目的 Autophagy is tightly regulated to maintain heart homeostasis.Impaired autophagy is closely associated with pathological cardiac hypertrophy.However, the relationship between autophagy and cardiac hypertrophy induced by chronic intermittent hypoxia (CIH) is not known.We tired to reveal the relationship between them and explore the mechanism of it.方法 In the present study, we measured autophagy-related genes and autophagosomes during 10 weeks of CIH in rats and 6 days in H9C2 cardiomyocytes, and showed that autophagy was impaired during the prolonged CIH treatment.This conclusion was further confirmed by the autophagy flux assay by measuring LC3 lipidation in absent or present of chloroquine.We detected significant hypertrophic pathological changes in the myocardium with impaired autophagy during CIH.Rapamycin, an autophagy enhancer, attenuated the cardiac hypertrophy induced by CIH, and silence of autophagy-related gene5 (ATG5) exerts the opposite effects.After identified the AMPK activation role of AICAR, the autophagy flux assay confirmed that cardiomyocyte autophagy is regulated by AMPK by modulating AMPK activity with AICAR.To investigate the mechanism of autophagy impairment, we compared phospho (p)-AMPK, p-Akt, and cathepsin D, cytosolic and nuclear NFAT3 levels, along with calcineurin activity, between sham and CIH groups.结果 CIH indeed impaired myocardium autophagy； Impaired autophagy induces significant cardiac hypertrophy； Autopahgy impairment under CIH goes through the AMPK pathway； Calcineurin is involved in the depress of AMPK during prolonged CIH； Calcineriun-NFAT3 pathway did not involved in this kind of cardiac hypertrophy under CIH.结论 CIH impairs autophagy and induces cardiac hypertrophy through calcineurin-AMPK pathway.