Li Kunzhe, Li Sujuan, Jia Hao, Song Yinping, Chen Zhixin, Wang Youhua
Institute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi'an 710119, China.
Institute of Sports Education, Henan College of Surveying and Mapping, Zhengzhou 450000, China.
Antioxidants (Basel). 2025 Jun 17;14(6):748. doi: 10.3390/antiox14060748.
Cardiac adaptations induced by aerobic exercise have been shown to reduce the risk of cardiovascular disease, and the autonomic nervous system is closely associated with the development of cardiovascular disease. Aerobic exercise intervention has been shown to enhance cardiac function and mitigate myocardial fibrosis and hypertrophy in heart failure mice. Further insights reveal that cardiomyocytes experiencing chronic heart failure undergo modifications in their lipidomic profile, including remodeling of multiple myocardial membrane phospholipids. Notably, there is a decrease in the total content of cardiolipin, as well as in the levels of total lysolipid CL and the CL (22:6). These alterations disrupt mitochondrial quality control processes, leading to abnormal expressions of proteins such as Drp1, MFN2, OPA1, and BNIP3, thereby resulting in a disrupted mitochondrial dynamic network. Whereas aerobic exercise ameliorated mitochondrial damage to a large extent by activating parasympathetic nerves, this beneficial effect was accomplished by modulating myocardial membrane phospholipid remodeling and restoring the mitochondrial dynamic network. In conclusion, aerobic exercise activated the parasympathetic state in mice and attenuated lipid peroxidation and oxidative stress injury, thereby maintaining mitochondrial dynamic homeostasis and improving cardiac function.
有氧运动诱导的心脏适应性变化已被证明可降低心血管疾病风险，且自主神经系统与心血管疾病的发生密切相关。有氧运动干预已被证明可增强心力衰竭小鼠的心脏功能，减轻心肌纤维化和肥大。进一步的研究表明，经历慢性心力衰竭的心肌细胞其脂质组学特征会发生改变，包括多种心肌膜磷脂的重塑。值得注意的是，心磷脂的总含量以及溶血磷脂CL和CL（22:6）的水平均有所下降。这些改变破坏了线粒体质量控制过程，导致Drp1、MFN2、OPA1和BNIP3等蛋白质的异常表达，从而导致线粒体动态网络紊乱。而有氧运动通过激活副交感神经在很大程度上改善了线粒体损伤，这种有益作用是通过调节心肌膜磷脂重塑和恢复线粒体动态网络来实现的。总之，有氧运动激活了小鼠的副交感神经状态，减轻了脂质过氧化和氧化应激损伤，从而维持线粒体动态稳态并改善心脏功能。
