Kontraktila

Kontraktila, or contractility, is the intrinsic ability of muscle tissue to develop tension and shorten in response to stimulation. It is a property of muscle fibers and some other contractile cells, and it underpins movement, circulation, respiration, and various organ functions. Contractility arises from the interaction of cytoskeletal proteins, primarily actin and myosin, powered by ATP, and is regulated by calcium signaling that coordinates cross-bridge cycling.

In skeletal and cardiac muscle, contraction is triggered by an increase in intracellular calcium. Calcium binds to troponin, causing a shift in the tropomyosin complex that exposes myosin-binding sites on actin. Myosin heads form cross-bridges, hydrolyze ATP, and slide actin filaments, shortening the muscle fiber. In smooth muscle, calcium activates calmodulin and myosin light-chain kinase, which phosphorylates myosin and enables interaction with actin, also leading to shortening, but with slower kinetics and longer-duration contractions.

Contractility varies by tissue type and physiological state. It is commonly measured as isometric force, shortening velocity, or in the heart, metrics such as ejection fraction. Pathologies can alter kontraktila function: reduced contractility is central in heart failure and certain cardiomyopathies, while aberrant contractility can contribute to hypertension, arrhythmias, or muscular dystrophies. Some non-muscle cells exhibit limited contractile activity, contributing to processes like cell migration, wound healing, and tissue remodeling.