Abstract
Endurance training by swimming (219-229 h) resulted in a significant protection against hypoxia/reoxygenation-induced injuries in Langendorff-perfused rat hearts. The protection was manifested as improved flow characteristics and a smaller release of creatine kinase into the perfusate. The concentration of thiobarbituric acid reactive substances (TBARS) was lower in the trained than in the respective control hearts. The trained hearts also showed a lower reoxygenation-induced increase in TBARS. The myocardium of the right ventricle and that of the left subepimyocardium were the most affected by reoxygenation. The swimming program induced a decrease in the activities of catalase and glutathione reductase in all parts of the myocardium measured. A decrease in vitamin E concentration in the subendomyocardium of the left ventricle and an increase in the activity of thioredoxin reductase also occurred. An increase in the concentration of reduced glutathione due to training was also observed, especially in the left subepimyocardium, whereas the glutathione disulfide concentration and the activity of superoxide dismutase were unaffected. The activity of glucose 6-phosphate dehydrogenase increased in the right ventricle. The results suggest both the importance of cellular redox state and the role of a lower degree of enzymatic antioxidants in training-induced protection against ischemic injuries.
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