The prevalence of obesity and type 2 diabetes mellitus (T2DM) among children is alarmingly increasing in the United States, and children born from obese mothers are at greater risk for diabetes and cardiovascular disease. Cardiac mitochondrial dysfunction may contribute to heart disease associated with T2DM and obesity. The purpose of this study was to test hypothesis that a maternal obesogenic diet would alter offspring cardiac mitochondrial function and systemic metabolism. Female CD‐1 mice were fed either a high‐fat, high‐sucrose diet (HFHS) or a refined low‐fat, low‐sucrose diet (LFLS) for eight weeks before initiation of pregnancy, gestation, and during lactation. At 21 days, male mice were randomly divided into 3 groups: offspring of HFHS dams weaned onto a standard chow diet (HC), HFHS diet (HH), or offspring of LFLS dams continue fed to LFLS diet (LL). Glucose and insulin tolerance tests were performed in 6 month‐old male offspring, followed by sacrifice for evaluation of cardiac mitochondrial respiratory function. HFHS diet‐induced maternal obesity impaired glucose tolerance and insulin sensitivity in HH offspring. Switching offspring to the control diet (HC) did not decrease body weight associated with maternal obesity, but significantly decreased subcutaneous fat mass compared to the HH, and preserved glucose tolerance and insulin responsiveness to near LL levels. In freshly isolated cardiac mitochondria, maximal oxidative phosphorylation (OXPHOS)‐linked respiratory capacity and coupling efficiency was significantly higher in the HC in the presence of fatty acid substrate (palmitoylcarnitine) compared to LL. In the absence of fatty acids, OXPHOS‐linked respiratory capacity and OXPHOS coupling control were not altered. These results indicate that both maternal and postnatal diet modulate offspring cardiac mitochondrial metabolism, favoring greater fatty acid oxidation in offspring fed a control diet following maternal obesity. Support or Funding Information This study was funded by the American Physiological Society Research Career Enhancement Award and the University of Texas at San Antonio, Office of the Vice President for Research and the College of Education and Human Developments.