PDF(Pubmed)
Abstract：
Higher intensity exercise, despite causing more tissue damage, improved aging conditions. We previously observed decreased p16INK4a mRNA in human skeletal muscle after high-intensity interval exercise (HIIE), with no change following equivalent work in moderate-intensity continuous exercise. This raises the question of whether the observed senolytic effect of exercise is mediated by inflammation, an immune response induced by muscle damage. In this study, inflammation was blocked using a multiple dose of ibuprofen (total dose: 1200 mg), a commonly consumed nonsteroidal anti-inflammatory drug (NSAID), in a placebo-controlled, counterbalanced crossover trial. Twelve men aged 20-26 consumed ibuprofen or placebo before and after HIIE at 120% maximum aerobic power. Multiple muscle biopsies were taken for tissue analysis before and after HIIE. p16INK4a+ cells were located surrounding myofibers in muscle tissues. The maximum decrease in p16INK4a mRNA levels within muscle tissues occurred at 3 h post-exercise (-82%, p < 0.01), gradually recovering over the next 3-24 h. A concurrent reduction pattern in CD11b mRNA (-87%, p < 0.01) was also found within the same time frame. Ibuprofen treatment attenuated the post-exercise reduction in both p16INK4a mRNA and CD11b mRNA. The strong correlation (r = 0.88, p < 0.01) between p16INK4a mRNA and CD11b mRNA in muscle tissues suggests a connection between the markers of tissue aging and pro-inflammatory myeloid differentiation. In conclusion, our results suggest that the senolytic effect of high-intensity exercise on human skeletal muscle is mediated by acute inflammation.
摘要：
高强度运动,尽管造成了更多的组织损伤，改善老化条件。我们先前观察到高强度间歇运动（IIIE）后人骨骼肌中p16INK4amRNA的减少，在中等强度连续运动的等效工作后没有变化。这提出了一个问题，即观察到的运动的衰老作用是否由炎症介导，肌肉损伤引起的免疫反应。在这项研究中,使用多剂量布洛芬（总剂量：1200毫克）阻断炎症，一种常用的非甾体抗炎药（NSAID），在安慰剂对照中，平衡交叉试验。12名20-26岁的男性在HIIE之前和之后以120％的最大有氧能力消耗布洛芬或安慰剂。在HIIE之前和之后进行多次肌肉活检以进行组织分析。p16INK4a+细胞位于肌肉组织中肌纤维周围。肌肉组织内p16INK4amRNA水平的最大下降发生在运动后3小时（-82％，p<0.01),在接下来的3-24小时内逐渐恢复。CD11bmRNA的同时减少模式(-87%，在相同的时间范围内也发现了p<0.01）。布洛芬治疗减弱了运动后p16INK4amRNA和CD11bmRNA的减少。肌肉组织中p16INK4amRNA和CD11bmRNA之间的强相关性（r=0.88，p<0.01）表明组织衰老标志物与促炎性骨髓分化之间存在联系。总之,我们的研究结果表明,高强度运动对人体骨骼肌的抗衰老作用是由急性炎症介导的.
