The Protective Mechanism of Moderate Intensity Continuous Training on TMAO-Induced Myocardial Injury Based on NMR Metabolomics

The purpose of this study was to explore the protective effect of 8 weeks of Moderate Intensity Continuous Training (MICT) on TMAO-induced myocardial injury in mice and its metabolic regulatory mechanism based on nuclear magnetic resonance (NMR) metabolomics methods. Male C57BL/6J mice were randomly allocated into the following groups: Control group (Con, n = 15), TMAO-induced myocardial injury group (TMAO, n = 15), and TMAO-induced with MICT intervention group (Exe, n = 15). TMAO and Exe groups underwent 8 weeks of high-dose TMAO gavage to establish a myocardial injury model, with the Exe group additionally receiving 8 weeks of MICT intervention (60 min/session, 5 sessions/week, 50% MRC). After the 8 weeks of interventions, the mouse heart function was tested using cardiac ultrasound equipment; myocardial histology was evaluated using HE staining; and myocardial tissue samples were collected for NMR metabolomics analysis. Compared with the Con group, the HR in the TMAO group was significantly increased, while EF and LVFS were significantly decreased. Compared with the TMAO group, the HR in the Exe group was significantly reduced, and EF and LVFS were significantly increased; NMR metabolomics analysis showed that, compared with the Con group, five metabolic pathways including phenylalanine metabolism, tyrosine metabolism, and TCA cycle were significantly altered in the TMAO group; compared with the TMAO group, ten metabolic pathways related to amino acid metabolism (such as alanine, glycine, etc.), energy metabolism (TCA cycle), and oxidative stress (purine metabolism) were significantly regulated in the Exe group. MICT could effectively alleviate TMAO-induced myocardial injury in mice by regulating multiple targets within the myocardial metabolic pathways. These findings provide a theoretical basis for the clinical application of exercise intervention in myocardial injury treatment.