Mechanical non-uniformity of myocardial wall is arrhythmogenic. Mechanical properties of non-uniform cardiac muscle are less known. Using non-uniform trabeculae by exposure to normal and low [Ca2+] o, we found 'weak' segments were stretched by 'strong' segments and produce 4-fold higher force than it would without being stretched. Based on force-velocity relationship (FVR), F increased 1.6 fold due to stretch of the 'weak' segment. FSLR may explain another 150% of the force increment by stretch.According to the 'single' cross-bridge FVR after correcting FVR by dynamic stiffness, FXB could only account for 10% force increment by stretch. Therefore, stretch increases force generation mainly by adjusting the number of cross-bridges which is dictated by the rate of cross-bridge weakening. The effect of velocity on the number of cross-bridges operates through the mechanical feedback coefficient g1. The effect resulting from stretch on the number of cross bridges by the FVR and by the FSLR explain the mechanics of non-uniform muscle.
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