Locked heart cgs4/1/2023 Ventricular filling sets the relationship between sarcomere length and tension development, and determines the degree of muscle shortening, which thereby regulates ventricular contraction and ejection. The ability of the heart to adjust the force of its contraction in response to changes in ventricular filling (end-diastolic volume, EDV) forms one of the main pillars of muscle physiology. Harvey’s description of the motion of blood greatly advanced the thinking of nineteenth century physiologists (Blasius 1872 Marey 1881 Dreser 1887 Frank 1895) and remains remarkably accurate to day. Patterson and Starling stated that “he working capacity of a pump is measured by its output.” (Patterson and Starling 1914) In the heart, cardiac output (CO) is the interdependence of blood volume ejected by the ventricles per contraction/heart beat-stroke volume (SV)-and the heart beat frequency-heart rate (HR)-occurring in 1 min (CO = SV × HR). And in like manner the intrinsic motion of the heart is not the diastole but the systole.” (Harvey 1889) It took 300 years before Wiggers ( 1921a, b) consolidated the meanings of systole and diastole that survive with minor modifications to day (Brutsaert and Sys 1989). William Harvey was the first to correctly define diastolic (relaxation) and systolic (contraction) phases of the heart “Whence the motion which is generally regarded as the diastole of the heart, is in truth its systole. Although the anatomy of the heart was well known to physicians at the time of Harvey, namely the existence of four cavities divided by an “impermeable” septum and valves that prevented backflow of material, it was however generally accepted that the heart was “a generator of vital spirits, and of heat” and that the propelling of blood was an “act of inspiration, and its flow to any part of the body determined by special excitation” (Fig. William Harvey’s (1628 publication) “ Exercitatio anatomica de motu cordis et sanguinis in animalibus” (On the motion of the heart and blood in animals) showed for the first time: (1) “that the blood moved in a ceaseless stream, as it were in a circle”, and (2) “that the heart is the great propelling power” (Harvey 1889). The heart, and its vessels, comprise the cardiovascular system responsible for the motion of blood throughout the body (Harvey 1889). It is the authors’ personal beliefs that much can be gained by understanding the Frank–Starling relationship at the cellular and whole organ level, so that we can finally, in this century, tackle the pathophysiologic mechanisms underlying heart failure. We “revive” a century of scientific research on the heart’s fundamental protein constituents (contractile proteins), to their assemblies in the muscle (the sarcomeres), culminating in a thorough overview of the several synergistically events that compose the Frank–Starling mechanism. The present review is a historic perspective on cardiac muscle function. As the Frank–Starling Law is a vital event for the healthy heart, it is of utmost importance to understand its mechanical basis in order to optimize and organize therapeutic strategies to rescue the failing human heart. Significant efforts have been attempted to identify a common fundamental basis for the Frank–Starling heart and, although a unifying idea has still to come forth, there is mounting evidence of a direct relationship between length changes in individual constituents (cardiomyocytes) and their sensitivity to Ca 2+ ions. The Frank–Starling Law mandates that the heart is able to match cardiac ejection to the dynamic changes occurring in ventricular filling and thereby regulates ventricular contraction and ejection. More than a century of research on the Frank–Starling Law has significantly advanced our knowledge about the working heart.
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