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Difference between revisions of "Jacobs 2013 Exp Physiol"

From Bioblast
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|tissues=Skeletal muscle
|tissues=Skeletal muscle
|preparations=Permeabilized tissue
|preparations=Permeabilized tissue
|couplingstates=LEAK, OXPHOS, ETS
|substratestates=CI, CII, CI+II
|substratestates=CI, CII, CI+II
|enzymes=Complex I, Complex II; Succinate Dehydrogenase
|enzymes=Complex I, Complex II; Succinate Dehydrogenase
}}
}}

Revision as of 22:05, 2 November 2012

Publications in the MiPMap
Jacobs RA, Boushel RC, Wright-Paradis C, Calbet JA, Robach P, Gnaiger E, Lundby C (2012) Mitochondrial function in human skeletal muscle following high altitude exposure. Exp Physiol [Epub ahead of print].

Β» PMID: 22636256

Jacobs RA, Boushel RC, Wright-Paradis C, Calbet JA, Robach P, Gnaiger E, Lundby C (2012) 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: DK Copenhagen Boushel RC, AT Innsbruck OROBOROS, CH Zurich Lundby C


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Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue  Enzyme: Complex I, Complex II; Succinate Dehydrogenase"Complex II; Succinate Dehydrogenase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property. 

Coupling state: LEAK, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property. 

HRR: Oxygraph-2k