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AJP - Endocrinology and Metabolism, Vol 254, Issue 5 E555-E561, Copyright © 1988 by American Physiological Society
ARTICLES |
E. A. Richter, B. Kiens, B. Saltin, N. J. Christensen and G. Savard
August Krogh Institute, University of Copenhagen, Denmark.
To study the role of muscle mass in glucoregulation, six subjects worked with the knee extensors of one leg on a specially constructed cycle ergometer. The knee extensors of one leg worked either alone or in combination with the knee extensors of the other leg and/or with the arms. Substrate usage was measured across both knee extensors by femoral arterial and venous catheterization and measurement of femoral venous blood flow. Glucose uptake by the working knee extensors was absolutely (by approximately 20%) or relatively decreased when arm cranking was added to knee extensions. The decrease in glucose uptake was not compensated for by increased uptake of free fatty acids but was accompanied by decreases in plasma insulin and increases in plasma epinephrine and norepinephrine. During work with large muscle masses, arterial lactate increased to approximately 6 mM, and net leg lactate release reverted to net lactate uptake. Decreased glucose uptake could not be explained by decreased perfusion. It is concluded that thigh muscle glucose uptake is affected by the size of the total muscle mass engaged in exercise. The decrease in thigh glucose uptake, when arm cranking was added and O2 uptake was increased above 50% of maximum aerobic capacity, may be elicited by neuroendocrine adjustments or lactate-induced inhibition of glycolysis and may represent a mechanism for protecting against premature hypoglycemia during prolonged exercise.
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