Purpose

This study aims to evaluate whether regular lifelong exercise has effects on age-related inflammatory cytokines, oxidative stress, and the skeletal muscle proteome.

Methods

Four groups of adult-aged (8-month-old) female Sprague Dawley rats were used: rats for which training was initiated at either 8 (8 M–MICT, moderate-intensity continuous training) or 18 months (18 M–MICT) and sedentary rats aged either 26 (26 M–SED) or 8 months (8M–SED), who served as aging and adult sedentary controls, respectively. Aged skeletal muscles were subjected to proteomic and Kyoto Encyclopedia of Genes and Genomes (KEGG) and immunoblotting analyses.

Results

Age-related loss of physical performance and anti-inflammatory steroid levels were lowest in the 8 M–MICT group, while the anti-oxidative activities remained unchanged compared to 18 M–MICT rats. The proteomic analysis demonstrated an amelioration of age-related changes to muscle contraction, focal adhesion signaling, mitochondrial function, apoptosis and regeneration, anti-oxidation, and protein processing in the endoplasmic reticulum in the 8 M–MICT. Additionally, neurotrophin (BDNF) and AKT/FOXO signaling pathways were upregulated in 8 M–MICT rats compared to 26 M–SED.

Conclusion

8 M–MICT exhibited greater beneficial effects in ameliorating age-related inflammation and physical performance loss, compared to 18 M–MICT. The amelioration is potentially related to the upregulation of autophagy activities via BDNF/AKT signaling.

中文翻译：

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终身运动对大鼠年龄相关的身体组成，氧化应激，炎性细胞因子和骨骼肌蛋白质组的影响。

目的

这项研究旨在评估定期的终身锻炼是否会对与年龄相关的炎症细胞因子，氧化应激和骨骼肌蛋白质组产生影响。

方法

使用四组成年（8个月大）雌性Sprague Dawley大鼠：在8（8 M–MICT，中等强度连续训练）或18个月（18 M–MICT）下开始训练的大鼠分别为年龄（26 M–SED）或8个月（8M–SED）的久坐大鼠，分别作为衰老和成年久坐的对照。对老年骨骼肌进行了蛋白质组学和《京都议定书》的基因和基因组百科全书（KEGG）并进行了免疫印迹分析。

结果

与年龄相关的体力丧失和抗炎类固醇水平在8 M–MICT组中最低，而抗氧化活性与18 M–MICT大鼠相比保持不变。蛋白质组学分析表明，在8 M–MICT内质网中，肌肉收缩，粘着信号传导，线粒体功能，细胞凋亡和再生，抗氧化和蛋白质加工的年龄相关变化得到改善。此外，相比于26 M–SED，8 M–MICT大鼠中的神经营养蛋白（BDNF）和AKT / FOXO信号通路被上调。

结论

与18 M–MICT相比，8 M–MICT在改善与年龄有关的炎症和身体机能丧失方面显示出更大的有益作用。改善可能与经由BDNF / AKT信号转导的自噬活性上调有关。