Latency relaxation in frog skeletal muscle

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1970

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Abstract

Latency relaxation, a reduction in resting tension which immediately precedes the twitch, has been observed in certain muscles. Its basic mechanism and physiological significance are not completely understood, but because it occupies a temporal position intermediate to stimulation and the development of positive tension it has been suggested as a mechanical manifestation of some phase of excitation-contraction coupling. To more closely investigate the relationship between latency relaxation and the accompanying twitch, frog sartorii were subjected to various procedures and the relative effects on latency relaxation and twitch were compared. The experimental variables included increasing resting tension, immersion into calcium-free Ringer solution with a chelating agent added, the presence of caffeine in the bathing medium, and increased temperature. Except in the presence of caffeine, latency relaxation amplitude was observed to either decrease more slowly than twitch, or increase while twitch decreased. Latency relaxation amplitude reached its maximum at consistently higher resting tensions than did the twitch. In muscles placed into the calcium-free solution, both latency relaxation and twitch decreased with increasing time of exposure, but the former at a slower rate than the latter. At moderate temperatures (25° to 32° C) latency relaxation was potentiated, the twitch less so, or not at all; at higher temperatures (up to 38°C) both events declined, but the twitch fell to a smaller percentage of the control value than did latency relaxation. With increasing time of exposure to a 1 mM caffeine solution, twitch amplitude increased while latency relaxation amplitude decreased. The dissimilarities in response of twitch and latency relaxation indicate separate basic mechanisms for the two events and demonstrate that the amplitude of latency relaxation is not indicative of the amplitude of the accompanying twitch. The results of these experiments were consistent with the suggestion that latency relaxation may arise from configurational changes along the thin muscle filaments associated with calcium-troponin interaction. In addition, the recorded latency relaxation amplitude may not only reflect the basic mechanism of the phenomenon itself, but, also, the delay in onset of contraction and the early twitch dynamics. Thus, factors which suppressed or slowed contraction tended to enhance latency relaxation and vice versa.

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