Key result
Aerobic exercise improves cardiac function and blunts oxidative stress in heart failure mice.
Why the study?
Aerobic exercise improves cardiac function and mitigates myocardial fibrosis and hypertrophy in heart failure mice, but the underlying lipidomic and mitochondrial quality control mechanisms require further elucidation.
Does aerobic exercise improve cardiac function and mitochondrial dynamic homeostasis in heart failure mice?
Does aerobic exercise improve cardiac function and mitochondrial dynamic homeostasis in heart failure mice?
Aerobic exercise improves cardiac function in heart failure mice by modulating lipidomics and restoring mitochondrial dynamic homeostasis via parasympathetic activation.
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.
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Li et al. (2025) studied Heart failure. Aerobic exercise was evaluated on Cardiac function, myocardial fibrosis, hypertrophy, and mitochondrial dynamic network. Aerobic exercise improved cardiac function and attenuated oxidative stress in heart failure mice by activating the parasympathetic state and maintaining mitochondrial dynamic homeostasis.
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