Augmented Carbohydrate Oxidation under Moderate Hypobaric Hypoxia Equivalent to Simulated Altitude of 2500 m

Abstract

Hypoxia itself stimulates glucose uptake mediated by a mechanism independent of insulin. However, whether moderate hypoxia causes similar metabolic effect in humans remains unclear. The present study aimed to determine glycemic regulation following glucose load at a simulated moderate altitude of 2,500 m. Eight healthy young males (mean ± standard error: 24 ± 1 years; 171.3 ± 1.6 cm; 66.9 ± 3.7 kg; 22.8 ± 1.0 kg/m(2)) consumed 75 g of glucose solution under either hypobaric condition (560 mmHg) or normobaric condition (745 mmHg). In the hypobaric chamber, the oxygen partial pressure is proportionally reduced with a reduction of atmospheric pressure, consequently leading to the hypoxic condition. Plasma glucose and serum insulin concentrations increased significantly following glucose load in both conditions (P < 0.05). However, no significant interaction (condition × time) or main effect for condition was observed. There were no significant differences in serum glycerol, plasma epinephrine, or plasma norepinephrine concentrations between the two conditions. No significant differences between the conditions were observed in changes in VO2 or VCO2. However, the hypobaric condition showed significantly higher respiratory exchange ratio (VCO2/VO2) at 90 and 120 min following glucose load (P < 0.05 vs. normobaric condition), suggesting that carbohydrate oxidation following glucose load was enhanced in moderate hypobaric hypoxia. In conclusion, acute exposure to moderate hypobaric hypoxia significantly augmented carbohydrate oxidation following the glucose load, without affecting glucose or insulin responses. Thus, a short-time exposure to moderate hypobaric hypoxia may be beneficial for people with impaired glucose tolerance.