Exercise Enhances Cardiomyocytic Mitochondrial Homeostasis to Alleviate Left Ventricular Dysfunction in Pressure Overload-Induced Remodelling

Background: This study aims to explore how exercise enhances mitochondrial regulation and mitigates pathological cardiac hypertrophy. Methods: Rat groups were assigned as CN, sham, SC, and SE. A bioinformatics analysis was conducted to uncover the underlying mechanisms.H9C2 cells were divided into: CON, Ang II, sh-GFP+Ang II, sh-ndufb10+Ang II, Ad-GFP+Ang II, and Ad-ndufb10+Ang II. Mitochondrial function was measured. mRNA and protein expression were assessed by qPCR or western blot analysis respectively. Results: In the SC group, a significant increase was observed in cardiomyocyte diameter, 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, and cardiomyocyte. 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 and apoptosis-related proteins showed significant upregulation. Overexpression of ndufb10 reversed pathological hypertrophy, mitochondrial autophagy, mitochondrial dysfunction, and cardiomyocyte in vitro. Conclusions: Swimming exercise improves mitochondrial abnormalities and reduces cardiomyocyte through regulation of the ndufb10 in left ventricular hypertrophy.