Abstract
As is evident in this review, significant advances have been made in the analysis of crossbridge cycling in cardiac muscle. It becomes apparent that the myocardial crossbridge cycling rate is altered by various factors such as: 1) changes in the intracellular constituents (Ca2+, MgATP, MgADP, Pi, and H+), 2) difference in the type of myosin isozyme, and 3) probably, troponin I, C-protein, and MLC2 phosphorylation. The physiological consequences of an altered crossbridge cycling rate may give rise to the changes in the contraction profile during twitch, tension cost (the ratio of ATPase activity to tension), and the thermal economy (the ratio of heat liberated to tension) of cardiac muscle. These findings and implications should be kept in mind when interpreting cardiac performance under different inotropic states.
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