The effects of intermittent hypoxia training on mitochondrial oxygen consumption in rats exposed to skeletal unloading.

Intermittent hypoxia training (IHT) may reduce the oxidative stress-induced damage caused by extreme influences such as ischemia, exhaustive physical exercise, acute hypoxia, and stress. The aim of the present study is to investigate the effects of IHT on hepatic mitochondrial oxygen consumption, lipid peroxidation, and selected biochemical parameters used as diagnostic tools in a skeletal unloading model in rats. Our data showed that the IHT method significantly improved liver tolerance of unloading by reorganizing mitochondrial energy metabolism due to NADH-dependent oxidation. Aminotransferase activity was decreased compared to levels in untreated rats. Succinate dehydrogenase activity and lipid peroxidation remained unchanged when compared between groups. Moreover, skeletal unloading in the growing rats induced an activation of the rate of mitochondrial respiration in state 3 at succinate oxidation and decreased oxygen consumption at α-ketoglutarate oxidation. Adaptation of rats to IHT in our experiment significantly improved the rate of oxidative phosphorylation and the efficiency of phosphorylation in liver mitochondria at α-ketoglutarate oxidation. IHT seems to be a hepatoprotective method, and its use in maintaining a healthy liver and preventing unloading-induced liver damage deserves consideration and further examination.