[Effect of endurance exercises on cross-striated muscle cells].
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Biomedical subjects
Publications and source records attributed to V Vihko.
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The effect of 10 weeks of running training and termination of training on the regional distribution of cardiac glucose uptake and protein synthesis were studied in isolated perfused hearts in male rats. The left ventricular glucose uptake in hearts from sedentary rats was 1.87 +/- 0.14 mumol/min per g protein (mean +/- SE), being about 30% higher in the subendocardial than in the subepicardial layer (p less than 0.05). The gradient of left ventricular glucose uptake was similar to the controls in the rats retired from training, but was absent in the trained animals. The altered transmural glucose uptake probably reflects differences in the adaptive response of various myocardial muscle layers to a long-term intermittent increase in cardiac work load. Phenylalanine incorporation was evenly distributed through the left ventricle in all the groups, but was lowered in the left and right ventricles of the trained rats. Phenylalanine incorporation returned to the control level 5 weeks after the cessation of training.
Male rats, aged 17 weeks at the end of experiments, were divided into four groups. Two groups lived in normal cage conditions with or without extra load (20% of the body weight) and two groups were trained by running with or without extra load for 8 weeks. Oxidation rates of succinate, glutamate + malate, palmitoylcarnitine, and pyruvate, and the activities of lactate dehydrogenase, citrate synthase, isocitrate dehydrogenase and cytochrome oxidase were measured in homogenates of the right ventricle and in those of the subendocardial and subepicardial layers of the left ventricle. Oxidation rates of succinate and palmitoylcarnitine tended to be higher in the subendocardium than in the subepicardium of sedentary control animals (p less than 0.1 and p less than 0.05, respectively). Transmural differences of succinate and palmitoylcarnitine oxidation rates were even more clear after running training (p less than 0.01 and p less than 0.05, respectively), after carrying extra load (p less than 0.001 and p less than 0.001, respectively) and after training carrying extra load (p less than 0.001 and p less than 0.05, respectively). Training also enhanced pyruvate oxidation rate in the subendocardium. Oxidation rates of all substrates were lower in the right ventricle than in the left ventricle. In control animals there were no regional differences in the myocardial enzyme activities and the training- or extra-load-induced changes were modest compared with the changes in the oxidation rates. The most significant change was the training-induced enhancement in the lactate dehydrogenase activity of the subendocardium (p less than 0.001 vs subepicardium). These results show greater subendocardial than subepicardial oxidation rates of certain substrates in the normal heart. These results also suggest that the myocardium adapts to increased work by increasing the subendocardial oxidation rate of some but not all substrates, indicating further that there may be qualitative mitochondrial differences in the different regions of the heart.
Regional glucose uptake in perfused hearts, and the activities of several glycolytic enzymes contributing to the glucose metabolism in perfused and nonperfused hearts were studied in male and female rats after 8-9 weeks of swimming training. The left ventricular glucose uptake showed a transmural gradient in the sedentary animals, the subendocardial uptake being 30% and 12% higher than that of the subepicardial layer in the males and females, respectively. Swimming exercise abolished the left ventricular glucose uptake gradient in male rats, and in female rats an opposite gradient was found, the subepicardial uptake being 23% higher than the subendocardial uptake. The activities of phosphofructokinase and 3-phosphoglyceraldehyde dehydrogenase also showed transmural gradients in the left ventricles. Training did not abolish these gradients. Training-induced changes in the activities of phosphofructokinase, 3-phosphoglyceraldehyde dehydrogenase, pyruvate kinase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, citrate synthase, and malate dehydrogenase were found in certain sites of the myocardium. Perfusion of isolated hearts for 50 min with insulin-containing Krebs-Ringer buffer especially affected the activities of phosphofructokinase, lactate dehydrogenase, and citrate synthase, increasing these activities in the left ventricles and decreasing them in the atria. These results indicate that there are regional differences between male and female rats in the cardiac glucose uptake rate after swimming training.
We studied the effects of running-training, heavy exercise and termination of training on the heart weight, the ratio heart to body weight and the cardiac muscle activities of actomyosin ATPase, citrate synthase, succinate dehydrogenase, cytochrome c oxidase, malate dehydrogenase, adenylate kinase and beta-glucuronidase with adult male NMRI-mice. Stable hypertrophy (6-7%), estimated by the ratio heart or ventricle weight to body weight, was achieved by 28 exercises and it was dependent on the running speed (20 vs. 25 m X min-1). The withdrawal of training for 5-61 days did not permanently decrease the heart weight or the heart to body weight ratio to the level of sedentary controls. The activity of enzymes of energy metabolism or actomyosin ATPase were not affected by training, heavy exercise or terminated training. beta-glucuronidase activity slightly (20-25%) increased in the trained animals and remained at a higher level during the period of terminated training. The results suggest that the capacity for aerobic metabolism of normal mice heart is sufficient to meet the enhanced demand for ATP imposed by running-training and that the heart enlargement occurs in equal proportions with the enzymatic potential of the cardiac tissue.