Abstract

Exercise (swimming 2 hr in water at 22°) results in a substantial increase in the activity of the kidney cortex phosphoenolpyruvate carboxykinase (EC 4.1.1.32) measured in the direction of oxaloacetate synthesis as well as in the direction of phosphoenolpyruvate formation. This increase probably is not due to de novo synthesis of the enzyme, since it is not counteracted by treatment with actinomycin d or cycloheximide. Blood lactate concentration sharply increases in the first 15 min of exercise and drops, also very rapidly, to the normal levels in 45 min. Renal phosphoenolpyruvate carboxykinase activity and gluconeogenic ability increase continuously during 2 hr of exercise. When the rats are previously treated with sodium bicarbonate, the increase in blood lactate is of the same order but its fall is considerably less pronounced than in normal exercised animals. In the bicarbonate treated rats, the phosphoenolpyruvate carboxykinase activity reaches only a slight enhancement in 2 hr. When swimming takes place in water at 37°—instead of 22°, as usual—the concentrations of blood lactate are only slightly higher than the normal values. In these conditions, the renal phosphoenolpyruvate carboxykinase activity is much lower, and the renal gluconeogenic capacity remains close to the normal values. The production of glucose and ammonia from glutamine is greater in kidney cortical slices from exercised rats than in the control animals, this increase being substantially overcome by previous treatment with bicarbonate. From these findings, it can be reasonably assumed that the increase in the renal phosphoenolpyruvate carboxykinase activity and gluconeogenic ability which takes place during exercise in our experimental conditions is mediated by the metabolic acidosis caused by overproduction of muscular lactate.

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