Cardiovascular disease causes the greatest mortality in the world today. It is now recognized that the quality of the fetal environment during early development is important for cardiovascular health in later life. Understanding the consequences of a poor in utero environment leading to cardiometabolic disease creates an exciting window of opportunity to diagnose, intervene and ultimately reduce the development of cardiovascular disease. Fetal hypoxia is one of the most common consequences of complicated pregnancies worldwide. Intrauterine hypoxia is associated with a variety of maternal, placental and fetal conditions, such as chronic maternal pulmonary disease, heart disease, acute respiratory infections, preeclampsia as well as placental insufficiency and hypoxic environments. Our studies use a model of chronic maternal hypoxia (rats housed at 11.5% oxygen for their last third of pregnancy) that leads to intrauterine growth restriction (referred to here as IUGR). For our vascular studies, we hypothesized that exposure to prenatal hypoxia would cause changes in vascular function that would impair vasodilation later in life in an age- or sex-dependent manner. We found that flow-induced vasodilation was unaffected at a young age (3 months old) but was significantly reduced in aging (12 months) IUGR animals compared to aging controls. Interestingly, nitric oxide (NO)-mediated vasodilation was significantly reduced in both young and aging IUGR males and females (1), suggesting altered pathways of vasodilation in offspring exposed to prenatal hypoxia for both sexes. Overall, our data suggest that a change in the mechanisms of vasodilation occurring at an earlier age in IUGR offspring may predispose them to adult cardiovascular diseases. In regard to cardiac function, we have used in vivo echocardiographic techniques that demonstrated that hypoxia-induced IUGR is associated with the development of chronic cardiopulmonary dysfunction (such as diastolic dysfunction and pulmonary hypertension) in offspring as the age (2). Moreover, cardiac tolerance to ischemia/reperfusion injury is reduced in hypoxic offspring by 4 months of age. Furthermore, we identified a mismatch in glucose metabolism leading to proton accumulation in the postischemic myocardium of offspring born IUGR as a potential mechanism involved (3). We further identified that in only the male offspring, IUGR was associated with an increase in myocardial oxidative stress as evidenced by an increased GSSH/GSH ratio (4). We further expanded our studies to address the impact of prenatal hypoxia on indices of metabolic syndrome. In IUGR offspring fed a high fat (HF)-diet, there was a relative increase in intra-abdominal fat deposition and size, as well as an increase in fasting plasma concentrations of leptin, triglyceride and free fatty acids by 3 months of age that was not evident in the control group. These changes were accompanied by in vivo insulin resistance and impaired glucose tolerance (5). Interestingly, we showed a synergistic effect of prenatal hypoxia and postnatal high fat diet to reduce the capacity for recovery from cardiac ischemia/reperfusion injury (6). Thus offspring exposed to prenatal hypoxia do not appear to have reserve against secondary insults such as high fat diet or aging. We next addressed a potential intervention strategy. Since resveratrol (Resv), the polyphenol produced by plants, exerts insulin-sensitizing effects, we tested whether Resv could prevent deleterious metabolic effects of being born IUGR. We showed that in only the IUGR offspring, feeding a HF diet supplemented with Resv for 9 weeks, from the time of weaning, prevented intra-abdominal fat deposition, improved the plasma lipid profile and ameliorated insulin resistance and glucose intolerance (7). Our results suggest that early, postnatal intervention can alleviate HF-diet induced pathologic metabolic phenotypes in young, adult offspring born from a complicated pregnancy associated with prenatal hypoxia. Overall, our laboratory has demonstrated that prenatal hypoxia leads to intrauterine growth restriction and impairs later life endothelial-dependent vascular function and decreases cardiac tolerance to ischemia/reperfusion injury. We have also noted that compromised offspring do not have the reserve to accommodate a secondary stress such as consuming a high fat diet. Understanding the impact of different interventions such as Resv will improve our knowledge of mechanisms and address potential strategies for early intervention for children at risk due to their prenatal history.