THE SIGNIFICANCE OF THE FRANK–STARLING MECHANISM IN CARDIAC FUNCTION: FROM THE CLASSICAL LAW TO MODERN MECHANOBIOLOGICAL CONCEPTS

The Frank–Starling mechanism is one of the major intrinsic autoregulatory mechanisms that enables the heart to change the force of contraction according to its filling without requiring direct nervous or hormonal regulation. This phenomenon represents the relationship between ventricular filling during diastole and the mechanical response during the subsequent systole. According to the classical physiological concept, an increase in venous return increases ventricular diastolic filling and leads to stretching of myocardial fibers. However, modern studies indicate that it is insufficient to explain the Frank–Starling mechanism solely by geometric stretching of muscle fibers. Changes in sarcomere length alter the Ca²⁺ sensitivity of myofilaments, actin–myosin interactions, the mechanical properties of titin, and the activation state of the thick filament. Therefore, the Frank–Starling mechanism is currently considered a multilevel mechanotransduction process. This article analyzes the classical physiological basis of the mechanism, molecular processes at the sarcomere level, the roles of titin and troponin, its interaction with the Anrep effect, as well as its significance in heart failure and other pathological conditions. Modern data indicate that the Frank–Starling mechanism does not have a single fully established molecular cause; rather, it is the overall result of several interconnected mechanical and biochemical processes.