In quantifying type B potentiation effects, given earlier merely qualitatively, it is found that Zn2+, 1—50 µM, causes increases in action potential duration, twitch tension, and twitch contraction period time, which are all directly proportional to the log of the concentration. Hence, the duration of the action potential, i.e. the magnitude of its mechanically effective period, is a causal factor quantitatively determining the degree of mechanical activation in the isometric twitch. In higher concentrations of Zn2+ up to 1000 µM, the spike duration and the contraction time continue to increase but the twitch tension is disproportionately smaller, evidently because the high zinc (500—1000 µM) raises the mechanical threshold of excitation-contraction (E—C) coupling and reduces the intrinsic strength of the contractile system. Eserine (1.5 mM) and also high Zn2+ not only cause type B potentiation effects, but also slow the rise of the spike, thus causing retardation of the very onset of tension production, which is even greater for high Zn2+ because of the raised mechanical threshold. This retardation is then succeeded by the faster tension output characteristic of type B potentiation resulting from spike prolongation. Thus, the changes in the consecutive, rising and falling phases of the action potential explicitly register their separate effects in the respective very earliest and directly following periods of twitch output; i.e., each phase of the action potential produces its own mechanical "transform." These transforms, and other effects, suggest that the release of activator Ca2+ from the sarcoplasmic reticulum during E—C coupling can be graded in both the rate and the total amount of the release.

This content is only available as a PDF.