• Korean Journal of Exercise Nutrition
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• v.16 no.2
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• pp.65-71
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• 2012

Oxygen is the final acceptor of electron transport from fat and carbohydrate oxidation, which is the rate-limiting factor for cellular ATP production. Under altitude hypoxia condition, energy reliance on anaerobic glycolysis increases to compensate for the shortfall caused by reduced fatty acid oxidation [1]. Therefore, training at altitude is expected to strongly influence the human metabolic system, and has the potential to be designed as a non-pharmacological or recreational intervention regimen for correcting diabetes or related metabolic problems. However, most people cannot accommodate high altitude exposure above 4500 M due to acute mountain sickness (AMS) and insulin resistance corresponding to a increased levels of the stress hormones cortisol and catecholamine [2]. Thus, less stringent conditions were evaluated to determine whether glucose tolerance and insulin sensitivity could be improved by moderate altitude exposure (below 4000 M). In 2003, we and another group in Austria reported that short-term moderate altitude exposure plus endurance-related physical activity significantly improves glucose tolerance (not fasting glucose) in humans [3,4], which is associated with the improvement in the whole-body insulin sensitivity [5]. With daily hiking at an altitude of approximately 4000 M, glucose tolerance can still be improved but fasting glucose was slightly elevated. Individuals vary widely in their response to altitude challenge. In particular, the improvement in glucose tolerance and insulin sensitivity by prolonged altitude hiking activity is not apparent in those individuals with low baseline DHEA-S concentration [6]. In addition, hematopoietic adaptation against altitude hypoxia can also be impaired in individuals with low DHEA-S. In short-lived mammals like rodents, the DHEA-S level is barely detectable since their adrenal cortex does not appear to produce this steroid [7]. In this model, exercise training recovery under prolonged hypoxia exposure (14-15% oxygen, 8 h per day for 6 weeks) can still improve insulin sensitivity, secondary to an effective suppression of adiposity [8]. Genetically obese rats exhibit hyperinsulinemia (sign of insulin resistance) with up-regulated baseline levels of AMP-activated protein kinase and AS160 phosphorylation in skeletal muscle compared to lean rats. After prolonged hypoxia training, this abnormality can be reversed concomitant with an approximately 50% increase in GLUT4 protein expression. Additionally, prolonged moderate hypoxia training results in decreased diffusion distance of muscle fiber (reduced cross-sectional area) without affecting muscle weight. In humans, moderate hypoxia increases postprandial blood distribution towards skeletal muscle during a training recovery. This physiological response plays a role in the redistribution of fuel storage among important energy storage sites and may explain its potent effect on changing body composition. Conclusion: Prolonged moderate altitude hypoxia (rangingfrom 1700 to 2400 M), but not acute high attitude hypoxia (above 4000 M), can effectively improve insulin sensitivity and glucose tolerance for humans and antagonizes the obese phenotype in animals with a genetic defect. In humans, the magnitude of the improvementvaries widely and correlates with baseline plasma DHEA-S levels. Compared to training at sea-level, training at altitude effectively decreases fat mass in parallel with increased muscle mass. This change may be associated with increased perfusion of insulin and fuel towards skeletal muscle that favors muscle competing postprandial fuel in circulation against adipose tissues.

• Journal of the Korean Society of Radiology
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• v.82 no.4
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• pp.953-958
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• 2021

High-altitude cerebral edema (HACE) is a potentially fatal neurological syndrome that develops in persons traveling to a high altitude. We report the case of a 49-year-old male who had traveled to a high altitude, and lost consciousness for a few hours. Susceptibility-weighted images revealed multiple, fine black pepper like microbleeds along the corpus callosum with several microbleeds in the left frontal and parietal subcortical white matter. The T2-weighted images did not show any abnormal signal intensities along the corpus callosum. The diffusion-weighted images revealed small nodular high signal intensities in the basal ganglia. This report describes the atypical radiologic findings of HACE showing multiple microbleeds along the corpus callosum, without abnormal high-signal intensity on T2-weighted images.

• The Journal of Internal Korean Medicine
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• v.29 no.4
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• pp.922-938
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• 2008

Objectives : Rhodiola rosea has been used in herbal medicine to treat various conditions, such as antimelancholia, antifatigue, improvement of work competence and prevention of altitude sickness. In this study, we investigated effects of Rhodiola rosea extract (KH101) on fatigue in forced swimming rats. Methods : Sprague-Dawley rats were induced with fatigue by forced swimming, then rats in each group were treated with KH101. We observed changes of glucose, LDH and cortisol in serum and LDH, glycogen, hexokinase, citrate synthase MDH, SDH and CK in muscle. Results : Obtained results were as follows: 1. Continuance times of exercise significantly increased in all groups at day 1, in the 50 mg/kg concentration group at day 2, in all groups at day 3 and in the 50 mg/kg conc. group at day 4. 2. In serum, glucose significantly decreased in all concentration groups. 3. In the soleus muscle, LDH significantly decreased in the 50 mg/kg concentration group. HK significantly decreased in the 100 mg/kg conc. group. SDH significantly increased in the 100 mg/kg conc. MDH were significantly decreased in all conc. groups. 4. In the gastrocnemius muscle, HK significantly decreased in all concentration groups, while MDH significantly increased all conc. groups. Conclusions : It is concluded that the KH101 has and anti-fatigue effect in rats. Additional studies are needed to find the mechanism of the association between each single herb.