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肝醣超補現象的分子調節過程研究—游泳運動后肌肉肝醣與GLUT4 mRNA的轉譯活性在16小時恢復過程中的變化

Molecular Regulatory Mechanism of Glycogen Supercompensation — Alteration in Musele Glycogen Storage and Translational Activity of GLUR4 mRNA within a 16-Hour Time Course after Swimming

摘要


在長時間高強度游泳運動造成肌肉肝醣減少後,如果有充分的砍水化合物補充肌肉的肝醣濃度會逐漸達到超補狀態。由於先前此現象發生的原因並不清楚,因此本研究的首要目的為觀察是否此超補現象與運動後在砍水化合物補充下肌肉調整葡萄糖運輸蛋白GLUT4的表現有關。在動物藉由游泳運動消耗肝醣後,紅肌(red gastrocnemius)與白肌(white gastrocnemius)的肝醣於90分鐘內已回補並恢復正常水準。五小時內兩種肌肉均已形成明顯的肝醣超補現象。在紅肌上GLUT4蛋白的表現量較白肌增加的快速。相同的,在肌肉肝醣的濃度的回補上也以紅肌較白肌為快。GLUT4 mRNA的表現數量在運動後立即測量發現比控制組高出45%。在運動後碳水化合物開始補充的前五小時內,GLUT4 mRNA的表現量明顯快速下降,但其轉譯速率卻反而明顯增加。GLUT4 mRNA與聚核醣體(P olysomes)的結合數量增加。當肝醣超補現象已發生後,GLUT4 mRNA數量與其轉譯才回複至正常水準。本研究證明了運動後砍水化合物補充造成GLUT4 mRNA轉譯活性增加,進而造成了GLUT4蛋白數量增加。由於筆者先前研究發現,在碳水化合物補充下肝醣的合成量與GLUT4蛋白量成正比,這個GLUT4 mRNA轉譯增加的現象也因此解釋了同時發生於肌肉的肝醣超補現象。

並列摘要


Skeletal muscle glycogen is largely depleted after a prolonged exercise bout and is hyperbolically repleted to a supercompensated level after an immediate post-exercise carbohydrate supplementation. The purpose of this study was to determine the effect of post-exercise carbohydrate supplementation on GLUT4 expression and its relationship to glycogen repletion. An immediate post-exercise carbohydrate load completely normalized glycogen levels within 90 mm in red and white gastrocnemius muscle, and reached supercompensation levels within 5 hours. In red gastrocnemius muscle, a faster and larger increase in GLUT4 protein and glycogen levels were observed within the 16-hour time course when compared to white gastrocnemius muscle. Red gastrocnemius GLUT4 mRNA was increased by 46% immediately after the glycogen depleting exercise. Red quadriceps GLUT4 mRNA engaged with polysomes was increased immediately post exercise and during the first 5 hours of recovery although the initial elevation in GLUT4 mRNA rapidly returned to control levels when glycogen was repleted. The current results demonstrate that a post-exercise carbohydrate supplementation increases translational activation of GLUT4 mRNA following an initial GLUT4 mRNA elevation, explaining the continuous rise in GLUT4 protein during recovery. The increase in GLUT4 protein availability may explain, in part, the concurrent glycogen supercompensation in the same muscle.

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