Exercise enhances cardiomyocyte mitochondrial homeostasis to alleviate left ventricular dysfunction in pressure overload induced remodelling.

This study aims to explore how exercise enhances mitochondrial regulation and mitigates pathological cardiac hypertrophy. Rat groups were assigned as the control group (CN, n = 8), sham group (sham, n = 8), model group (SC, n = 16) and exercise group (SE, n = 20). A bioinformatics analysis was conducted to uncover the underlying mechanisms.H9C2 cells were divided into: the Ang II 0 h group (CON), Ang II 48 h group (Ang II), Ang II 48 h + sh-control group (sh-GFP + Ang II), Ang II 48 h + sh-ndufb10 group (sh-ndufb10 + Ang II), Ang II 48 h + overexpressedndufb10 control group (Ad-GFP + Ang II) and Ang II 48 h + over-expressedndufb10group (Ad-ndufb10 + Ang II). Mitochondrial function was measured. mRNA and protein expression were assessed by qPCR or western blot analysis respectively. In the SC group, a significant increase was observed in cardiomyocyte diameter, cardiac function, autophagy, and apoptosis. After 8 weeks of swimming exercise, there was a substantial reduction in cardiomyocyte diameter, an improvement in cardiac function, a mitigation of mitochondrial fission and autophagy. Ndufb10 was markedly enriched in oxidative phosphorylation and downregulated in the SC group, while it was upregulated in the SE group. In the sh-ndufb10 group, mitochondrial fusion was suppressed; fission and autophagy were further facilitated; mitochondrial membrane potential, mPTP, and ROS levels increased; and TUNEL positive nuclei and apoptosis-related proteins showed significant upregulation. Overexpression of ndufb10 reversed pathological hypertrophy, mitochondrial autophagy, mitochondrial dysfunction, and cardiomyocyte apoptosis in vitro. Swimming exercise improves mitochondrial abnormalities and reduces cardiomyocyte hypertrophy through regulation of the ndufb10 in left ventricular hypertrophy.