The principle describes the heart’s ability to regulate stroke volume based on venous return. An increase in venous return leads to a greater end-diastolic volume, which in turn stretches the myocardial fibers. This stretching optimizes the overlap of actin and myosin filaments, resulting in a more forceful contraction and a larger stroke volume. For example, during exercise, increased venous return causes the heart to fill more completely, leading to a more powerful ejection of blood with each beat.
This intrinsic regulatory mechanism is crucial for maintaining cardiac output in response to varying physiological demands. It allows the heart to adapt to changes in blood volume and peripheral resistance without the need for external regulation from the nervous or endocrine systems. Historically, its understanding has been fundamental to the development of treatments for heart failure and related cardiovascular conditions.
