运动对人体肌肉的老化效应需要急性炎症
Wei-Horng Jean1,2, Yin-Chou Lin2,3, Pei-Yao Ang4
1Department of Anesthesiology, Far East Memorial Hospital, New Taipei City 220, Taiwan.
Aging
|May 16, 2024
概括
高强度运动通过触发炎症来减少肌肉中的衰老标志物. 用布洛芬阻断这种炎症会使运动诱导的衰老标志物减少,这表明炎症介导了老化作用.
科学领域:
- 运动生理学 运动生理学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 高强度间歇运动 (HIIE) 已显示出潜在的老化作用,减少骨肌中的p16INK4a mRNA等衰老标志物.
- 急性炎症的作用,即对肌肉损伤的免疫反应,在调解运动诱导的老化中仍然不清楚.
- 了解这种机制对于优化对衰老的运动干预至关重要.
研究的目的:
- 调查HIIE对人类骨肌的老化作用是否由急性炎症介导.
- 检查布洛芬阻断炎症对运动诱导的衰老和炎症标志物变化的影响.
主要方法:
- 一个安慰剂控制的,平衡的交叉试验,涉及12名年轻男子 (年龄20-26岁).
- 参与者接受了HIIE (120%的最大有氧功率) 后,消费或ibuprofen (1200毫克总量) 或安慰剂.
- 运动前和运动后收集肌肉活检以分析p16INK4a和CD11bmRNA水平.
主要成果:
- HIIE显著降低了肌肉组织中的p16INK4amRNA (-82%) 和CD11b mRNA (-87%) 水平,在运动后3小时达到峰值.
- 易布洛芬治疗减轻了p16INK4a和CD11bmRNA的运动后减少.
- 在p16INK4a和CD11bmRNA之间观察到强烈的正相关性 (r=0.88),这表明衰老标志物和炎症之间存在联系.
结论:
- 高强度运动对人类骨肌肉的老化效应似乎是由急性炎症介导的.
- 用像布洛芬这样的NSAIDs阻断炎症可以减轻运动诱导的细胞衰老标志物的减少.
- 这些发现突出了运动,炎症和细胞衰老之间的复杂相互作用.
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