EFFECT OF PHYSICAL-TRAINING ON MITOCHONDRIAL-FUNCTION IN SKELETAL-MUSCLE OF NORMAL AND DIABETIC RATS

The study was designed to assess the impact of physical training on th e oxidative phosphorylation rate (OPR) in mitochondria isolated from t wo different skeletal muscles of rats with or without chronic diabetes mellitus. Diabetes was induced by an intravenous injection of strepto zotocin (50 mg/kg), and only animals with a blood glucose level betwee n 14 and 22 mmol/L 1 week later were kept in the protocol. Exercise tr aining was performed on a treadmill with a progressive 10-week program . Rats were killed by decapitation at the end of the training program, and mitochondria were isolated from the gastrocnemius and the red vas tus lateralis muscles. When the data were expressed as per milligrams of protein, OPR was significantly depressed by diabetes mellitus in th e mitochondria from each muscle; a similar negative impact also appear ed to be produced by physical training in mitochondria isolated from t he red vastus lateralis muscle. However, due to changes in mitochondri al protein yield between groups, the capacity to oxidize pyruvate and malate was also calculated per gram of muscle. Adenosine triphosphate (ATP) production rate appeared to be unaffected by diabetes hut signif icantly increased by training in both muscles of diabetic and nondiabe tic rats. This effect of training was not associated with any improvem ent in plasma glucose or insulin levels in diabetic animals. However, the large increase in plasma levels of beta-hydroxybutyric acid in sed entary diabetic rats was partly reversed by training (1,079 +/- 472 v 3,424 +/- 618 mu mol/L, P < .001). These results suggest. that the tra ining-induced increase in the capacity of skeletal muscles to oxidize substrates and generate energy may also contribute to reduce the eleva ted plasma beta-hydroxybutyric acid levels observed in a state of insu lin deficiency. This may have clinical relevance, since ketoacidosis r emains a life-threatening event in insulin-dependent diabetic subjects . Copyright (C) 1996 by W.B. Saunders Company