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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。
Objective: To investigate the relationship between mitochondrial oxidative stress and age-related skeletal muscle loss and to further reveal the mechanism of endurance exercise on the loss of aged skeletal muscle. Methods: Forty ICR mice were randomly divided into 4 groups: young control group (YC), youth group (YR ), Aged control group (AC) and aged exercise group (AR); 10 rats in each group. The mice of different ages were tested for exercise ability with increasing load. The mice of YR and AR groups were trained for 65% ~ 75% of the maximum load and trained for 1 hour per day for 4 weeks. Gastrocnemius muscle and quadriceps femoris were weighed. ROS production and membrane potential of gastrocnemius muscle were detected by fluorescent probe method. The content of 8-OH-dG in gastrocnemius muscle was detected by ELISA. Results: 1) The wet weight of gastrocnemius and left quadriceps of 4-month-old group was significantly higher than that of 2, 6 and 8 months old group (P <0.05) Significantly affected. 2) The 8-OH-dG content in 8-month-old group was significantly higher than that in 2, 4 and 6-month old group (P <0.01) (P <0.05). The content of 8-OH-dG in AR group was significantly higher than that in AC group (P <0.05). 3) Compared with 2-month-old group, mitochondrial membrane potential of 4, 6 and 8-month old group decreased significantly (P <0.01). Compared with 4 and 6-month old group, mitochondrial membrane potential of 8-month- 0.01). Mitochondrial membrane potential in AR group was significantly higher than that in AC group (P <0.05). CONCLUSION: Mitochondrial membrane potential decreases, DNA oxidative damage is exacerbated and ROS production rate increases at different stages of aging skeletal muscle loss. Endurance exercise with maximum intensity of 65% -75% increased the mitochondrial membrane potential of skeletal muscle in aged mice, indicating that endurance exercise is important for maintaining the mitochondrial function and preventing myocyte apoptosis in aged mice, but may also aggravate DNA oxidative damage. It is recommended that older people need endurance exercise but not too much exercise intensity.