Memory T cells are critical for long-term immunity against reinfection and require interleukin-7 (IL-7), but the mechanisms by which IL-7 controls memory T cell survival, particularly metabolic fitness, remain elusive. We discover that IL-7 induces expression of the glycerol channel aquaporin 9 (AQP9) in virus-specific memory CD8+ T cells, but not naive cells, and that AQP9 is vitally required for their long-term survival. AQP9 deficiency impairs glycerol import into memory CD8+ T cells for fatty acid esterification and triglyceride (TAG) synthesis and storage. These defects can be rescued by ectopic expression of TAG synthases, which restores lipid stores and memory T cell survival. Finally, we find that TAG synthesis is a central component of IL-7-mediated survival of human and mouse memory CD8+T cells. This study uncovers the metabolic mechanisms by which IL-7 tailors the metabolism of memory T cells to promote their longevity and fast response to rechallenge. Display omitted Display omitted •IL-7 induces glycerol channel AQP9 expression in CD8+ T cells•AQP9 is required for memory CD8+ T cell survival and self-renewal•AQP9 imports glycerol, promotes TAG synthesis, and sustains ATP levels in T cells•IL-7 enhances TAG synthesis to promote memory CD8+ T cell survival Interleukin-7 induces expression of the glycerol channel aquaporin 9, allowing memory CD8+ T cells to import glycerol, use it for triglyceride synthesis and storage, and sustain ATP levels required for long-term metabolic fitness and fast responses to reinfection.