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Difference between revisions of "Jacobs 2013 Exp Physiol"

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|abstract=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. Therefore the aim of this study was to investigate mitochondrial function in response to high altitude acclimatization through measurements of respiratory control in the m. vastus lateralis. Skeletal muscle biopsies were obtained from ten lowland natives prior to and again after a total of 9-11 days of exposure to 4,559 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, as 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, as both coupling and respiratory control did not change in response to hypoxic exposure. High altitude acclimatization did, however, show a tendency (p=0.059) to limit mass specific maximal oxidative phosphorylation capacity. This data suggests that 9-11 days of exposure to high altitude does not markedly modify 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.
|abstract=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. Therefore the aim of this study was to investigate mitochondrial function in response to high altitude acclimatization through measurements of respiratory control in the m. vastus lateralis. Skeletal muscle biopsies were obtained from ten lowland natives prior to and again after a total of 9-11 days of exposure to 4,559 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, as 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, as both coupling and respiratory control did not change in response to hypoxic exposure. High altitude acclimatization did, however, show a tendency (p=0.059) to limit mass specific maximal oxidative phosphorylation capacity. This data suggests that 9-11 days of exposure to high altitude does not markedly modify 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.
|keywords=High altitude acclimatization
|keywords=High altitude acclimatization
|mipnetlab=SE Stockholm Boushel RC, AT Innsbruck OROBOROS, CH Zurich Lundby C, AT Innsbruck Gnaiger E, CA Vancouver Boushel RC, ES CN Las Palmas Calbet JA, US CO Colorado Springs Jacobs RA
|mipnetlab=SE Stockholm Boushel RC, AT Innsbruck Oroboros , CH Zurich Lundby C, AT Innsbruck Gnaiger E, CA Vancouver Boushel RC, ES CN Las Palmas Calbet JA, US CO Colorado Springs Jacobs RA
}}
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Revision as of 10:32, 23 January 2019

Publications in the MiPMap
Jacobs R, Boushel RC, Wright-Paradis C, Calbet JA, Robach P, Gnaiger E, Lundby C (2013) Mitochondrial function in human skeletal muscle following high altitude exposure. Exp Physiol 98:245-55.

Β» PMID: 22636256 Open Access

Jacobs R, Boushel RC, Wright-Paradis C, Calbet JA, Robach P, Gnaiger E, Lundby C (2013) Exp Physiol

Abstract: 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. Therefore the aim of this study was to investigate mitochondrial function in response to high altitude acclimatization through measurements of respiratory control in the m. vastus lateralis. Skeletal muscle biopsies were obtained from ten lowland natives prior to and again after a total of 9-11 days of exposure to 4,559 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, as 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, as both coupling and respiratory control did not change in response to hypoxic exposure. High altitude acclimatization did, however, show a tendency (p=0.059) to limit mass specific maximal oxidative phosphorylation capacity. This data suggests that 9-11 days of exposure to high altitude does not markedly modify 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. β€’ Keywords: High altitude acclimatization

β€’ O2k-Network Lab: SE Stockholm Boushel RC, AT Innsbruck Oroboros, CH Zurich Lundby C, AT Innsbruck Gnaiger E, CA Vancouver Boushel RC, ES CN Las Palmas Calbet JA, US CO Colorado Springs Jacobs RA


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style 

Stress:Ischemia-reperfusion  Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Regulation: Coupling efficiency;uncoupling  Coupling state: LEAK, OXPHOS, ET  Pathway: F, N, S, NS  HRR: Oxygraph-2k 


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