Previous studies have reported that glucose tolerance can be improved by short-term altitude living and activity. However, not all literature agrees that insulin sensitivity is increased at altitude. The present study investigated the effect of a 25-day mountaineering activity on glucose tolerance and its relation to serum levels of dehydroepiandrosterone-sulfate (DHEA-S) and tumor necrosis factor-alpha (TNF-alpha) in 12 male subjects. On day 3 at altitude, we found that serum DHEAS was reduced in the subjects with initially greater DHEA-S value, whereas the subjects with initially lower DHEA-S remained unchanged. To further elucidate the role of DHEA-S in acclimatization to mountaineering activity, all subjects were then divided into lower and upper halves according to their sea-level DHEA-S concentrations: low DHEA-S (n = 6) and high DHEA-S groups (n = 6). Glucose tolerance, insulin level, and the normal physiologic responses to altitude exposure, including hematocrit, hemoglobin, erythropoietin (EPO), and cortisol were measured. We found that glucose and insulin concentrations on an oral glucose tolerance test were significantly lowered by the mountaineering activity only in the high DHEA-S group. Similarly, hematocrit and hemoglobin concentration in altitude were increased only in the high DHEA-S group. In contrast, the low DHEA-S subjects exhibited an EPO value at sea level and altitude greater than the high DHEA-S group, suggesting an EPO resistance. The findings of the study imply that DHEA-S is essential for physiologic acclimatization to mountaineering challenge.

Swimmers tend to have greater body fat than athletes from other sports. The purpose of the study was to examine changes in body composition after altitude hypoxia exposure and the role of blood distribution to the skeletal muscle in swimmers. With a constant training volume of 12.3 km/day, young male swimmers (N = 10, 14.8 ± 0.5 years) moved from sea-level to a higher altitude of 2,300 meters. Body composition was measured before and after translocation to altitude using dual-energy X-ray absorptiometry (DXA) along with 8 control male subjects who resided at sea level for the same period of time. To determine the effects of hypoxia on muscle blood perfusion, total hemoglobin concentration (THC) was traced by near-infrared spectroscopy (NIRS) in the triceps and quadriceps muscles under glucose-ingested and insulin-secreted conditions during hypoxia exposure (16% O2) after training. While no change in body composition was found in the control group, subjects who trained at altitude had unequivocally decreased fat mass (-1.7 ± 0.3 kg, -11.4%) with increased lean mass (+0.8 ± 0.2 kg, +1.5%). Arterial oxygen saturation significantly decreased with increased plasma lactate during hypoxia recovery mimicking 2,300 meters at altitude (~93% versus ~97%). Intriguingly, hypoxia resulted in elevated muscle THC, and sympathetic nervous activities occurred in parallel with greater-percent oxygen saturation in both muscle groups. In conclusion, the present study provides evidence that increased blood distribution to the skeletal muscle under postprandial condition may contribute to the reciprocally increased muscle mass and decreased body mass after a 3-week altitude exposure in swimmers.

The aim of this study was to investigate the effect of mountain living conditions and high altitude hiking activities on glucose tolerance. In study I, we performed an oral glucose tolerance test on nine untrained subjects before and after 3 days of mountain living. In study II, the same measurement was used to determine the effect of high altitude hiking in two distinct geographic environments; participants included 19 professionally trained mountaineers. We found that trained mountaineers displayed significantly better sea-level glucose tolerance than sedentary subjects of a similar age (p < 0.05). This result suggests that mountaineering training could produce a beneficial effect on glucose tolerance. More importantly, in study I we demonstrated that 3 days of high altitude living (altitude approximately 2400 m) was sufficient to improve glucose tolerance. Furthermore, hiking in a relatively flat plateau area (Pamirs highland area, China, altitude approximately 4000 m) generated significantly better improvement in glucose tolerance than hiking in a mountain that contained many rough hills at a similar altitude (Mountain Snow, Taiwan, altitude approximately 3800 m). In conclusion, we found that living at a high altitude for the short term can significantly improve glucose tolerance. Additionally, the improving effect of hiking at high altitudes on glucose tolerance appears to be influenced by the geographic environment. These preliminary results suggest that high altitude living conditions and activities may possibly be developed as potential natural medicines for the prevention and treatment of type II diabetes in the future.

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Chen, Chi-Hsien, Yuh-Feng Liu, Shin-Da Lee, Wen-Chih Lee, Ying-Lan Tsai, Chien-Wen Hou, Chih-Yang Huang, and Chia-Hua Kuo. Altitude hypoxia increases glucose uptake in human heart. High Alt. Med Biol. 10:83-86, 2009.-Cardiac muscle is a highly oxygenated tissue that produces ATP mainly from fat oxidation. However, when the rate of oxygen demand exceeds oxygen supply, energy reliance on the carbohydrate substrate becomes crucial for sustaining normal cardiac function. In this study, the effect of acute altitude hypoxia on glucose uptake from circulation was determined, for the first time, in the human heart, using [18F]-2-deoxy-2-fluoro-D-glucose positron emission tomography (FDG-PET) in a simulated altitude condition (14% O(2), corresponding to approximately 3000 m above sea level) or room air (21% O(2)). Our results showed that subjects (n = 6) started to experience difficulty in sustaining the hypoxic condition at approximately 45 min. This was concurrent with a substantially increased blood lactate concentration, which reflects an accelerated rate of anaerobic glycolysis. Hypoxia elevated FDG uptake above control by approximately 70% in heart, but not in limbs (representing primarily skeletal muscle), brain, and liver. This study provides the first human evidence for the hypoxia-stimulated glucose uptake in heart. At this hypoxia level, the previously observed hypoxia-stimulated glucose uptake in rat skeletal muscle was not confirmed in the human study.