Cardiac function and modulation of sarcomeric function by length.
The Frank-Starling relationship provides beat-to-beat regulation of ventricular function by matching ventricular input and output. This review addresses the subcellular mechanisms by which the ventricle adjusts its output (i.e. stroke volume) by changes in end-diastolic volume. The subcellular processes are placed in the context of the four phases of the cardiac cycle with emphasis on the sarcomeric properties that mediate the number of force-generating cross-bridges recruited during pressure development. Additional mechanistic insight is provided regarding the factors that regulate myocyte loaded shortening speeds, which are paramount for dictating ejection volume. Emphasis is placed on the interplay between cross-bridge-induced cooperative activation of the thin filament and cooperative deactivation of the thin filament induced by muscle shortening. The balance of these two properties seems to determine systolic haemodynamics, and how this balance is modulated by sarcomere length, in part, underlies the Frank-Starling relationship.
Hanft
Laurin M
LM
Department of Medical Pharmacology & Physiology, MA 415, Medical Sciences Building, School of Medicine, University of Missouri, Columbia, MO 65212, USA.
Korte
Fredrick S
FS
McDonald
Kerry S
KS
D008841:Actin Cytoskeleton / Q000378:metabolism; D000818:Animals; D048430:Cell Shape; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D053580:Muscle Strength; D009200:Myocardial Contraction; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism; D009210:Myofibrils / Q000378:metabolism; D012518:Sarcomeres / Q000378:metabolism*; D013318:Stroke Volume; D016277:Ventricular Function, Left; D017725:Ventricular Pressure