Alessandra Ferri1, Xu Yan1, Jujiao Kuang1, Cesare Granata1,2, Rodrigo S F Oliveira1, Christopher P Hedges1, Adriano E Lima-Silva3, Francois Billaut1,4, David J Bishop5. 1. Institute for Health and Sport, Victoria University, Melbourne, VIC, Australia. 2. Department of Diabetes, Central Clinical School, Monash University, Alfred Medical Research and Education Precinct, Melbourne, VIC, Australia. 3. Human Performance Research Group, Federal University of Technology-Parana (UTFPR), Curitiba, Brazil. 4. Département de Kinésiologie, Université Laval, Québec, Canada. 5. Institute for Health and Sport, Victoria University, Melbourne, VIC, Australia. David.Bishop@vu.edu.au.
Abstract
PURPOSE: To investigate within the one study potential molecular and cellular changes associated with mitochondrial biogenesis following 15 days of exposure to moderate hypoxia. METHODS: Eight males underwent a muscle biopsy before and after 15 days of hypoxia exposure (FiO2 = 0.140-0.154; ~ 2500-3200 m) in a hypoxic hotel. Mitochondrial respiration, citrate synthase (CS) activity, and the content of genes and proteins associated with mitochondrial biogenesis were investigated. RESULTS: Our main findings were the absence of significant changes in the mean values of CS activity, mitochondrial respiration in permeabilised fibers, or the content of genes and proteins associated with mitochondrial biogenesis, after 15 days of moderate normobaric hypoxia. CONCLUSION: Our data provide evidence that 15 days of moderate normobaric hypoxia have negligible influence on skeletal muscle mitochondrial content and function, or genes and proteins content associated with mitochondrial biogenesis, in young recreationally active males. However, the increase in mitochondrial protease LON content after hypoxia exposure suggests the possibility of adaptations to optimise respiratory chain function under conditions of reduced O2 availability.
PURPOSE: To investigate within the one study potential molecular and cellular changes associated with mitochondrial biogenesis following 15 days of exposure to moderate hypoxia. METHODS: Eight males underwent a muscle biopsy before and after 15 days of hypoxia exposure (FiO2 = 0.140-0.154; ~ 2500-3200 m) in a hypoxic hotel. Mitochondrial respiration, citrate synthase (CS) activity, and the content of genes and proteins associated with mitochondrial biogenesis were investigated. RESULTS: Our main findings were the absence of significant changes in the mean values of CS activity, mitochondrial respiration in permeabilised fibers, or the content of genes and proteins associated with mitochondrial biogenesis, after 15 days of moderate normobaric hypoxia. CONCLUSION: Our data provide evidence that 15 days of moderate normobaric hypoxia have negligible influence on skeletal muscle mitochondrial content and function, or genes and proteins content associated with mitochondrial biogenesis, in young recreationally active males. However, the increase in mitochondrial protease LON content after hypoxia exposure suggests the possibility of adaptations to optimise respiratory chain function under conditions of reduced O2 availability.
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