FrankStarling

The Frank-Starling law, also known as the Frank-Starling mechanism, describes the intrinsic property of the heart in which the stroke volume increases in response to an increase in end-diastolic volume (preload), within physiological limits. In other words, the heart pumps more forcefully when it is filled more during diastole, so that cardiac output matches venous return.

Mechanism: As ventricular muscle fibers are stretched toward an optimal length, the overlap between actin and myosin filaments improves, enhancing cross-bridge formation and force generation. Stretch-related changes in intracellular calcium handling and myofilament sensitivity also contribute. Consequently, within the normal range, greater end-diastolic stretch yields greater systolic pressure and stroke volume. The relation plateaus at high volumes and can be affected by disease, aging, or altered contractility.

History: The mechanism is named for Otto Frank and Ernest Starling, who described related observations in the late 19th and early 20th centuries. The term Frank-Starling law or Starling's law is used in physiology texts to denote the same concept.

Clinical relevance: In practice, the Frank-Starling relationship helps explain how venous return influences cardiac output in healthy individuals and in several disease states. It interacts with afterload and contractility, and its usefulness can be limited in severe heart failure or extreme preload conditions.