Despite the remarkable clinical efficacy achieved by immune checkpoint blockade (ICB) and adoptive T cell therapy, the majority of patients with solid tumors still fail to achieve long-term responses to immunotherapy. One important reason is the complex metabolic patterns and inhibitory signals within the tumor microenvironment (TME), which induce metabolic reprogramming in immune cells and thereby impair their anti-tumor efficacy. This review summarizes the metabolic preferences of CD8⁺ T cells across various differentiation states, explores the metabolic changes that occur during their interaction with tumor cells and the TME, and discusses how these metabolic changes affect differentiation, function, and stemness of CD8⁺ T cells. Additionally, strategies that target metabolic molecules or pathways are highlighted to enhance the antitumor ability of CD8⁺ T cells, thereby improving the efficacy of chimeric antigen receptor gene-modified T lymphocyte (CAR-T cell) immunotherapy and ICB therapy.