Abstract
ALTHOUGH there is a paucity of direct supporting evidence for the postulate that the immediate source of the energy for muscular contraction is the dephosphorylation of adenosine triphosphate, this view has been accepted by most authors1–3. The usual finding that there is no net decrease in the amount of adenosine triphosphate present in the working muscle is attributed to its rapid resynthesis by transfer of the phosphate group of phosphocreatine. However, Fleckenstein et al. 4 found no evidence for such transfers of phosphate groups in a tracer study on drug-induced contracture of muscles of the frog, and Dixon and Sacks5 found no evidence for equilibration of isotopic phosphorus between the terminal phosphorus of adenosine triphosphate and phosphocreatine in the course of a tetanic contraction of the cat gastrocnemius muscle of 30 sec. duration. Nor was there any equilibration of the isotope between the middle phosphorus of adenosine triphosphate and the corresponding phosphorus of adenosine diphosphate, such as would be expected to result from mixing of any adenosine diphosphate formed during the tetanus with that initially present in the resting muscle.
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References
Szent-Györgyi, A., “Chemistry of Muscular Contraction”, 2nd ed. (Academic Press, New York, 1951).
Weber, H. H., and Portzehl, H., “Progress in Biophysics and Biophysical Chemistry”, 4, 60 (1954).
Buchthal, F., Svensmark, O., and Rosenfalck, P., Physiol. Rev., 36, 503 (1956).
Fleckenstein, A., Janke, J., Davies, R. E., and Richter, W., Arch. Exp. Path. u. Pharm., 228, 596 (1956).
Dixon, G. J., and Sacks, J., Amer. J. Physiol., 193, 129 (1958).
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SACKS, J. Prolonged Muscular Activity without Phosphate Exchange. Nature 183, 825–826 (1959). https://doi.org/10.1038/183825b0
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DOI: https://doi.org/10.1038/183825b0
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