摘要
探讨运动疲劳引起大鼠骨骼肌纤维GLUT4mRNA和蛋白表达的变化及其可能机制。方法:Wistar大鼠40只,随机选取10只为正常对照组(D组),其余采用多级递增负荷跑台运动建立运动疲劳模型,留其成功的20只为疲劳组(P组);测试力竭运动后2组大鼠血糖、血尿素氮、血乳酸、血清胰岛素含量,采用逆转录-聚合酶链反应(RT-PCR)法测定股四头肌细胞GLUT4mRNA的表达,运用免疫组化法观测该部GLUT4蛋白的表达。结果:力竭运动后即刻,实验组大鼠血糖、血清胰岛素含量均显著低于(P<0.05)D组大鼠,而血乳酸水平却显著高于(P<0.05)D组大鼠,骨骼肌纤维GLUT4mRNA及蛋白的表达均较D组大鼠显著上调(P<0.05)。结论:运动疲劳后大鼠能量基本耗竭、通过非胰岛素途径迫使机体以上调骨骼肌纤维GLUT4mRNA和蛋白表达来应激,以此延搁由能量衰竭所引起的级联反应,从而形成一种适应性保护反应来减缓运动性外周疲劳的发生。
The adaptive immediate changes of GLUT4 mRNA and protein expression in skeletal muscle fiber and possible mechanism were discussed after sports fatigue in rat.10 rats were randomly chosen as normal control group from 40 Wistar rats.The sports fatigue model was built through multistage increasing load treadmill exercise,after which 20 Wistar rats were chosen as fatigue experimental group.The blood glucose,blood urea nitrogen,blood lactic acid,serum insulin were tested,and the expression level of GLUT4 mRNA and protein were observed by using RT-PCR and immunohistochemical method in two groups.The results showed that immediately after exhaustion sports,the blood glucose and blood serum insulin in experimental group were significantly(P0.05)lower than those indexes in control group;but the blood lactic acid and the expression level of GLUT4 mRNA and protein of skeletal muscle fiber were significantly(P0.05)higher than control group rat.Conclusions:the energy was exhausted after sports fatigue in rats,forced the body to stress through up-regulation expression level of GLUT4 mRNA and protein of skeletal muscle fiber by non-insulin mediate way.Through this way,the cascade reaction induced by energy exhaustion was delayed,thus forming a kind of adaptive protective reaction to slow the happening of sports peripheral fatigue.
作者
龚云
王超
GONG Yun;WANG Chao(College of Physical Education, Northwest Normal University, Lanzhou 730070,China;Dongfanghong Primary School,Qingyang 745000,China.)
出处
《首都体育学院学报》
CSSCI
北大核心
2017年第2期182-187,共6页
Journal of Capital University of Physical Education and Sports
基金
西北师范大学青年教师科研能力提升计划项目(SKQNGG-13018)