Contractility

Contractility refers to the intrinsic ability of muscle tissue to develop force and shorten in response to stimulation, independent of changes in muscle length (preload) or loading conditions (afterload). In the heart this property is often described as the strength of ventricular contraction and its impact on stroke work.

In cardiac muscle, contractility is governed by intracellular calcium handling and myofilament responsiveness to calcium. A greater calcium transient during systole increases cross-bridge formation and force. Sympathetic stimulation via beta-adrenergic receptors raises cAMP, activates protein kinase A, enhances calcium influx and release, and increases myofilament sensitivity, producing a positive inotropic effect. By contrast, pharmacologic or pathologic factors that reduce calcium availability or myofilament responsiveness produce negative inotropy.

In smooth muscle, contractility is initiated by calcium binding to calmodulin, which activates myosin light-chain kinase and promotes cross-bridge cycling. Myosin light-chain phosphatase reduces phosphorylation and relaxes the muscle. Thus, smooth muscle contractility is governed by calcium signaling and kinase activity rather than the troponin-based regulation seen in striated muscle.

Measurement and clinical relevance: For the heart, contractility is inferred from indices such as the maximal rate of pressure rise (dP/dt max), ejection fraction, or end-systolic elastance; load-independent measures are preferred when possible. Reduced contractility occurs in heart failure and cardiomyopathy; increased contractility can occur with catecholamine surges. Treatments aimed at modifying contractility include inotropes (dobutamine, milrinone) and calcium sensitizers (levosimendan), used with caution due to risks such as arrhythmia and increased oxygen demand.