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) over dotO(2) (max) after which the contribution of lipids decreases both in relative and absolute terms. In the high-intensity domain (> 60% (V) over dotO(2 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.