[Intermittent hypoxic training with exogenous nitric oxide improves rat liver mitochondrial oxidation and phosphorylation during acute hypoxia].

It have been shown that NO plays primary role in several mitochondrial functions. Our objective for this study was to investigate whether exogenous NO (L-arginine) modulates the adaptive reactions of rat liver tissue respiration and lipid peroxidation on intermittent hypoxic training (IHT). In control animals the test with acute hypoxia (7% O2, 30 min) provoked sharp augmentation of ADP-stimulating 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 with the inhibition of aminotranspherase Krebs cycle substrates supply mechanism. The twice augmentation of malon dialdehyde content (MDA) was observed. The same hypoxic test but after 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 aminotranspherase pathway, the marked increase of ADP/O ratio on the background of a decrease of MDA content by 32%. The combination of IHT with L-arginine treatment (600 Mg/Kg intraperitoneally, daily before IHT sessions) provoked a decrease of tissue oxygen consumption, the inhibition of both aminotranspherase and succinateoxidase Krebs cycle substrates supply mechanism on the background of pronounced MDA decrease (by 120%) in comparison with untrained animals. L-arginine effects abolished by the NO-synthase blocker L-NNA. We conclude that the combination of IHT which promotes the increase of inner adaptive mechanisms with NO-donors treatment could significantly increase the tolerance to episodes of acute hypoxia.