Calcium activation and maximum unloaded shortening velocity. Investigations on glycerinated skeletal and heart muscle preparations

Summary

In the present paper a method is described which allows differentiation of direct and indirect, shortening-induced effects of any parameter on maximum unloaded shortening velocity. It is shown that curvature of the length trace in isotonic quick releases should be attributed to shortening-induced changes in the afterload per cross bridge during such a quick release, caused, for example, by either a shortening-induced, internal load or a deactivation of the contractile system.

To evaluate shortening behaviour throughout the total course of isotonic quick releases, shortening velocity was plotted against the momentary length during the releases. These length-velocity relations yield straight lines when graphed on a floating-point scale, i.e., shortening velocity decreases exponentially with increasing amount of shortening during an isotonic release. Extrapolation of the length-velocity plots to the initial length of the releases allows determination of shortening velocity without alteration by shortening-induced increase in cross-bridge after-load.

Using this method, it is shown that sarcoplasmic Ca⁺⁺ concentration neither has an effect on maximum unloaded shortening velocity in skeletal muscle, nor in cat myocardium. Furthermore, it is demonstrated that the described shortening-induced changes in cross-bridge afterload resulting in a decrease in shortening velocity may be the source of the Ca⁺⁺ dependence of V_max published by different authors.

Supported by the Deutsche Forschungsgemeinschaft.