Affiliation:
1. Exercise Biology Institute, Tartu University, Estonia.
Abstract
To evaluate glucocorticoid participation in the control of alanine metabolism during exercise, experiments were performed on adrenalectomized and normal male rats. The adrenal insufficiency prevented the rises induced by 3 h of swimming in alanine levels of blood plasma, red portion of quadriceps, and liver. In normal rats, the rise in alanine content by 65% in blood, 50% in fast-twitch oxidative fibers, and 93% in liver was associated with increased activity of alanine aminotransferase in fast-twitch oxidative-glycolytic fibers (by 23%). In adrenalectomized rats, enzyme activity during exercise did not change in muscles and decreased in hepatic tissue (by 25%). The dependence of exercise-induced changes in alanine aminotransferase activity on glucocorticoids was confirmed by an increased enzyme activity (by 53%) in exercised adrenalectomized rats treated with 125 micrograms corticosterone. In normal rats, training prevented both the rise of blood corticosterone and the activation of hepatic alanine aminotransferase during exercise. The results support the view that the stimulation of the glucose-alanine cycle by glucocorticoids promotes alanine supply and utilization in liver during exercise. In adrenalectomized rats, hepatic arginase activity was decreased during exercise and no elevation of urea levels was found in blood, liver, or skeletal muscles. Consequently, the use of products of the deamination of alanine (and other amino acids) for urea formation also depends on glucocorticoids.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
16 articles.
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