Acute and Chronic Exercise Increases Insulin Sensitivity Insulin Receptor Density and Glucose Transport into Muscle

Though skeletal muscle is omnivorous, its work intensity and duration, training status, inherent metabolic capacities, and substrate availability determine its energy sources. For very short-term exercise, stored phosphagens (ATP and creatine phosphate) are sufficient for crossbridge interaction between actin and myosin, even maximal efforts lasting 5 to 10 seconds require little or no glycolytic or oxidative energy production. When work to exhaustion is paced to be somewhat longer in duration, glycolysis is driven (particularly in fast glycolytic fibers) by high intramuscular ADP concentrations, and this form of anaerobic metabolism, with its by-product lactic acid, is the major energy source. The carbohydrate provided to gly-colysis comes from stored, intramuscular glycogen or blood-borne glucose. Exhaustion from work in this intensity range (50 to 90% of the maximal oxygen uptake) is associated with carbohydrate depletion. Accordingly, factors that increase carbohydrate availability improve fatigue resistance. These include prior high dietary carbohydrate, cellular training adaptations that increase the enzymatic potential for fatty acid ox idation (thereby sparing carbohydrate stores), and oral carbohydrate intake during exercise. Frank hypoglycemia rarely occurs in healthy people during even the most prolonged or intense physical activity. When it does, it is usually in association with the depletion of muscle and hepatic stores and a failure to supplement carbohydrate orally.

Exercise suppresses insulin secretion by increasing sympathetic tone at the pancreatic islets. Despite acutely falling levels of circulating insulin, both non-insulin-dependent and insulin-dependent muscle glucose uptake increase during exercise. Exercise recruits glucose transporters from their intracellular storage sites to the plasma membrane of active skeletal muscle cells. Because exercise increases insulin sensitivity, patients with type 1 diabetes (insulin-dependent) require less insulin when activity increases. However, this positive result can be treacherous because exercise can accelerate hypoglycemia and increase the risk of insulin coma in these individuals. Chronic exercise, through its reduction of insulin requirements, up-reg-ulates insulin receptors. This effect appears to be due less to training than simply to a repeated acute stimulus, the effect is full-blown after 2 to 3 days of regular physical activity and can be lost as quickly. Consequently, healthy active people show strikingly greater insulin sensitivity than do their sedentary counterparts (Fig. 30.7). In addition, up-

Insulin Exercise Response

Repeated daily exercise and the blood glucose and insulin response to glucose ingestion. Both responses are blunted by repeated exercise, demonstrating increased insulin sensitivity.

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