The last week of gestation is a critical period for the sexual differentiation of the brain in the rat. Exposure to prenatal stress during this period has been shown to demasculinize and/or feminize adult male sexual behavior. Many of the neurochemical and endocrine responses to hypoxia are similar to that observed under stressful conditions such as restraint stress. Therefore, we examined the postnatal consequences on reproductive and nonreproductive sexually dimorphic behaviors in male offspring of dams exposed to chronic hypoxia during the last week of gestation. In addition, we examined sensorimotor development in offspring of both sexes. Pregnant Sprague-Dawley dams were exposed to continuous hypoxia (10.5% O2 from gestational day 15 to 21). Offspring were weaned at 22 days of age and group housed. Behavioral tests were conducted with littermate representatives. In adulthood, male rats prenatally exposed to hypoxia had significantly delayed initiation latencies of masculine sexual behavior and decreased number of ejaculations, but did not display a significant increase in feminine sex behavior potentials. Developmentally, animals exposed to prenatal hypoxia did not differ significantly from controls with respect to day of eye or ear opening, or the in times of righting reflex, negative geotaxis or cliff avoidance. Wire hanging latencies in hypoxic exposed animals were significantly greater than controls around the time of eye opening, but did not differ at earlier or later ages. A significant effect of hypoxia was detected on stride length at 95 days of age, but other aspects of gait patterns were similar to controls. No group differences in gait patterns were observed at 17 or 45 days of age. In addition, no significant differences were observed in open field activity, circadian locomotor activity, saccharin preference, or Morris water maze test. This hypoxia regimen did not influence the occurrence of the prenatal or postnatal surge of plasma testosterone. Overall, these results provide some evidence that, in males, mild, chronic prenatal hypoxia may result in incomplete masculinization of adult reproductive behavior in the absence of overt changes in perinatal testosterone surges.