低氧训练介导的细胞自噬激活对于小鼠体重控制与游泳运动能力提高的研究

发布时间：2018-04-09 18:48

本文选题：低氧训练　切入点：运动能力　出处：《武汉体育学院》2016年硕士论文

【摘要】：目的低氧训练是一种有效的辅助运动训练手段,在低氧环境刺激下,机体能够产生一系列抵抗缺氧的生理反应,从而有效增强机体的运动适应与有氧代谢能力、优化身体成分、提高运动表现与成绩。本文旨在通过高住低练的方式,并采用低压氧舱设备建立氧浓度设定为15.0%(相当于海拔高度2500 m)的小鼠运动实验模型,来考察低氧游泳训练对于小鼠的游泳运动能力提高及其相关分子机制。方法取8周龄昆明小鼠60只随机分为3组:常氧对照组(normoxia control,NC),常氧训练组(normoxia exercise,NE),低氧训练组(hypoxia exercise,HE),每组小鼠20只。NC和NE组小鼠在常氧环境下饲养,HE组小鼠则放入低氧舱内进行居住,低氧训练组和常氧训练组小鼠均在常氧条件下进行为期8周的游泳训练,每周训练5天、每天训练45 min。游泳训练结束后,每组部分小鼠给予力竭游泳运动以考察其运动能力。另一部分则分别采取小鼠血清、腓肠肌、比目鱼肌和心肌以ELISA方法测定SOD和MDA的含量;以Western blot方法检测自噬相关蛋白Beclin1、p62、LC-3、AMPK、p-AMPK及抗凋亡蛋白Bcl-2的表达。结果1、与NC相比,HE组和NE组小鼠体重均显著性降低(P0.05),而且HE小鼠体重较NE组也明显下降(P0.05)。2、与NC相比,HE组和NE组小鼠的力竭运动时间均明显地增加(P0.05);HE与NE组相比,小鼠力竭运动时间也具有显著性的提高(P0.05)。3、与NC组相比,NE组和HE组小鼠比目鱼肌和腓肠肌中SOD活力明显升高(P0.05),HE组小鼠比目鱼肌和腓肠肌中SOD活力增高更为明显(P0.05),同时,NE组和HE组小鼠比目鱼肌和腓肠肌中,MDA含量也明显地降低。4、与NC组相比,NE组和HE组小鼠心肌中SOD活力有所增高,但各组小鼠心肌中的MDA含量无显著差异。5、在心肌、腓肠肌和比目鱼肌中,与NC组相比,HE和NE组小鼠肌肉组织中AMPK、p-AMPK、Beclin1、LC3-I、LC3-II均呈现显著性的升高(P0.05),并且在HE组中的升高幅度显得更为明显(P0.05);与NC组相比,HE和NE组小鼠肌肉组织中p62显著性的降低(P0.05),并且在HE组小鼠肌肉组织中的降低更加明显(P0.05)。6、在腓肠肌和比目鱼肌中,HE组小鼠肌肉组织Bcl-2蛋白表达量显著性地高于NC和NE组(P0.05);NE组小鼠比目鱼肌和心肌组织中Bcl-2蛋白表达量相对于NC组亦具有显著性的升高(P0.05)。结论适当的低氧暴露联合游泳训练的双重或协同刺激以有效地实现小鼠体重降的低或控制、身体体脂成分的优化、运动适应能力的加强、以及运动能力的提高;相应地,对于这些功能性的改善与提高,低氧暴露联合游泳训练诱导的细胞自噬的激活在其中对于能量代谢与利用、代谢废物的清除、内环境稳态的维持起到十分重要的作用。
[Abstract]:Objective hypoxic training is an effective means of supplementary exercise training. Under the stimulation of hypoxic environment, the body can produce a series of physiological responses to resist hypoxia, thereby effectively enhancing the ability of sports adaptation and aerobic metabolism of the body, and optimizing the body composition.Improve performance and performance.The purpose of this paper is to establish an experimental model of exercise in mice with oxygen concentration of 15.0 (equivalent to 2500 m above sea level) by means of living high and training low, and using low-pressure oxygen chamber equipment.To investigate the effects of hypoxic swimming training on the swimming ability of mice and its related molecular mechanisms.Methods Sixty 8-week-old Kunming mice were randomly divided into three groups: normoxia control group, normoxia exercise group, hypoxia exercise group and hypoxia exercise group.The mice in hypoxia training group and normoxic training group were trained for 8 weeks under normoxic condition for 5 days a week for 45 mins a day.After swimming training, some mice in each group were given exhaustive swimming to test their athletic ability.In the other part, the contents of SOD and MDA in serum, gastrocnemius muscle, soleus muscle and myocardium were determined by ELISA method, and the expression of AMPK p-AMPK and anti-apoptotic protein Bcl-2 were detected by Western blot method.Results 1. Compared with NC, the body weight of mice in HE group and NE group was significantly lower than that in NC group, and the body weight of HE group was significantly lower than that of NE group. Compared with NC group, the exhaustive exercise time of HE group and NE group were significantly increased compared with NE group.The content of MDA in soleus muscle and gastrocnemius muscle decreased significantly in NE group and HE group. Compared with NC group, the activity of SOD in myocardium of NE group and HE group was higher than that of NC group.However, there was no significant difference in the content of MDA in myocardium of each group. 5. In myocardium, gastrocnemius muscle and soleus muscle,Compared with NC group, the expression of P0. 05 was also significantly increased (P 0. 05).Conclusion proper hypoxia exposure combined with dual or cooperative stimulation of swimming training can effectively realize the low or control of weight loss, the optimization of body fat composition, the enhancement of sports adaptability and the improvement of exercise ability in mice.The activation of autophagy induced by hypoxic exposure combined with swimming training plays an important role in energy metabolism and utilization, metabolic waste removal and homeostasis.
【学位授予单位】：武汉体育学院
【学位级别】：硕士
【学位授予年份】：2016
【分类号】：G804.2

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