A high potential for lipid oxidation is a sign of metabolic fitness and is important not
only for exercise performance but also for health promotion. Despite considerable
progress during recent years, our understanding of how lipid oxidation is controlled
remains unclear. The rate of lipid oxidation reaches a peak at 50-60% of v·O2 max after
which the contribution of lipids decreases both in relative and absolute terms. In the
high-intensity domain (>60% v·O2 max), there is a pronounced decrease in energy state,
which will stimulate the glycolytic rate in excess of the substrate requirements of
mitochondrial oxidative processes. Accumulation of glycolytic products will impair
lipid oxidation through an interaction with the carnitine-mediated transfer of FA into
mitochondria. Another potential site of control is Acyl-CoA synthetase (ACS), which
is the initial step in FA catabolism. The activity of ACS may be under control of
CoASH and energy state. There is evidence that additional control points exist
beyond mitochondrial influx of fatty acids. The electron transport chain (ETC) with
associated feed-back control by redox state is one suggested candidate. In this review
it is suggested that the control of FA oxidation during heavy exercise is distributed
between ACS, CPT1, and ETC.