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首页> 外文期刊>Proceedings of the Nutrition Society >Does skeletal muscle carnitine availability influence fuel selection during exercise?
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Does skeletal muscle carnitine availability influence fuel selection during exercise?

机译:骨骼肌肉毒碱可用性是否会影响运动期间的燃料选择?

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摘要

Fat and carbohydrate are the major fuel sources utilised for oxidative, mitochondrial ATP resynthesis during human skeletal muscle contraction. The relative contribution of these two substrates to ATP resynthesis and total energy expenditure during exercise can vary substantially, and is predominantly determined by fuel availability and exercise intensity and duration. For example, the increased ATP demand that occurs with an increase in exercise intensity is met by increases in both fat and carbohydrate oxidation up to an intensity of approximately 60–70 % of maximal oxygen consumption. When exercise intensity increases beyond this workload, skeletal muscle carbohydrate utilisation is accelerated, which results in a reduction and inhibition of the relative and absolute contribution of fat oxidation to total energy expenditure. However, the precise mechanisms regulating muscle fuel selection and underpinning the decline in fat oxidation remain unclear. This brief review will primarily address the theory that a carbohydrate flux-mediated reduction in the availability of muscle carnitine to the mitochondrial enzyme carnitine palmitoyltransferase 1, a rate-limiting step in mitochondrial fat translocation, is a key mechanism for the decline in fat oxidation during high-intensity exercise. This is discussed in relation to recent work in this area investigating fuel metabolism at various exercise intensities and taking advantage of the discovery that skeletal muscle carnitine content can be nutritionally increased in vivo in human subjects.
机译:脂肪和碳水化合物是用于氧化,线粒体ATP在人骨骼肌收缩期间用于氧化的主要燃料源。锻炼期间这两个基板对ATP重新合成和总能量消耗的相对贡献可以基本上变化,并且主要通过燃料可用性和运动强度和持续时间来确定。例如,通过脂肪和碳水化合物氧化的增加,通过脂肪和碳水化合物氧化的增加,增加了随着运动强度的增加而发生的提高的提高需求增加到最大氧消耗的约60-70%。当运动强度超出此工作量的增加时,骨骼肌碳水化合物利用率加速,导致减少和抑制脂肪氧化对总能源消耗的相对和绝对贡献。然而,调节肌肉燃料选择和支撑脂肪氧化下降的精确机制仍不清楚。本简要综述主要是解决了碳水化合物通量介导的理论,即肌肉肉毒碱的可用性降低线粒体酶肉碱肉豆蔻酰基转移酶1,是线粒体脂肪易位的速率限制步骤,是脂肪氧化期间下降的关键机制高强度运动。这与最近在该地区的最近作品中讨论了在各种运动强度下调查燃料代谢,并利用骨骼肌肉碱含量可以在人类受试者体内营养增加的发现。

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