Nonuniform activation and the mechanics of myocardial trabeculae with fast or slow myosin.

Left ventricular (LV) wall motion abnormalities reflect regional nonuniform contraction which may be arrhythmogenic. We studied sarcomere mechanics and force development (F) in uniform and nonuniform trabeculae using a model in which half of the muscle can be rendered weak by exposure to low [Ca2+](o). Stretch allowed the weak muscle segment to generate a force that was four-fold higher than force when the whole muscle was exposed to low [Ca2+](o). The sarcomere force-velocity relationships (FSVR) and the force-sarcomere-length relationships (FSLR) explained the force increase in the weak segment and the decrease of force in the strong segment such that both carried the same force. Correction for muscle stiffness converted the FSVR into a [Ca2+](o)-independent linear FVRXB for "the single cross-bridge (XB)." Stretch increased XB force < 10% above FXB-max, but recruited more XBs by feedback of V to the rate of XB, weakening (g = g(0) + g(1)V). The g(1) here was indistinguishable from g(1) of XBs in slow myosin of aged animals. The mechanics of nonuniform muscle can be explained by a linear FVRXB combined with the effect of V on the XB weakening rate.