to its inhibiting position on the active site of actin, and effectively ending contraction.