Introduction: During normal pregnancy, the placenta supplies the fetus with sufficient oxygen (O2) and nutrients to match its demands for growth. The placenta is responsive to environmental cues and is capable of adapting its capacity for substrate transfer to favour fetal growth during adverse conditions, like undernutrition(1). However, relatively little is known about adaptation of placental function to hypoxia; a major cause of fetal growth restriction (FGR)(2,3) and pregnancy complications at high altitude(4,5). Thus, this study aimed to determine the effect of hypoxia on placental transport and fetal growth. Methods: C57BL/6 female mice were time-mated and exposed to either 13% or 10% atmospheric O2 (13% H and 10% H, respectively) from day (D)14-D19 of pregnancy (term=D20). As exposure to hypoxia reduced maternal food intake, dams in 21% O2 fed ad libitum (ad lib) or pair-fed to the intake of hypoxic mice (13% PF and 10% PF) were used as controls. On D19, placental transport of 14C-methyl aminoisobutyric acid (MeAIB) was assessed in vivo and related to fetal growth. Litter means were analysed using ANOVAs with Bonferroni Post-hoc tests, unless stated otherwise. Results: Maternal body weight was significantly reduced by 13% and 10% hypoxia compared to ad lib controls (Table 1). Fetuses of 10% H, but not 13% H, mice weighed significantly less than fetuses from ad lib mice (Table 1). Fetuses of 10% PF mice also weighed significantly less than those from ad lib mice but more than 10% H pups (Table 1). Placental weight did not differ significantly between groups although placental efficiency, measured as the ratio of fetal to placental weight, was significantly reduced in 10% H mice compared to all other groups (Table 1). Placental transport of MeAIB tended to be lower in all hypoxic and pair fed groups but was only significantly reduced in 10% H compared to ad lib mice (Figure 1). Conclusions: In late pregnancy, placental efficiency and fetal growth were maintained in response to 13% O2, despite reduced maternal food intake and body weight. At the more severe insult of 10% O2, placental efficiency and transport were both compromised in association with reduced fetal weight. The data indicate that there is a threshold between 13% and 10% maternal inspired O2, at which the placenta can no longer support normal fetal growth during hypoxia. They also suggest that, at 10% O2, it is the combined effect of hypoxia and undernutrition which determines maternal nutrient allocation to the fetus, via changes in placenta nutrient transfer capacity. This has implications for the mechanisms of FGR in pregnancies complicated by hypoxaemia.