A. KATZ AND K. SAHLIN National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Phoenix, Arizona 85016; and Department of Clinical Physiology, Karolinska Institute, Huddinge University Hospital, S-14186 Huddinge, Sweden KATZ, A., AND K. SAHLIN. Regulation of lactic acid production during exercise. J. Appl. Physiol. 65(Z): 509418, 1988.-Lactic acid accumulates in contracting muscle and blood beginning at GO-70% of the maximal O2 uptake, well before the aerobic capacity is fully utilized. The classical explanation has been that part of the muscle is O2 deficient and therefore lactate production is increased to provide supplementary anaerobically derived energy. Currently, however, the predominant view is that lactate production during submaximal dynamic exercise is not 02 dependent. In the present , data and arguments in support of and against the hypothesis of 02 dependency have been scrutinized. Data underlying the conclusion that lactate production during exercise is not 02 dependent were found to be 1) questionable, or 2) interpretable in an alternative manner. Experiments in human and animal muscles under various conditions demonstrated that the redox state of the muscle is reduced (i.e., NADH is increased) either before or in parallel with increases in muscle lactate. Based on experimental
Journal of Applied Physiology – The American Physiological Society
Published: Aug 1, 1988
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