Objective To investigate the effect of intermittent hypoxia (IH) intervention on myocardial fatty acid metabolism and its mechanism through p-STAT3/CPT-1 regulation in post-myocardial infarction (MI) mice.Methods Thirty-two 6-8-week-old male C57BL6/J mice were randomly divided into four groups (n = 8/group): sham-normoxia (SED), sham-IH, MI-normoxia (MI-SED), and MI-IH. MI was induced by left anterior descending coronary artery ligation. After 1-week recovery, IH groups received 4 h/day, 5 days/week hypoxia (simulated 5 000 m altitude, 13% O?) for 4 weeks. We assessed body weight, exercise tolerance, left ventricular ejection fraction (LVEF), myocardial fibrosis, mitochondrial ultrastructure, ATP content, citrate synthase (CS) activity, and protein expression (CD36, LCAD, ACOX1, p-STAT3, CPT1)Results Compared with MI-SED, MI-IH showed: improved exercise tolerance (P < 0.05), increased LVEF (P < 0.05), reduced fibrosis (P < 0.05), preserved mitochondrial structure, elevated ATP (P < 0.05) and CS activity (P < 0.05). Fatty acid oxidation proteins (CD36, LCAD, ACOX1) and p-STAT3 expression increased significantly. Both protein and gene expression of CPT1 were upregulated (all P < 0.05).Conclusion IH improves post-MI cardiac function by enhancing fatty acid oxidation via p-STAT3/CPT-1 pathway, preserving mitochondrial integrity and reducing fibrosis.