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The increased energy demand that occurs with incremental exercise intensity is met by increases in the oxidation of both endogenous fat and carbohydrate stores up to an intensity of ~70% V˙O2max in trained individuals. However, when exercise intensity increases beyond this workload, fat oxidation rates decline, both from a relative and absolute perspective. As endogenous glycogen use is accelerated, glycogen stores can become depleted, ultimately resulting in fatigue and the inability to maintain high intensity, submaximal exercise ( > 70% V˙O2max ). Despite a considerable accumulation of knowledge that has been gained over the past half century, the precise mechanism( s ) regulating muscle fuel selection and underpinning the aforementioned decline in fat oxidation remain largely unclear. A greater understanding would undoubtedly lead to novel strategies to increase fat utilization and, as such, improve exercise capacity. The present review primarily addresses one of the most prominent theories to explain the phenomenon of diminished fat oxidation during high intensity, submaximal exercise; a reduced availability of muscle free carnitine for mitochondrial fat translocation. This is discussed in the light of recent work in this area taking advantage of the discovery that muscle carnitine content can be increased in vivo in humans. Furthermore, the evidence supporting the recently proposed theory that reduced muscle co-enzyme A availability to several key enzymes in the fat oxidation pathway may also exert a degree of control over muscle fuel selection during exercise is also considered. Strong correlational evidence exists that muscle free carnitine availability is likely to be a key limiting factor to fat oxidation during high intensity, submaximal exercise. However, it is concluded that further intervention studies manipulating the muscle carnitine pool in humans are required to establish a direct causal role. In addition, it is concluded that while a depletion of muscle coenzyme A availability during exercise also offers a viable mechanism for impairing fat oxidation, at present, this remains speculative.


Mary MacKillop Institute for Health Research

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Journal Article

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