Increasing epidemiological evidences have revealed the association between ambient fine particulate matter (PM(2.5)) pollution and cardiovascular disease\'s morbidity and mortality. However, how seasonal PM(2.5) exposure influence cardiac function and the underlying mechanism converged in energy metabolic remodeling remain to be elucidated. This study focused on seasonal PM(2.5)-induced cardiac dysfunction and metabolic remodeling, and the toxicity differences of PM(2.5) samples from different sampling seasons and different exposure dosages were discussed. The results showed that seasonal haze caused cardiac dysfunctions, including decreases in heart rate (HR) and heart rate variability (HRV), abnormal changes in hemodynamic and echocardiographic parameters. Concurrently, the energy production in myocardial tissues was evidently disturbed. In particular, low dose of PM(2.5) exposure notably induced the elevation of beta oxidation (beta-oxidation) and tricarboxylic acid cycle (TCA cycle) as the compensation for the disturbed energy metabolism in animals, whereas high dose of PM(2.5) exposure attenuated this process and the glycolysis levels were strikingly promoted, thus causing the reduced energy production and cardiac dysfunction. Comparatively, winter PM(2.5) exposure caused more severe cardiac toxicity than did summer haze samples, possibly due to the existence of different components and pollutant levels in seasonal hazes. The findings on seasonal PM(2.5) induced cardiac dysfunction and myocardial metabolic remodeling provided new insights into cardiovascular disease risks from haze exposure.