Continuous Adaptation of Rats to Hypobaric Hypoxia Prevents Stressor Hyperglycemia and Optimizes Mitochondrial Respiration in Acute Hypoxia

Oxygen consumption, glucose level in the blood, and respiration of the liver mitochondria were investigated in male Wistar rats, permanently living in middle altitude (2100 m, Elbrus region). The animals were characterized by reduced oxygen consumption and blood glucose level, as well as by intensified utilization of NAD-dependent substrates in mitochondrial respiratory chain and increased indices of ADP-stimulated respiration, in comparison with rats residing in the low land. As a result of adaptive rebuilding of oxidative metabolism in those rats residing in the midland, the nature and severity of metabolic responses to acute hypoxia were also changed. An exposure of the rats residing in the lowland to barochamber on the "altitude" 5600 m for 3 hours resulted in both transient hypometabolic reaction, and a stressor hyperglycemic one. Rapid adaptation of mitochondrial function occurred due to an increase in the rate of PAD-dependent substrate oxidation accompanied by a decrease in the effectiveness of phosphorylation. In midland rats, by contrast, hypoglycemic reaction was developed, and further reduction of aerobic metabolism was limited. Rapid adaptation of mitochondrial function to acute hypoxia in those rats was more intense than in the low land animals. This was achieved by a significant increase in the rate of NAD-dependent substrate oxidation, especially lipids, and an improved efficiency of mitochondrial respiration and an increased economy of oxygen utilization.