Aging and obesity are two major causes of female subfertility. Mitochondrial dysfunction has been proposed as an underlying cause however, there is little holistic understanding of metabolism dynamics with the ovarian follicle. To address this, we used real time metabolic analysis (Seahorse XFe96) to map energy metabolism dynamics (mitochondrial respiration, glycolysis and fatty acid oxidation) in mouse granulosa cells and cumulus-oocyte complexes (COCs) across a detailed timecourse in the lead up to ovulation. ATP production in granulosa cells was increased at 8hrs after hCG and maximal at 12hrs post-hCG, due to increased mitochondrial respiration, glycolysis and fatty acid oxidation. In stark contrast, total ATP production of COCs showed a rapid increase at 4 hours of hCG, and then gradually decreased until ovulation. The effects of obesity and aging on ATP production was examined in preovulatory follicles. Mitochondrial respiration, but not glycolysis, was reduced in granulosa cells of obese mice; and females that were both obese and reproductively old mice showed a marked decrease in both mitochondrial respiration and glycolysis. Similar metabolic alterations were observed in the ovarian stromal faction. To translate these findings, the metabolic profile of granulosa cells was measured in a cohort of 130 women undergoing IVF/ICSI cycles, and correlated with clinical parameters and cycle outcomes. Increased age, BMI and total FSH dose resulted in significant alterations in granulosa cell metabolic profile. Further, the follicular metabolic profile was significantly correlated with IVF outcomes. Overall, we demonstrate dynamic increases in multiple energy metabolism pathways in response to the LH-surge in key ovarian follicle cells. Mitochondrial respiration and glycolysis were impaired with obesity and aging, in mice and women, providing new insights into the cellular mechanisms of subfertility, by demonstrating specific metabolic perturbations that are associated with poor oocyte quality.