Increased force levels after shortening and restretching skinned cardiac muscle.

At steady calcium activation, changes in loading conditions were imposed on single skinned cardiac myocytes and on multicellular skinned cardiac muscle. Despite the initial steady level of activation, an increase in isometric force (i.e. force gain) was observed after stretching following a period of shortening. Force gain was most pronounced at low levels of free activating calcium, but it was present at any level of free calcium, including maximal activation. The extent of shortening did not influence the amount of force gain. An increased level of shortening (i.e. shortening gain) was observed after clamping a single myocyte under afterloaded conditions. Since no membranous systems were present, the mechanism causing force and shortening gain were shown to be located at the level of the contractile proteins. The hypothesis is suggested that different steady states of the crossbridges could exist despite a constant steady level of calcium activation.