Abstract
The study relates to the control of the mechanical activity of the cardiac muscle by coupling calcium kinetics with crossbridge cycling. Two main feedback mechanisms affect the performance of the contractile filaments: 1) cooperativity, in which the affinity of troponin for calcium is a function of the number of cycling crossbridges, and 2) mechanical feedback where the velocity of filament sliding affects crossbridge turnover rate from the strong to the weak conformation. This intracellular control mechanism describes the performances of the skinned and intact cardiac muscle at various loading conditions, i.e. the force-length and the force-velocity relationships and the control of relaxation. The model can also describe the effect of various loading conditions on the work and ATP consumption. Using this approach, a mechanism for the time varying elastance of the left ventricle is proposed.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">></ETX>
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