已知運動訓練可有效避免胰島素阻抗(insulin resistance)與第二型糖尿病(type 2 diabetes),部分原因為運動過程造成肌肉相對缺氧,誘發正面的調適生理反應。而低氧運動訓練可增強組織的相對缺氧,使得身體對於醣類能源依賴比重增加。運動與低氧可透過活化AMP-activated protein kinase (AMPK)來促進第四型葡萄糖轉運體(glucose transporter type4, GLUT-4)蛋白由細胞內轉移到細胞膜來增加血液中的葡萄糖轉運進入細胞。低氧運動訓練可能透過與PI-3 kinase及AMPK信息傳導路徑來影響肌肉醣類代謝機制。本篇文章將透過深入的文獻探討幫助讀者瞭解低氧運動訓練對胰島素阻抗與骨骼肌肉可能發生的作用機轉。這些知識可能對於未來發展低氧運動處方用來預防胰島素阻抗與第二型糖尿病有幫助。
Physical exercise is known to prevent insulin resistance and type 2 diabetes, mediated in part by beneficial adaptation of tissue hypoxia in exercised muscle. Hypoxia training can further reduce tissue oxygenation and increase energy dependence on carbohydrate. It has been shown that activation of AMP-activated protein kinase (AMPK) by hypoxia can increase glucose transporter type 4 (GLUT4) translocation to plasma membrane and thus enhances trans-membrane glucose transport. This article provides extensive review on existing evidence regarding to the role of PI-3 kinase and AMPK signal transduction pathways on glucose transport system in response to hypoxia and exercise training. We aimed to provide insight into how hypoxia exercise training affects carbohydrate metabolism in skeletal muscle. Such knowledge may be important for the possibility of using hypoxia exercise training in the prevention and treatment of type 2 diabetes.