Intramuscular mechanisms regulating fatty acid oxidation during exercise

Abstract

Fatty acid oxidation increases in response to exercise, but at high intensities the contribution of fatty acid oxidation to energy production decreases. The carnitine palmitoyl transferase (CPT) complex appears to be a plausible site of regulation of fatty acid oxidation at rest and during exercise. Muscle malonyl-CoA, a potent inhibitor of CPT I, decreases during muscle contraction as a consequence of phosphorylation and inactivation of acetyl-CoA carboxylase (ACC) by AMP-activated protein kinase (AMPK). When AMPK is artificially activated with AICA riboside, ACC is inactivated, malonyl-CoA decreases, and fatty acid oxidation increases. Factors other than the muscle malonyl-CoA concentration are likely responsible for the decline in fatty acid oxidation during exercise at high intensities.