Abstract:

BACKGROUND: The plasma fatty acid to the working muscle is primarily supplied from lipolysis of triacylglycerol stored in adipose tissue. The inability of fatty acid oxidation to support the energy demand during high intensity exercise can reflect a limitation in skeletal muscle to oxidize fatty acids.
OBJECTIVE: To review findings of research on which related to the regulation mechanism about fatty acid oxidation during exercise, and to propose the problems that need to be solved on mechanism about fatty acid oxidation.
METHODS: The PubMed database was used to search the articles on the regulation mechanism about fatty acid oxidation during exercise published from 1995 to 2012 with the key words of “exercise, fatty acid oxidation, intensity, carnitine, acetylcarnitine, mitochondria” in English. The repetitive contents were deleted.
RESULTS AND CONCLUSION: A total of 94 articles were collected after the initial search, the repetitive contents were deleted, and finally 56 articles were classified and sorted. Fatty acid oxidation during exercise involves multiple possible regulatory steps, ranging from adipose tissue lipolysis to mitochondrial metabolism in skeletal muscle. It seems that the most attractive regulatory candidate for fatty acid oxidation is the muscle metabolite carnitine, which is essential in carnitine palmitoyl transferase-1 regulation and fatty acid oxidation. At high intensity exercise, the rapid glycolysis provides the mitochondria with excess Acetyl coenzyme A which buffered by free carnitine to form acetylcarnitine. Accordingly, a fall in muscle concentration of free carnitine may reduce carnitine palmitoyl transferase-1 activity, and thus the ability to transport fatty acid into the mitochondria, and therefore also the rate of fatty acid oxidation. In this way, rapid glycogen decomposition and glycolysis are suggested to have a major impact on inhibiting fatty acid oxidation.