Increasing the amount of energy derived from fat is likely to have important health and performance applications. This thesis applied contemporary knowledge in order to investigate strategies for optimising whole-body fat oxidation, in male subjects. Study 1 investigated the efficacy of Xenadrine EFXTM (Gx), a weight-loss supplement containing bitter orange, green tea, and guarana, in promoting fat metabolism during 6 h rest. The ingredients in Gx are purported to increase lipolysis and fat oxidation. Indeed, a metabolic effect of Gx was evident. However, carbohydrate oxidation was increased by 15.5 ± 5.6 g over the 6 h period with a concomitant decrease in fat oxidation of -5.9 ± 3.1 g, while the metabolic rate remained unchanged. Study 2 extended the work from the first experimental study, by examining the acute effects of GX during 60 min sub-maximal treadmill walking. Although the onset of the walking exercise resulted in an approximately five-fold increase in the rate of fat oxidation, a reduction in the energy derived from fat, and increase in the energy derived from carbohydrate, was again evident with Gx. In Study 3 the intensity of exercise was manipulated, during treadmill running, in order to determine the exercise intensity eliciting the highest rate of fat oxidation (Fatmax). There was a large variation in the rate of fat oxidation across the range of exercise intensities investigated, with Fatmax occurring at 65.9 ± 1.0 % V02max, while individual peak rates of fat oxidation were 0.54 ± 0.04 g·min-1. This study highlighted the need for careful consideration of the intensity of exercise in order to optimise fat oxidation. Study 4 identified a relationship between Fatmax and the lactate threshold, during treadmill exercise. Analysis of plasma glycerol and NEF A concentrations indicated that the reduced rates of fat oxidation at high exercise intensities were not mediated by reduced lipolysis or plasma FA availability. These finding's were interpreted as supporting either depletion of the free carnitine pool, or inhibition of CPTI by a reduction in intra-cellular pH, as mediating the reduction in fat oxidation at exercise intensities in excess of Fatmax. Based upon the hypothesis that a reduction in intra-cellular pH might contribute to the reduced rates of fat oxidation at high exercise intensities, Study 5 sought to increase intra-cellular H+ buffering capacity. Four weeks supplementation with ~-alanine resulted in a significant increase in the muscle concentration of carnosine, an imidazole dipeptide contributing to intra-cellular physico-chemical H+ buffering. Despite the augmented carnosine concentration there were no changes in substrate utilisation across the range of exercise intensities studied, whilst Fatmax remained unchanged. This data suggests that a reduction in intra-cellular pH does not mediate reduction in fat oxidation during intense exercise. Taken together, the findings of this thesis demonstrate the importance of exercise as an intervention for facilitating fat metabolism, and highlight the primacy of carbohydrate metabolism within the fat-carbohydrate interaction.