The relationship between the pathogenesis of cardiovascular diseases in individuals and maternal obesity (MO) has attracted much recent attention. In addition to jeopardizing maternal health, MO increases the heart-attack risk in the offspring by affecting the development of the cardiovascular system. High prenatal calorie intake leads to fetal overnutrition, which affects the use of fatty acids, glucose, and ketones in cardiomyocytes. MO has been shown to affect the offspring via cardiomyocyte metabolism and remodeling, as well as increasing reactive oxygen species in the heart, thereby stimulating the mammalian target of rapamycin and Hippo pathways to induce cardiomyocyte proliferation and hypertrophy. Notably, the Hippo pathway could represent a potential therapeutic target for cardiomyocyte hypertrophy. This review considers the role of MO in regulating fetal cardiomyocyte metabolism and hypertrophy in the offspring, and the related epigenetic mechanism. We also discuss the long-term effects of MO on offspring cardiomyocyte health. The findings suggest that metabolic memory, cross-generational genetic effects, and early-life interventions may be important avenues for future research.