Abstract

AbstractThis chapter summarizes how fatty acid (FA) oxidation is regulated in skeletal muscle during exercise and the role of obesity in regulation of FA oxidation in skeletal muscle. The substrates fueling increased FA oxidation in skeletal muscle during exercise are mainly circulating FAs, although hydrolysis of circulating triacylglycerol (TG) in very-low-density lipoproteins (VLDL-TG) and especially lipolysis of intramuscular TG (IMTG) also appear to contribute to some extent. Several steps are involved in FA uptake and oxidation in skeletal muscle and could all be of importance in the regulation of FA oxidation during exercise. Besides trans-sarcolemmal FA uptake via fatty acid transporters, it appears that intramyocellular carnitine content plays an important regulatory step in regulation of substrate selection during exercise. Interestingly, individuals with obesity exhibit a compromised ability to oxidize FAs and to increase FA oxidation in response to lipid exposure (reduced metabolic flexibility). Skeletal muscle mitochondrial function appears to be related to this defect. It remains controversial whether this impaired FA oxidative capacity in obesity diminishes the ability to increase and properly regulate FA oxidation during an acute, single exercise bout. However, despite these initial impairments in FA oxidation capacity in the obese situation, endurance exercise training can rescue the capacity for FA oxidation and the metabolic flexibility in the skeletal muscle of individuals with obesity at least to equivalent levels of their lean counterparts.KeywordsFatty acid oxidationExerciseSkeletal muscleMitochondriaObesityExercise trainingLipid metabolism

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