| Summary: | 碩士 === 輔仁大學 === 營養科學系 === 96 === Glucose transporter 4 (GLUT4) and fatty acid translocase (FAT/CD36) are membrane-associated transporters of glucose and long chain fatty acids, respectively. Previous studies indicated that upon stimulation by muscle contraction or insulin, intracellular pools of GLUT4 and FAT/CD36 could be mobilized to the plasma membrane. Stimulation of muscle contraction or insulin also resulted in elevated GLUT4 and FAT/CD36 levels. The aim of the present study was to examine whether meals with different glycemic indices (GI) after an endurance bicycle exercise has differential influences on the expression of GLUT4 and FAT/CD36 in human skeletal muscle. Six healthy untrained male subjects received three treatments: high GI meal (HGI), low GI meal (LGI) and fast, separated by 3 weeks. In each trial, following an overnight fast, subjects randomly consumed the test meal after performing a single bout of bicycle ergometer exercise with 70% peak oxygen consumption for 60 minutes. Blood samples were measured for glucose, insulin, free fatty acid and glycerol concentrations. Musculus vastus lateralis were analyzed for the mRNA and protein expression of GLUT4 and FAT/CD36. Post-exercise supplementation of HGI resulted in higher plasma glucose and serum insulin responses than LGI and exercise-fasting (P<0.05). In contrast, plasma free fatty acid concentrations were significantly lower following HGI and LGI compared with exercise-fasting (P<0.05). GLUT4 mRNA levels were significantly lowered in subjects receiving the carbohydrate meal during 3-h recovery period. GLUT4 protein levels were increased in three experimental conditions, and GLUT4 protein content was higher in HGI trail than that of LGI or exercise-fasting trial. In addition, post-exercise supplementation of HGI or LGI resulted in decreased FAT/CD36 mRNA and protein expression. In conclusion, the results indicate that carbohydrate supplementation after exercise will enhance GLUT4 protein expression by increasing translational efficiency but suppress FAT/CD36 expression. It is speculated that these outcomes are likely associated with increased glucose availability and may promote glucose transport and improve muscle glycogen resynthesis.
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