ABSTRACT Obstructive sleep apnea (OSA), marked by intermittent hypoxia, is associated with obesity, type 2 diabetes and metabolic associated fatty liver disease. In pregnancy, it remains underdiagnosed despite links to gestational diabetes, hypertension, and foetal growth restriction. Intermittent hypoxia may alter foetal programming and increase the risk of long‐term metabolic issues in offspring. This study evaluates the effects of gestational OSA on offspring metabolic function, focusing on weight gain, glucose homeostasis, insulin sensitivity, hepatic glucose metabolism, inflammation and oxidative stress. Experiments were performed on pregnant female Wistar rats submitted to a chronic intermittent hypoxia (CIH) protocol during the last 2 weeks of pregnancy. Offspring were evaluated for body weight, glucose tolerance and insulin sensitivity at 1, 3, and 12 months of age. Liver western blot analysis was performed to assess markers of glucose metabolism (glucokinase, pyruvate kinase and glucose‐6‐phosphatase), inflammation (NF‐kB, IL‐1R, IL‐6R, TNF‐ɑR and NRLP3) and antioxidant enzymes (catalase, SOD‐1 and iNOS). CIH did not modify body weight, glucose tolerance and insulin sensitivity at 1, 3 and 12 months of age, except for a transient increase in glucose intolerance observed in 3‐month‐old females, which was attenuated by 12 months. Moreover, no evidence was found of modifications caused by gestational CIH on markers of hepatic glucose metabolism, inflammation or antioxidant defence. However, there was a gradual increase in inflammation with age. No sexual dimorphism was observed. Overall, these findings suggest that gestational CIH does not predispose offspring to long‐term metabolic dysfunction later in life and does not affect biological ageing, regardless of sex.