急性高原低氧和力竭运动对大鼠骨骼肌AMPK磷酸化水平的影响

Effects of acute hypobaric hypoxia and exhaustive exercise on AMP-activated protein kinase phosphorylation in rat skeletal muscle

本文旨在探讨急性高原低氧和力竭运动对大鼠骨骼肌磷酸化AMP激活的蛋白激酶(phosphorylated AMP-activated pro-tein kinase,pAMPK)水平的影响及其意义。Sprague-Dawley(SD)大鼠随机分为平原组和高原组,高原组大鼠置模拟海拔5000m低压舱中24h,平原组大鼠在舱外饲养。测定大鼠在模拟高原和平原条件下的游泳力竭时间以及力竭运动后骨骼肌糖原、血乳酸含量。Western blot检测骨骼肌组织中pAMPK/AMPK比值。结果显示,急性低氧可显著缩短大鼠游泳力竭时间。运动力竭时,高原组大鼠骨骼肌剩余糖原含量显著高于平原组大鼠,而血乳酸含量显著低于平原组大鼠。无论是在平原还是在模拟高原条件下,运动力竭时,各组大鼠骨骼肌pAMPK/AMPK比值都显著升高,但高原组大鼠骨骼肌pAMPK/AMPK比值明显低于平原组大鼠。以上结果表明,急性高原低氧可显著降低大鼠运动能力,但运动力竭时骨骼肌pAMPK/AMPK比值低于平原条件下水平,提示骨骼肌能量代谢因素可能不是导致进入高原早期运动能力降低的主要因素。

The present study was aimed to explore the changes of phosphorylated AMP-activated protein kinase （pAMPK） level in skeletal muscle after exposure to acute hypobaric hypoxia and exhaustive exercise.Thirty-two male Sprague-Dawley （SD） rats were randomly divided into sea level and high altitude groups.The rats in high altitude group were submitted to simulated 5 000 m of high altitude in a hypobaric chamber for 24 h,and sea level group was maintained at normal conditions.All the rats were subjected to ex-haustive swimming exercise.The exhaustion time was recorded.Before and after the exercise,blood lactate and glycogen content in skeletal muscle were determined;AMPK and pAMPK levels in skeletal muscle were detected by Western blot.The results showed that the exhaustion time was significantly decreased after exposure to high altitude.At the moment of exhaustion,high altitude group had lower blood lactate concentration and higher surplus glycogen content in gastrocnemius compared with sea level group.Exhaustive exercise significantly increased the pAMPK/AMPK ratio in rat skeletal muscles from both sea level and high altitude groups.However,high altitude group showed lower pAMPK/AMPK ratio after exhaustion compared to sea level group.These results suggest that,after exposure to acute hypobaric hypoxia,the decrement in exercise capacity may not be due to running out of glycogen,accumulation of lactate or disturbance in energy status in skeletal muscle.