Endurance training at submaximal levels of VO2 increases the oxidative capacity of muscle without causing muscle hypertrophy. Muscle size does not change but there are increases in the number of mitochondria and enzymes for fatty acid oxidation, the citric acid cycle, and the electron transport chain. Capillary density and myoglobin also increase to enhance O2 transport. Muscles must be activated during training to undergo these changes, so higher levels of VO2 are necessary to train fast-twitch glycolytic fibers than slow-twitch oxidative fibers. Activating fast-twitch fibers with heavy training increases mitochondrial enzymes, and the fibers change their biochemistry to a more oxidative pattern.
VO2 increases more rapidly after training because there are more mitochondria and the metabolism of glucose and free fatty acids increases faster. ADP does not build up as quickly, resulting in less lactic acid and better preservation of phosphocreatine stores. Increased capillary density and perhaps membrane transporters enhance the transport of free fatty acids from the circulation into muscle. Transporters on mitochondrial membranes improve the uptake of free fatty acids from the myoplasm, and enzymes for fatty acid metabolism in the mitochondria are increased. Glucose uptake is enhanced by insulin-independent and -dependent transporters, which remain elevated for several hours following exercise and are upregulated in trained muscles.
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