摘要
目的:探讨线粒体氧化应激与增龄性骨骼肌流失之间的关系,进一步揭示耐力运动对增龄性骨骼肌流失的影响机制。方法:选用40只ICR小鼠建立2、4、6、8月龄增龄性骨骼肌流失模型;另选用40只ICR小鼠分为4组:青年对照组(YC)、青年运动组(YR)、老龄对照组(AC)和老龄运动组(AR);每组10只。对不同月龄小鼠采用递增负荷进行运动能力测试,YR、AR组小鼠按最大负荷的65%～75%进行耐力训练,每天训练1h,持续4周。取腓肠肌、股四头肌称重,荧光探针法检测腓肠肌线粒体活性氧(ROS)产率与膜电位,ELISA法检测腓肠肌8-羟基-脱氧鸟苷(8-OH-dG)含量。结果:1)4月龄组腓肠肌、左右股四头肌湿重显著高于2、6、8月龄组(P<0.05);但耐力运动对AR、YR组小鼠骨骼肌湿重均无显著影响。2)8月龄组线粒体ROS产率显著高于2、4、6月龄组(P<0.01),6、8月龄组8-OH-dG含量显著高于2月龄、4月龄组(P<0.05)。AR组8-OH-dG含量显著高于AC组(P<0.05)。3)与2月龄组比较,4、6、8月龄组线粒体膜电位显著下降(P<0.01);与4、6月龄组比较,8月龄组线粒体膜电位进一步显著下降(P<0.01)。AR组线粒体膜电位显著高于AC组(P<0.05)。结论:在增龄性骨骼肌流失的不同时期,先后出现线粒体膜电位下降、DNA氧化损伤加剧、ROS产率增加。65%～75%最大强度的耐力运动提高了老龄小鼠骨骼肌的线粒体膜电位,表明耐力运动对老龄小鼠维持线粒体功能、防止肌细胞凋亡有重要意义,但也可能加剧DNA氧化损伤。建议老年人有必要从事耐力运动但不宜采用过高的运动强度。
Purpose： To investigate the relationship between mitochondrial oxidative stress and skeletal muscle loss, and the effects of ageing and endurance training on muscle atrophy. Methods： 2,4,6 or 8 month old ICR mice were established an experimental model of ageing-induced muscle loss, another 40 ICR mice （1 or 6 month old） were distributed into four groups： young and sedentary （ YC, n = 10）, young and trained （ YR, n = 10）, old and sedentary （ AC, n = 10） or old and trained （AR, n= 10）. Running test was firstly used to determine the maximum running capacity of young or old mice, exercise training consisted of 60 min of treadmill exercise at 65% -75% maximum running capacity per day, 6 days/wk. Gastrocnemius and quadriceps were excised and weighed after 4-week training, fluorescence probe was used to detect mitochondrial ROS production and membrane potential, ELISA was used to detect the content of 8-OH-dG in mice gastrocnemius. Results： 1 ） Gastrocnemius and quadriceps wet weight of 4 month old mice was higher than that of 2,6,8 month old （P〈0. 05）. However, exercise training had no significant effect on muscle wet weight in YR and AR mice. 2 ） Mitochondrial ROS level of 8 month old mice was higher than that of 2,4,6 month old （P〈0. 01）. The content of 8-OH-dG of 6,8 month old mice was higher than that of 2,4 month old （P〈0.05）. The content of 8-OH-dG of AR mice was increased than AC mice （P〈0.05）. 3） Mitochondrial membrane potential （△ψ） of 4,6,8 month old mice was decreased than 2 month old （P 〈0.01 ）, the △ψ of 8 month old mice was more decreased than 4,6 month old （P〈 0.01）. The △ψ of AR mice was increased than AC mice （P〈0.05）. Conclusion： During the ageing process and skeletal muscle loss, the decreased membrane potential occurred firstly, DNA oxidative damage was increased secondly, and ROS production was increased finally. Endurance training with 65-75 % maximum running capacity increased mitoehondrial membrane potential in ageing skeletal muscle, suggesting that endurance training was likely to maintain mitochondrial function and prevent muscle apoptosis, but induce more DNA damage in skeletal muscle. Our results suggested it is necessary for old people to do endurance exercise, but it is not proper to take a program with high intensity.
出处
《体育科学》
CSSCI
北大核心
2010年第10期46-51,共6页
China Sport Science
基金
国家自然科学基金资助项目(30871212)
教育部2007年度新世纪优秀人才支持计划(790013P8)
