This preclinical study demonstrates that elasticity changes and tension development in frog skeletal muscle during potassium-induced contractures are driven by two distinct processes with different time courses.
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Caution against extrapolating frog skeletal muscle results to human myocardium; hypothesis-generating for distinct elasticity-tension mechanisms.
The responses to rapid stretches applied just prior to or during potassium‐induced contractures were investigated using small bundles of muscle fibres. In submaximal contractures induced by 27 or 42 mM KCl (in choline‐Ringer's) the “resistance to stretch” (i. e., the extra tension recorded about 0.1 sec following the start of the stretch) and the tension developed without stretching followed different time courses. When stretched during the rise in tension the muscles always developed greater tensions than when the same stretch was applied before exposure to the elevated potassium. The “resistance to stretch” was small at the start of the contracture, it was maximal about halfway through the rise in tension and it declined slowly thereafter. By a proper selection of the amount of stretch and the instant of stretching it was possible to obtain tensions equal to or greater than the maximal tensions induced by isotonic KCl. In contractures induced by isotonic KCl the “resistance to stretch” was maximal near the start, it declined slowly during the rise of tension, and it declined rapidly during the fall in tension. These results suggest that the changes in elasticity (as indicated by the ‘resistance to stretch’) and the ability to develop tension resulted from two distinct processes and in potassium‐induced contractures they follow different time courses which can be varied experimentally.
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George B. Frank (1965) studied this question.
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