GLUCOCORTICOIDS IN METABOLIC CONTROL DURING EXERCISE - ALANINE METABOLISM

To evaluate glucocorticoid participation in the control of alanine met abolism during exercise, experiments were performed on adrenalectomize d and normal male rats. The adrenal insufficiency prevented the rises induced by 3 h of swimming in alanine levels of blood plasma, red port ion of quadriceps, and liver. In normal rats, the rise in alanine cont ent by 65% in blood, 50% in fast-twitch oxidative fibers, and 93% in l iver was associated with increased activity of alanine aminotransferas e in fast-twitch oxidative-glycolytic fibers (by 23%). In adrenalectom ized rats, enzyme activity during exercise did not change in muscles a nd decreased in hepatic tissue (by 25%). The dependence of exercise-in duced changes in alanine aminotransferase activity on glucocorticoids was confirmed by an increased enzyme activity (by 53%) in exercised ad renalectomized rats treated with 125 mu g corticosterone. In normal ra ts, training prevented both the rise of blood corticosterone and the a ctivation of hepatic alanine aminotransferase during exercise. The res ults support the view that the stimulation of the glucose-alanine cycl e by glucocorticoids promotes alanine supply and utilization in liver during exercise. In adrenalectomized rats, hepatic arginase activity w as decreased during exercise and no elevation of urea levels was found in blood, liver, or skeletal muscles. Consequently, the use of produc ts of the deamination of alanine (and other amino acids) for urea form ation also depends on glucocorticoids.