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[Nitric oxide as a factor in the antihypoxic effect of adaptation to physical loading].

It is known that adaptation to exercise enhances the organism resistance to acute hypoxia. However the mechanism of this cross protective effect have been insufficiently studied. The analysis of literature suggests that NO may play a role in the development of the antihypoxic effect of adaptation to exercise. The aim of the present study was to test this hypothesis: first, by evaluating the influence of NO donor and NO-synthase inhibitor on the antihypoxic effect of adaptation to exercise and, second, by evaluating the changes of NO production in acute hypoxia and after a course of adaptation to exercise. It was shown that the NO donor could both reproduce and considerably (three times) potentiate the antihypoxic effect of adaptation to exercise. At the same time, the NO-synthase inhibitor completely suppressed the development of the protective antihypoxic effect of adaptation. After adaptation to exercise, the cerebral NO production was unchanged, while the hepatic NO production doubled. Acute hypoxia induced a biphase change in tissue NO production; initial increase (twofold in the brain) preceded a decrease (by 25% in liver and 37% in the brain as compared to the control). Therefore, the increased NO production following adaptation to exercise can underlie the antihypoxic effect of such an adaptation.