高强度间歇运动改善骨骼肌损伤和提高大鼠运动能力的机制  被引量:1

Mechanism by which high-intensity intermittent exercise improves skeletal muscle injury and enhances exercise capacity in rats

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作  者:张六妹 刘菁菁 林晓烨 刘琳[1] 陆矫 Zhang Liumei;Liu Jingjing;Lin Xiaoye;Liu Lin;Lu Jiao(School of Sports and Health,Nanjing Sport Institute,Nanjing 210014,Jiangsu Province,China;School of Sports and Health,Shanghai University of Sport,Shanghai 200000,China;Jiangsu Collaborative Innovation Center for Sport and Health,Nanjing 210014,Jiangsu Province,China)

机构地区:[1]南京体育学院运动健康学院,江苏省南京市210014 [2]上海体育学院运动健康学院,上海市200000 [3]江苏省体育与健康协同创新中心,江苏省南京市210014

出  处:《中国组织工程研究》2023年第35期5603-5609,共7页Chinese Journal of Tissue Engineering Research

基  金:国家自然科学基金项目(32000829),项目负责人:刘琳;江苏省高校自然科学研究(19KJB180019),项目负责人:陆矫;江苏省体育与健康协同创新中心项目(JSCIC-YP21003),项目负责人:陆矫;国家重点研发计划项目(2020YFC2007002),项目负责人:陆矫。

摘  要:背景:高强度间歇运动增强机体适应性,提高运动表现,其潜在机制可能与骨骼肌内腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)的磷酸化水平有关。目的:明确高强度间歇运动减轻力竭运动诱导的骨骼肌损伤与提高运动能力的作用,并阐明此过程中AMPK介导葡萄糖转运蛋白4的变化与作用机制。方法:取45只雄性SD大鼠,采用随机数字表法分为对照组、力竭运动组、高强度间歇+力竭运动组,每组15只。对照组大鼠不进行任何干预;力竭运动组大鼠以25-28 m/min的速度在跑台上运动至力竭;高强度间歇+力竭运动组进行3 d的高强度间歇运动训练(每天以28 m/min的速度在跑台上运动4次,每次10 min,穿插10 min休息),高强度间歇运动结束后24 h复制力竭运动模型;记录大鼠运动距离。力竭运动后,检测各组大鼠血浆肌酸激酶、超氧化物歧化酶水平,TUNEL染色与Western Blot检测腓肠肌细胞凋亡情况,Western Blot检测腓肠肌组织内AMPK磷酸化水平,免疫荧光染色与Western Blot检测腓肠肌组织内葡萄糖转运蛋白4表达与易位情况。结果与结论:①高强度间歇+力竭运动组大鼠的运动距离大于力竭运动组(P<0.05);与对照组比较,力竭运动组肌酸激酶、超氧化物歧化酶水平升高(P<0.05);与力竭运动组比较,高强度间歇+力竭运动组肌酸激酶、超氧化物歧化酶水平降低(P<0.05);②TUNEL染色与Western Blot检测显示,力竭运动组腓肠肌细胞凋亡率大于对照组(P<0.05),高强度间歇+力竭运动组腓肠肌细胞凋亡率小于竭运动组(P<0.05),3组间凋亡相关蛋白Bax和Bcl-2表达无差异(P>0.05);③Western Blot检测显示,与对照组比较,力竭运动组AMPK和p-AMPK蛋白表达升高(P<0.05);与力竭运动组比较,高强度间歇+力竭运动组AMPK蛋白表达降低(P<0.05),p-AMPK蛋白表达升高(P<0.05);④免疫荧光染色与Western Blot检测显示,与对照组相比,力竭运动组骨骼肌纤维的细胞BACKGROUND:The potential mechanism of high-intensity intermittent exercise to enhance body adaptability and improve exercise capacity may be related to the phosphorylation level of AMP-activated protein kinase(AMPK)in skeletal muscle.OBJECTIVE:To clarify the role of high-intensity intermittent exercise in reducing skeletal muscle damage induced by exhaustion and improving exercise capacity and to elucidate the mechanism of AMPK-mediated changes in glucose transporter protein 4 during this process.METHODS:Forty-five Sprague-Dawley rats were randomly divided into control group,exhaustive exercise group(EE group)and high-intensity intermittent exercise group(HIIT+EE group),with 15 rats in each group.No intervention was given in the control group.The EE group was exhausted on the treadmill at the speed of 25-28 m/min.The HIIT+EE group underwent high-intensity intermittent exercise:running on the treadmill,4 times a day at the speed of 28 m/min,once for 10 minutes,with an interval of 10 minutes,for 3 consecutive days,and then experienced exhaustive exercise at 24 hours after the completion of high-intensity intermittent exercise to reproduce animal models of exhaustive exercise.The exercise distance of the rats was recorded.After exhaustive exercise,plasma creatine kinase and superoxide dismutase levels were measured in each group.Apoptosis of cells in gastrocnemius muscle was detected by TUNEL staining and western blot.AMPK phosphorylation in gastrocnemius muscle was detected by western blot.Glucose transporter protein 4 expression and translocation in gastrocnemius muscle was detected by immunofluorescence staining and western blot.RESULTS AND CONCLUSION:The exercise distance of rats in the HIIT+EE group was greater than that in the EE group(P<0.05).The levels of creatine kinase and superoxide dismutase were increased in the EE group compared with the control group(P<0.05).The levels of creatine kinase and superoxide dismutase were decreased in the HIIT+EE group compared with the EE group(P<0.05).TUNEL staining and

关 键 词:高强度间歇运动 运动损伤 力竭运动 凋亡 腺苷酸活化蛋白激酶(AMPK) 葡萄糖转运蛋白4(GLUT4) 

分 类 号:R459.9[医药卫生—治疗学] R349.6[医药卫生—临床医学] R648

 

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