Endurance exercise training can result in increased rates f insulin-stimulated glucose uptake in skeletal muscle; however, this effect may be lost rapidly once training ceases. To examine a mechanism for these changes, the skeletal-muscle glucose transport system of female rats exercise-trained in wheelcages for 6 wk were studied against a group of untrained female rats. The trained rats were studied immediately following and 2 and 5 days after removal from wheelcages; both trained and untrained rats were studied 30 min after insulin (90 nmol/rat, intraperitoneal) or saline injection. The total number of skeletal-muscle plasma-membrane glucose transporters (Ro), total muscle-homogenate and plasma-membrane GLUT4 protein, and rates of plasma-membrane vesicle D-facilitated glucose transport were higher in the exercise-trained rats immediately after exercise training and did not decrease significantly during the 5 days after cessation of training. On the other hand, exercise training did not alter microsomal-membrane total glucose-transporter number or GLUT4 protein, nor did training alter GLUT1 protein in total muscle homogenates nor either membrane fraction. The carrier-turnover number, an estimate of average functional activity of glucose transporters in the plasma membrane, was elevated slightly, but not significantly, in the trained muscle. In both the trained and untrained muscle, insulin administration resulted in translocation of glucose transporters from the microsomal-membrane fraction to the plasma membrane and an increase in the carrier-turnovernumber. These data suggest that increased rates of glucose uptake in endurance-trained skeletal muscle results primarily from an increase in the number—and not an increase in the average functional activity—of glucose transporters present in the plasma membrane. Furthermore, these increases persist for several days after cessation of exercise training. The specific increase in the GLUT4, but not the GLUT1 glucose-transporter isoform, in response to training demonstrates that a common, chronic physiological stimulus can regulate the expression of the two glucose-transporter isoforms present in skeletal-muscle tissue differentially.

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