Cao Yangfan, Zhou Jiawei, Quan Helong, Li Wei, Li Ting, Wang Lifeng
College of Physical Education and Health Sciences, Zhejiang Normal University, Jinhua, China.
College of Physical Education, Northeast Normal University, Changchun, China.
Front Immunol. 2025 Jun 3;16:1597222. doi: 10.3389/fimmu.2025.1597222. eCollection 2025.
Age related muscle atrophy is associated with chronic inflammation and impaired autophagy. Resistance training serves as an effective intervention for enhancing skeletal muscle hypertrophy.
This study utilized a naturally aged mouse model to investigate the role of the mammalian target of rapamycin complex 1 (mTORC1) pathway in mediating the effects of resistance training on chronic inflammation and autophagy in aged skeletal muscle.
Our findings demonstrate that resistance training increased the wet weight of the gastrocnemius (GAS) and quadriceps (Quad), absolute number of fibers and the cross-sectional areas (CSA) of skeletal muscles, as well as enhanced the maximum load and maximum grip strength. These findings indicate that resistance training improved the quality and strength of skeletal muscles in aging mice. Resistance training alleviated inflammation in aged skeletal muscle by promoting M2 macrophage polarization, reducing the mRNA levels of tumor necrosis factor alpha (TNF-α), nuclear factor-kappaB (NF-κB) and interleukin-1beta (IL-1β), and increasing the mRNA levels of interleukin-6 (IL-6) and interleukin-10 (IL-10). In aged skeletal muscle, resistance training decreased the protein expression of mTOR, regulatory-associated protein of mTOR (Raptor), p70 ribosomal protein s6 kinase (p70S6K), IL-1β, and hypoxia-inducible factor 1-alpha (HIF-1α) without affecting protein kinase B (AKT) activity. Moreover, autophagy, which is reduced in aged muscle, was increased by resistance training through increased AMP-activated protein kinase (AMPK) activity and increased BCL-2-interacting protein 1 (Beclin1) and transcriptional factor EB (TFEB) expression.
Our study suggests that resistance training was associated with alleviated inflammation and regulated autophagy, potentially involving the mTORC1-HIF-1α and mTORC1-AMPK pathways, which may contribute to improved skeletal muscle mass in aged mice.
与年龄相关的肌肉萎缩与慢性炎症和自噬受损有关。抗阻训练是增强骨骼肌肥大的有效干预措施。
本研究利用自然衰老小鼠模型，探讨雷帕霉素复合物1（mTORC1）通路在介导抗阻训练对衰老骨骼肌慢性炎症和自噬影响中的作用。
我们的研究结果表明，抗阻训练增加了腓肠肌（GAS）和股四头肌（Quad）的湿重、肌纤维绝对数量和骨骼肌横截面积（CSA），并增强了最大负荷和最大握力。这些结果表明，抗阻训练改善了衰老小鼠骨骼肌的质量和力量。抗阻训练通过促进M2巨噬细胞极化、降低肿瘤坏死因子α（TNF-α）、核因子κB（NF-κB）和白细胞介素1β（IL-1β）的mRNA水平以及增加白细胞介素6（IL-6）和白细胞介素10（IL-10）的mRNA水平，减轻了衰老骨骼肌中的炎症。在衰老骨骼肌中，抗阻训练降低了mTOR、mTOR调节相关蛋白（Raptor）、p70核糖体蛋白S6激酶（p70S6K）、IL-1β和缺氧诱导因子1α（HIF-1α）的蛋白表达，而不影响蛋白激酶B（AKT）活性。此外，衰老肌肉中减少的自噬通过增加AMP激活的蛋白激酶（AMPK）活性以及增加BCL-2相互作用蛋白1（Beclin1）和转录因子EB（TFEB）的表达而被抗阻训练所增强。
我们的研究表明，抗阻训练与减轻炎症和调节自噬有关，可能涉及mTORC1-HIF-1α和mTORC1-AMPK通路，这可能有助于改善衰老小鼠的骨骼肌质量。
