减量训练对心肌mTOR上游信号蛋白PI3K和Akt的影响

来源 :北京体育大学学报 | 被引量 : 0次 | 上传用户:yanjiawei2005
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减量训练对于防止运动性疾病和过度疲劳的发生起重要作用,对于促进心脏朝着有利于运动员机能提高的方向发展至关重要。研究利用72只SPF级7周龄雄性SD大鼠,经过1周适应性训练后,随机分为8组:3周大运动量训练组、3 d、6 d和2周减量训练组及其相应的对照组。3周大运动量训练采用中等强度和大强度交替进行,运动时间逐渐延长,然后进行减量训练。训练后取左心室肌组织,测定PI3K、Akt的蛋白和磷酸化采用Western blotting方法。结果显示:减量训练过程中,心肌PI3K P85蛋白表达有升高趋势。PI3K是减量训练诱导心肌保护的重要调节物。不同的运动负荷对Akt蛋白表达量和磷酸化产生不同的影响。在3周大运动量训练后进行减量训练,心肌Akt蛋白表达显著增加。在3周大运动量训练后进行6 d减量训练,AktSer473磷酸化显著增加,2周减量训练后,心肌AktSer473磷酸化显著增加。减量训练过程中,心肌Akt蛋白表达和AktSer473磷酸化有升高趋势。减量训练通过增加Akt蛋白表达和AktSer473磷酸化对心肌起保护作用。 Decreasing training plays an important role in preventing the occurrence of motor sickness and fatigue, which is crucial for promoting the development of the heart in the direction of improving the performance of athletes. In this study, 72 SPF male Sprague-Dawley (SD) rats, aged 7 weeks, were randomly divided into 8 groups: 3-week exercise training group, 3-day, 6-day and 2-week reduction training group and their corresponding Control group. Three weeks of large amount of exercise training using medium-intensity and high intensity alternation, exercise time gradually extended, and then reduce training. Left ventricular muscle tissue was obtained after training, and the protein and phosphorylation of PI3K and Akt were determined by Western blotting. The results showed that the expression of PI3K P85 protein in myocardium tended to increase during training. PI3K is an important regulator of diminished training in induction of myocardial protection. Different exercise loads have different effects on Akt protein expression and phosphorylation. After 3 weeks of training, the amount of Akt protein expression was significantly increased. After 6 weeks training, the AktSer473 phosphorylation increased significantly after 3 weeks training. The AktSer473 phosphorylation increased significantly after 2 weeks training. Decreased training, myocardial Akt protein expression and AktSer473 phosphorylation have an increasing trend. Decreasing training protects the myocardium by increasing Akt protein expression and AktSer473 phosphorylation.
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