Symposium: Limits to fat oxidation by skeletal muscle during exercise--introduction

Lipids, in the form of adipose tissue triacylglycerol (TG), intramuscular triglyceride (IMTG), and dietary-derived fatty acids (FA) from plasma TG (chylomicrons), and very low-density lipoproteins (VLDL), represent the largest store of nutrient energy in humans. Yet despite the abundance of endogenous TG, there is limited capacity for FA oxidation during exercise: there are no mechanisms that match the availability and metabolism of FA to the rate of energy expenditure. Because of the body's limited carbohydrate (CHO) stores, and because depletion of muscle and liver glycogen reserves often coincide with exhaustion, there is interest in several nutritional interventions that increase FA availability and rates of fat oxidation during exercise: such strategies have the potential to slow the rate of glycogen utilization and delay the onset of fatigue. The five papers comprising this symposium provide a synopsis of 1) the regulation of fat oxidation in human skeletal muscle during aerobic exercise; 2) selected nutritional techniques that increase fat oxidation, spare endogenous CHO stores, and modify exercise capacity; and 3) dietary manipulations that alter macronutrient availability and muscle gene expression.