A characteristic of memory T (T_M) cells is their ability to mount faster and stronger responses to reinfection than naïve T (T_N) cells do in response to an initial infection. However, the mechanisms that allow this rapid recall are not completely understood. We found that CD8 T_M cells have more mitochondrial mass than CD8 T_N cells and, that upon activation, the resulting secondary effector T (T_E) cells proliferate more quickly, produce more cytokines, and maintain greater ATP levels than primary effector T cells. We also found that after activation, T_M cells increase oxidative phosphorylation and aerobic glycolysis and sustain this increase to a greater extent than T_N cells, suggesting that greater mitochondrial mass in T_M cells not only promotes oxidative capacity, but also glycolytic capacity. We show that mitochondrial ATP is essential for the rapid induction of glycolysis in response to activation and the initiation of proliferation of both T_N and T_M cells. We also found that fatty acid oxidation is needed for T_M cells to rapidly respond upon restimulation. Finally, we show that dissociation of the glycolysis enzyme hexokinase from mitochondria impairs proliferation and blocks the rapid induction of glycolysis upon T-cell receptor stimulation in T_M cells. Our results demonstrate that greater mitochondrial mass endows T_M cells with a bioenergetic advantage that underlies their ability to rapidly recall in response to reinfection.