We have reported that muscular exercise (swimming in water at 22'C for 2 h)enhances the activity of phosphoenolpyruvate carboxykinase and the gluconeogenic capacity of rat kidney cortex [I ,2]. These effects are probably mediated by the metabolic acidosis which takes place during exercise as result of muscular overproduction of lactate [3].The increase of renal gluconeogenesis in experimental metabolic acidosis seems to be related to the enhancement of the reaction catalyzed by phosphoenolpyruvate carboxykinase, as indicated by the concentrations of intermediate metabolites of this process [4,5]. Consequently, we have measured the content of gluconeogenic intermediates in kidney after 2 h of swimming in order to obtain further evidence on the relation between the effect of exercise on gluconeogenesis and metabolic acidosis.
Materials aud methodsFemale Wistar rats (150-200 g) were used. The animals were forced to swim in a water bath (22°C) for 2 h. At the end of exercise, they were sacrificed by cervical dislocation. A-portion of liver or one of the kidneys was rapidly excised and clamped between metal tongs precooled in liquid nitrogen [6]. The time elapsing between dislocation of the neck and freezing the organ was 8-10 s. The frozen tissue was pulverized in a mortar, extracted with perchloric acid solution and neutralized with KOII, as in 171.Lactate was determined as in [8] ; aspartate as in
Results and diicussionIn the liver from exercised rats the content of lactate was decreased whereas the concentrations of malate, aspartate ,2-phosphoglycerate , fructose 6-phosphate and glucose 6-phosphate were increased (table 1). Assuming that the content of malate and aspartate reflect that of oxalacetate (which is unstable and present in small concentrations in tissues), the rise in malate and aspartate in connection with the absence of a significant e~~cement for phosphoenolpyruvate indicate a low activity of phosphoenolpyruvate carboxykinase . Therefore, the decrease in lactate content is not likely due to gluconeogenesis but to oxidative consumption in the tricarboxylic acid cycle. On the other hand, the rise in fructose 6-phosphate and glucose 6-phosphate can be explained by the operation of glycogenolysis. It is well established that glycogen degradation takes place during exercise [14].The effect of exercise on the renal content of ghrconeogenic intermediates is shown in table 2. Like in liver, lactate was decreased and there was a rise in the content of fructose 6-phosphate and glucose 6-phosphate. On the contrary, mrtlate and 2-phosphoglycerate did not charge, asparate and fructose bisElsevier/North-IioIkmd Biomedical Press