|Title:||Mitochondrial function in human skeletal muscle following high-altitude exposure||Authors:||Jacobs, Robert A.
Calbet, Jose A. L.
|UNESCO Clasification:||241106 Fisiología del ejercicio||Keywords:||Operation Everest-Ii
Down-Regulation, et al
|Issue Date:||2013||Publisher:||0958-0670||Journal:||Experimental Physiology||Abstract:||New Findings What is the central question of this study? Are the enzymatic alterations in human skeletal muscle observed following 9–11 days of exposure to high altitude reflected in mitochondrial function? What is the main finding and its importance? The main findings of this study are that the capacity fat oxidation, individualized respiration capacity through mitochondrial complex I and II, and electron coupling efficiency are not greatly affected by 9–11 days of exposure to high altitude. The importance of this data is that high altitude exposure failed to affect integrated measures of mitochondrial functional capacity in skeletal muscle despite significant decrements to enzyme concentrations involved in the tricarboxylic acid (TCA) cycle and oxidative phosphorylation. Studies regarding mitochondrial modifications in human skeletal muscle following acclimatization to high altitude are conflicting, and these inconsistencies may be due to the prevalence of representing mitochondrial function through static and isolated measurements of specific mitochondrial characteristics. The aim of this study, therefore, was to investigate mitochondrial function in response to high-altitude acclimatization through measurements of respiratory control in the vastus lateralis muscle. Skeletal muscle biopsies were obtained from 10 lowland natives prior to and again after a total of 9–11 days of exposure to 4559 m. High-resolution respirometry was performed on the muscle samples to compare respiratory chain function and respiratory capacities. Respirometric analysis revealed that mitochondrial function was largely unaffected, because high-altitude exposure did not affect the capacity for fat oxidation or individualized respiration capacity through either complex I or complex II. Respiratory chain function remained unaltered, because neither coupling nor respiratory control changed in response to hypoxic exposure. High-altitude acclimatization did, however, show a tendency (P = 0.059) to limit mass-specific maximal oxidative phosphorylation capacity. These data suggest that 9–11 days of exposure to high altitude do not markedly modify integrated measures of mitochondrial functional capacity in skeletal muscle despite significant decrements in the concentrations of enzymes involved in the tricarboxylic acid cycle and oxidative phosphorylation.||URI:||http://hdl.handle.net/10553/50932||ISSN:||0958-0670||DOI:||10.1113/expphysiol.2012.066092||Source:||Experimental Physiology[ISSN 0958-0670],v. 98 (1), p. 245-255|
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