[Intermittent hypoxic training and L-arginine as corrective agents for myocardial energy supply under acute hypoxia].

It NO has been shown play to the primary role in several mitochondrial functions. Our aim for this study was to investigate whether exogenous NO (L-arginine) or NO blocker L-NNA modulated the adaptive reactions of rat myocardial tissue respiration on intermittent hypoxic training (IHT). In the control rats an acute hypoxic test (inhalation of 7% O2, 30 min) provoked sharp augmentation of ADP-stimulated tissue respiration with the increase of respiratory coefficient and phosphorylation rate, the decrease of O2 uptake efficacy and switching the energy supply to succinate oxidation pathway. The same hypoxic test but following 14 days of IHT (11% O2, 15-min sessions with 15 min rest intervals, 5 times daily) produced a stimulation of oxidative phosphorylation with primary activation of NAD-dependent pathway, the marked increase of ADP/O ratio. The combination of IHT with L-arginine treatment (600 mg/kg intraperitoneally, daily before IHT sessions) provoked the decrease of tissue oxygen consumption in comparison with untrained animals. L-arginine effects abolished by the NO-synthase blocker L-NNA. Its effects on mitochondrial function deals with succinic acid inhibition utilizatin (increasing level ADP/O) and activation NADH-dependent oxidation. We conclude that the combination of IHT with NO-precursor treatment was capable to increase significantly the tolerance to episodes of acute hypoxia.