力竭运动过程中大鼠纹状体葡萄糖/乳酸代谢的实时观察

Real-Time Monitor of Glucose and Lactate Metabolism in Rats Striatum during Exhaustion Exercise

目的:通过实时观察一次性力竭运动过程中大鼠纹状体葡萄糖和乳酸浓度的动态变化规律,揭示运动性中枢疲劳形成过程中脑能量代谢的特征。方法:8周龄雄性Wistar大鼠20只分为两组,纹状体葡萄糖、乳酸测定组(第1组)和外周血葡萄糖、乳酸测定组(第2组),每组10只。采用微透析-电化学联用的活体检测技术,实时监测大鼠(第1组)在一次性力竭运动过程中纹状体细胞外液中葡萄糖和乳酸的代谢变化,并从尾静脉采血动态监测大鼠(第2组)外周血液中葡萄糖和乳酸浓度的变化。结果:(1)与安静状态相比,运动初期大鼠纹状体胞外乳酸浓度显著升高(P<0.05),运动后期直至恢复期均显著降低(P<0.05,P<0.01);而胞外葡萄糖浓度在运动初期无明显变化,在运动后期开始下降,甚至在恢复期的90分钟内仍显著低于安静水平(P<0.05,P<0.01)。(2)大鼠外周血糖浓度随着运动时间的延长而显著降低,在运动力竭以及恢复期血糖水平均显著低于安静水平(P<0.05,P<0.01);大鼠血乳酸浓度在力竭运动过程中显著高于安静时水平(P<0.05),而在运动结束后即迅速恢复至安静时水平。结论:力竭运动过程中,持续的外周低血糖导致脑对于葡萄糖摄取不足,出现脑葡萄糖和乳酸浓度降低,中枢能量物质葡萄糖和乳酸代谢的显著降低可能是产生运动性中枢疲劳的一个重要的神经生物学机制。

Objective We used a real-time technique to continuously monitor the dynamic changes in glucose and lactate level in rat striatum during exhaustion exercise. Methods Twenty 8 weeks old male Wistar rats were randomly divided into two groups： group 1（n=10,testing glucose and lactate in striatum）and group 2（n =10,testing peripheral glucose and lactate）. Combination of microdialysis and electrochemical detection technique was applied for real-time analysis of extracellular levels of glucose and lactate in rats striatum in vivo during exhaustion exercise.Changes in the plasma glucose and lactate were evaluated with drawing blood from vena caudalis. Results （1） There was a significant increase in the concentration of extracellular lactate in rats striatum at the beginning of exercise（P ﹤0.05） and a significant decrease during the later period of exercise and recovery period,as compared with that at rest （P ﹤ 0.01）;the glucose concentration remained unchanged at the beginning of exercise,whereas decreased significantly during the later period of exercise（P﹤0.05）and recovery period（P﹤0.01）.（2）The plasma glucose level decreased with prolonging of exercise,and was significant after exhaustion （P 〈0.05）and during the 90-minute recovery period （P 〈0.01）as compared with that at rest. The plasma lactate during exercise was significantly higher than that at rest, and returned to normal level soon after exercise. Conclusion The brain glucose availability was limited by hypoglycaemia induced by exhaustion exercise. The significantly decreased brain glucose and lactate metabolisms could be one of the neurobiological mechanisms causing exercise-induced central fatigue.