Levett et al conducted an acclimatization study to

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Levett et al conducted an acclimatization study to the skeletal muscle mitochondria at high altitude hypoxia. No significant changes in mitochondrial density were found, after 19 days exposure to high
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altitude hypoxia. (Levett et al., 2012) This result does not correspond with the results of the study of Jacobs et al. They studied the effects of high altitude (3454 m) with a maintained energetic balance. The subjects tried to have the same physical activity level and the same diet. They found that the skeletal muscle mitochondrial volume densityincreased, with specific increased intermyofibrillar mitochondrial volume density and constant subsarcolemmal mitochondrial volume density. (Jacobs et al., 2015) The explanation for the difference can be found in the difference of energetic balance. Jacobs et al. maintained the energetic balance, were Levett et al. conclude that loss of body mass is something that occurs on altitude exposure due to loss of efficiency. Besides that, both experiments used only few subjects (6 subjects in the experiment of Levett and 9 in Jacobs’ experiment) which makes it hard to have significant results. Edwards et al studied also the response to high altitude hypoxia. They studied the skeletal muscle function and concluded that the skeletal muscle function is maintained, although significant atrophy was measured. (Edwards et al., 2010)Levett also measured an trend of UCP3 mRNA and protein upregulation, which seems to protect mitochondria from excessive ROS. The mitochondrial density and citrate synthase seems to reduce, with down-regulation of PGC1α. These adaptations suggest a coordinated response to downregulate the mitochondrial biogenesis to correspond the oxygen availability with the oxygen consumption. This is in contradiction with the response to exercise, where mitochondrial biogenesis is induced.Notably, Levett et al. did not found increased HIF-1α during the altitudeexperiments, this can be explained with a possible degradation of HIF-1during sampling of the biopsies. The PPAR-α expression is increased, what can result in a switch to fatty acid oxidation, Levett et al. found non-significant loss of intramyocellular fat stores, which supports the capacity to use fat as substrate. (Levett et al., 2012)SummaryHigh altitude reduces the partial oxygen pressure in blood levels, what causes reduced haemoglobin-oxygen saturation and reduced total oxygen content of blood. To compensate for this hypoxic stress, physiological adaptations are initiated. There are no studies found that measured the cellular oxygen levels. So we cannot say that at high altitude cellular hypoxia occurs, but we know that in the muscular
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capillary P02 is also reduced. To compensate for hypoxic stress, the oxidative phosphorylation reduces and the anaerobe fermentation increases. The glycolytic pathway increases to maintain the cellular ATP levels. This switch is regulated by HIF-1. With this switch, the oxygen consumption reduces. If the mitochondrial density changes
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