Biochemical adaptation to endurance training on skeletal muscle in aged mice.

老年小鼠骨骼肌耐力训练的生化适应。

• 批准号: 62580105
• 负责人: HIGUCHI Mitsuru
• 金额: $ 1.28万
• 依托单位: National Institute of Nutrition
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1987
• 资助国家: 日本
• 起止时间: 1987 至 1988
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-62580105/
• 关键词: Senescent accelerated mouse (SAM); Endurance training; Skeletal muscle; Mitochondria; Citrate synthase; 3-hydroxyacyl CoA dehydrogenase; 老化促進モデルマウス(SAM); スーパーオキシドディスムターゼ

This study was undertaken to determine if aging musele adapts to endurance training with an enhancement of mitochondrial oxidative enzyme activities and of enzymatic defenses against free radical damage by using senescent accelerated mice (SAM). A program of 8 week endurance running induced 30-40% increases in citrate synthase and 3-OH acyl CoA debydrogenase acvitities in leg muscles of either SAM-P/2 strain or SAM-R mice aged 6 and 10 months. The training also resulted in 20-30% increases in mitochondrial superoxide dismutase activities in leg muscle of different age-groups. These findings suggest that aging does not result in a progressive impairment in the ability for increasing the oxidative enzymes and free radical scavenging enzyme in muscle mitochondria in response to chronic endurance exercise in healthy mice.

本研究旨在通过衰老加速小鼠（SAM）来确定老化肌肉是否能通过增强线粒体氧化酶活性和酶防御自由基损伤来适应耐力训练。8周耐力跑步可诱导6个月和10个月的SAM-P/2系或SAM-R小鼠腿部肌肉中柠檬酸合成酶和3-OH酰基辅酶A脱氢酶活性增加30-40%。训练还导致不同年龄组腿部肌肉线粒体超氧化物歧化酶活性增加20-30%。这些发现表明，在健康小鼠慢性耐力运动中，衰老不会导致肌肉线粒体中增加氧化酶和自由基清除酶的能力进行性损害。