Ovarian aging is a significant cause of female infertility. As women age, the quantity and quality of their oocytes decline, leading to reduced ovarian reserve function. This decline is a key indicator of ovarian aging and is influenced by changes in oocyte energy metabolism. These changes affect ATP production and the quality of oocytes, which in turn impact fertility. The review focuses on the energy metabolism of oocytes in age-related ovarian aging and its potential impact on oocyte quality, as well as therapeutic strategies that may influence oocyte metabolism. The metabolism of oocytes is crucial for their development and maturation, affecting nutrient absorption, energy production, and cellular redox status. Mitochondrial-nuclear communication plays a critical role in cellular adaptability, organismal health, and energy metabolism. The energy metabolism of oocytes is complex, involving the TCA cycle, oxidative phosphorylation, lipid metabolism, glutamine metabolism, and the adenosine salvage pathway. Age-related changes in these metabolic pathways can impact oocyte quality, leading to reduced fertility. The TCA cycle activity decreases with age, leading to reduced levels of NAD+ and FAD, which are essential for energy metabolism and cell survival. The decline in oxidative phosphorylation due to mitochondrial dysfunction is an important marker of human aging. The respiratory chain components, such as CoQ, play important roles in cells, and their decline can lead to mitochondrial dysfunction and reduced reproductive performance. Age-dependent changes in lipid metabolism, including fatty acid oxidation and triglyceride synthesis, can impact oocyte quality. The accumulation of free fatty acids and reduced long-chain polyunsaturated fatty acids are associated with oocyte quality decline. Glutamine metabolism is also important for oocyte quality, with increased glutamine levels in aging oocytes. The adenosine salvage pathway is involved in ATP production and oocyte quality. Glycolysis and the pentose phosphate pathway are crucial for oocyte maturation, with the pentose phosphate pathway playing a more significant role. Sirtuins, such as SIRT1-7, regulate energy metabolism in oocytes, with age-related changes in their expression affecting mitochondrial function and oocyte quality. FoxO3a is involved in cell survival and energy metabolism, with age-related changes in its expression impacting mitochondrial function. Epigenetic changes, including DNA methylation and histone modification, can influence oocyte energy metabolism and quality. Non-coding RNAs and miRNAs also play roles in regulating energy metabolism in oocytes. The surrounding environment of follicles, including follicular stromal cells and immune cells, can impact oocyte quality. Age-related changes in the ovarian environment, such as fibrosis and inflammation, can affect oocyte energy metabolism. Overall, understanding the changes in oocyte energy metabolism during ovarian aging is crucial for developing therapeutic strategies to improve oocyte quality and fertility.Ovarian aging is a significant cause of female infertility. As women age, the quantity and quality of their oocytes decline, leading to reduced ovarian reserve function. This decline is a key indicator of ovarian aging and is influenced by changes in oocyte energy metabolism. These changes affect ATP production and the quality of oocytes, which in turn impact fertility. The review focuses on the energy metabolism of oocytes in age-related ovarian aging and its potential impact on oocyte quality, as well as therapeutic strategies that may influence oocyte metabolism. The metabolism of oocytes is crucial for their development and maturation, affecting nutrient absorption, energy production, and cellular redox status. Mitochondrial-nuclear communication plays a critical role in cellular adaptability, organismal health, and energy metabolism. The energy metabolism of oocytes is complex, involving the TCA cycle, oxidative phosphorylation, lipid metabolism, glutamine metabolism, and the adenosine salvage pathway. Age-related changes in these metabolic pathways can impact oocyte quality, leading to reduced fertility. The TCA cycle activity decreases with age, leading to reduced levels of NAD+ and FAD, which are essential for energy metabolism and cell survival. The decline in oxidative phosphorylation due to mitochondrial dysfunction is an important marker of human aging. The respiratory chain components, such as CoQ, play important roles in cells, and their decline can lead to mitochondrial dysfunction and reduced reproductive performance. Age-dependent changes in lipid metabolism, including fatty acid oxidation and triglyceride synthesis, can impact oocyte quality. The accumulation of free fatty acids and reduced long-chain polyunsaturated fatty acids are associated with oocyte quality decline. Glutamine metabolism is also important for oocyte quality, with increased glutamine levels in aging oocytes. The adenosine salvage pathway is involved in ATP production and oocyte quality. Glycolysis and the pentose phosphate pathway are crucial for oocyte maturation, with the pentose phosphate pathway playing a more significant role. Sirtuins, such as SIRT1-7, regulate energy metabolism in oocytes, with age-related changes in their expression affecting mitochondrial function and oocyte quality. FoxO3a is involved in cell survival and energy metabolism, with age-related changes in its expression impacting mitochondrial function. Epigenetic changes, including DNA methylation and histone modification, can influence oocyte energy metabolism and quality. Non-coding RNAs and miRNAs also play roles in regulating energy metabolism in oocytes. The surrounding environment of follicles, including follicular stromal cells and immune cells, can impact oocyte quality. Age-related changes in the ovarian environment, such as fibrosis and inflammation, can affect oocyte energy metabolism. Overall, understanding the changes in oocyte energy metabolism during ovarian aging is crucial for developing therapeutic strategies to improve oocyte quality and fertility.