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Skeletal muscle energy metabolism in environmental hypoxia: climbing towards consensus.


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Authors

Horscroft, James A 
Murray, Andrew J 

Abstract

Skeletal muscle undergoes metabolic remodelling in response to environmental hypoxia, yet aspects of this process remain controversial. Broadly, environmental hypoxia has been suggested to induce: (i) a loss of mitochondrial density; (ii) a substrate switch away from fatty acids and towards other substrates such as glucose, amino acids and ketone bodies; and (iii) a shift from aerobic to anaerobic metabolism. There remains a lack of a consensus in these areas, most likely as a consequence of the variations in degree and duration of hypoxic exposure, as well as the broad range of experimental parameters used as markers of metabolic processes. To attempt to resolve some of the controversies, we performed a comprehensive review of the literature pertaining to hypoxia-induced changes in skeletal muscle energy metabolism. We found evidence that mass-specific mitochondrial function is decreased prior to mass-specific mitochondrial density, implicating intra-mitochondrial changes in the response to environmental hypoxia. This loss of oxidative capacity does not appear to be matched by a loss of glycolytic capacity, which on the whole is not altered by environmental hypoxia. Environmental hypoxia does however induce a selective attenuation of fatty acid oxidation, whilst glucose uptake is maintained or increased, perhaps to support glycolysis in the face of a downregulation of oxidative metabolism, optimising the pathways of ATP synthesis for the hypoxic environment.

Description

Keywords

High altitude, Hypoxia, Metabolism, Mitochondria, Skeletal muscle

Journal Title

Extrem Physiol Med

Conference Name

Journal ISSN

2046-7648
2046-7648

Volume Title

3

Publisher

Springer Science and Business Media LLC
Sponsorship
JAH receives a PhD studentship from the BBSRC. AJM thanks the Research Councils UK for supporting his academic fellowship and Action Medical Research, the British Heart Foundation and the BBSRC for supporting research projects in his laboratory.