Solid tumors exhibit abnormal vasculature and elevated glycolysis, depleting glucose in the tumor microenvironment (TME) and impairing CD8⁺ effector T cell function. Glucose is scarce but fructose is often enriched due to low expression of the fructose transporter GLUT5 in most tumors and immune cells. Therefore, we developed anti-EphA2 chimeric antigen receptor (CAR) T cells ectopically express GLUT5 (GT5), enabling fructose utilization to sustain metabolic fitness in glucose-poor TMEs. GT5 CAR T cells produced lactate from fructose at levels comparable to glucose, demonstrating that substrate availability limits of glycolytic flux. GT5 cells also maintained higher glycolytic activity upon restimulation in vitro, suggesting resistance to metabolic exhaustion. Under chronic stimulation in low-glucose, high-fructose conditions in vitro, GT5 cells showed reduced CTLA-6 and TIM-3 with modestly increased PD-1, consistent with sustained activation and less terminal exhaustion. GT5 cells also exhibited enhanced cytotoxicity against EphA2⁺ cancer cell lines, particularly under low antigen density in vitro and in vivo, suggesting that improved metabolic fitness lowers T cell activation threshold. These findings suggest that T cell exhaustion arises from a mismatch between activation demand and metabolic capacity. GT5 engineering restores this balance by enabling fructose utilization, preserving effector functions in nutrient-restricted TMEs.