Skeletal muscle energy metabolism in environmental hypoxia: climbing towards consensus.
Skeletal muscle energy metabolism in environmental hypoxia: climbing towards consensus.
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DOI：
10.1186/2046-7648-3-19
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发表时间：
2014
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影响因子：
--
通讯作者：
Murray AJ
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文献类型：
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作者：
Horscroft JA;Murray AJ
骨骼肌经历代谢重塑，以应对环境缺氧，但这个过程的方面仍然存在争议。广义上，环境缺氧已被认为诱导：（i）线粒体密度的损失;（ii）底物从脂肪酸转向其他底物，如葡萄糖、氨基酸和酮体;以及（iii）从有氧代谢转变为无氧代谢。在这些领域仍然缺乏共识，最有可能是由于缺氧暴露的程度和持续时间的变化，以及广泛的实验参数作为代谢过程的标志物。为了试图解决一些争议，我们进行了一个全面的审查有关的文献缺氧引起的骨骼肌能量代谢的变化。我们发现的证据表明，特定质量的线粒体功能下降之前，特定质量的线粒体密度，暗示线粒体内的变化，在环境缺氧的反应。这种氧化能力的丧失似乎与糖酵解能力的丧失不匹配，糖酵解能力总体上不受环境缺氧的影响。然而，环境缺氧确实诱导脂肪酸氧化的选择性衰减，同时维持或增加葡萄糖摄取，可能是为了在氧化代谢下调的情况下支持糖酵解，优化缺氧环境的ATP合成途径。本文的在线版本（doi：10.1186/2046 - 7648 - 3 - 19）包含补充材料，可供授权用户使用。
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. The online version of this article (doi:10.1186/2046-7648-3-19) contains supplementary material, which is available to authorized users.