过度训练对大鼠骨骼肌自由基代谢和MAPK信号通路p38蛋白表达的影响

Effect of Overtraining on Free Radical Metabolism and Activity of PKB in Rat Skeletal Muscle

目的:为探讨过度训练的机制,观察6周过度训练对大鼠骨骼肌自由基代谢MAPK信号通路p38的影响。方法:将30只Wistar大鼠随机分成两组,即安静对照组和过度训练组,过度训练组进行6周的递增负荷过度训练,通过整体机能状态和常规生化指标评定其运动疲劳的程度,并进一步测定其骨骼肌丙二醛(MDA)、超氧化物歧化酶(SOD)、总抗氧化能力及p38蛋白表达。结果:过度训练大鼠血清皮质醇、睾酮/皮质酮和血红蛋白显著下降(P<0.01),血尿素氮显著升高(P<0.01),且运动组大鼠睾酮、睾酮皮质酮比值、血红蛋白较正常组分别下降71.81%、85.21%和23.12%,皮质酮较正常组升高94.79%,分别超过30%、30%、20%和20%的人类过度训练诊断参考标准。同时,骨骼肌MDA含量明显升高(P<0.01),SOD活性和总抗氧化能力明显下降(P<0.05)。肌糖原含量没有显著的变化,血糖出现了显著下降,p38的蛋白表达出现显著的升高(P<0.01)。结论:过度训练引起的肌能量大量消耗,自由基生成加强,抗氧化能力减弱,过剩的自由基通过p38激活了MAPK系统,但这种激活并没有增加肌糖原的含量,推测MAPK对骨骼肌代谢的调节作用可能被低血糖水平所抑制。

Objective：to investigate the mechanism of overtraining and observe the influence to p38 MAPK on free radical Metabolism of skeletal muscle caused by overtraining for six weeks.Methods：thirty male SD rats were randomly divided into control group without training and overtraining group.The rats in the overtraining groups took incremental over training for 6 weeks;Fatigue was evaluated by overall functional status and conventional biochemical indicators.In the further determination,the MDA,SOD,total antioxidant capacity and the protein expression of p38 were determined.Results：serum cortisol,Testosterone/Corticosterone,Hb of the rats in overtraining group decreased significantly（P0.01）,BUN increased significantly（P0.01）.Serum cortisol,Testosterone/Corticosterone,Hb in overtraining group is decreased by 71.81%,85.21% and 23.12% respectively.Corticosterone in overtraining group is 94.79% higher than that in the control group.They overtook reference standard for diagnosis of human over-training for 30%,30%,20%,20%.Each MDA in skeletal muscle increased significantly（P0.01）,SOD and simultaneously total antioxidant capacity in skeletal muscle decreased significantly（P0.05）,simultaneously.Muscle glycogen content did not change significantly,glucose decreased significantly,and the protein expression of p38 increased significantly（P0.01）.Conclusion：large amount of energy consumption in skeletal muscle,the increasing of radical generation,the reduced antioxidant capacity,excess radical caused by overtraining activated MAPK,but didn＇t increase the content of muscle glycogen.It is speculated that MAPK regulates skeletal muscle metabolic may be inhibited by the low glucose.