We have previously shown that when pregnant Wistar dams are housed in a chamber containing 12% O2, the adult male offspring (CHU) show altered skeletal muscle vasodilator responses to acute hypoxia (breathing 8% O2). Relative to normal (N) rats, these dilator responses showed a reduced functional role for nitric oxide (NO) in rats exposed to CHU for the first half of pregnancy (early: ECHU) but not in those in those exposed to CHU for the second half (late: LCHU) of pregnancy (1). We also showed that this could not explained simply by a reduction in the expression of endothelial nitric oxide synthase (eNOS) protein. In the adult rat, chronic hypoxia induces angiogenesis in skeletal muscle (2) and also modulates the profile of muscle fibre type (3). Thus, in this study, we have examined the oxidative capacity of the hindlimb muscle extensor digitorum longus (EDL) by measuring fibre type and capillarity in 9-10 week old ECHU (n=4) and LCHU (n=5) rats compared to normal (N) rats (n=4). Sections (10µm) were cut from snap frozen muscles. Results are expressed as mean±SEM and comparison to N rats was made by ANOVA. Capillarity was measured using rhodamine-conjugated lectin and fibre typing was performed using myosin ATPase staining. Western blot analysis of whole muscle homogenate from EDL confirmed our previous findings in other hindlimb muscles (1) that eNOS protein expression was not reduced in either ECHU or LCHU rats (ECHU: 9.6±19%; LCHU 27±19% relative to N). Capillary:fibre (C:F) ratio increased significantly in both ECHU (p<0.01) and LCHU (p<0.001) compared to N rats (N: 1.57±0.03, ECHU: 2.06±0.06, LCHU: 2.06±0.08). Type I (slow oxidative) fibre size and number were not affected by CHU. However, cross sectional area of type IIa (fast oxidative glycolytic) fibres was significantly increased in both CHU groups compared to N (ECHU 117±34%, p<0.01; LCHU 93±23%, p<0.05). The number of type IIb (fast twitch glycolytic) fibres was also decreased significantly in both CHU groups compared to N rats (ECHU: -19±6.1%, p<0.05; LCHU -32±3.1%, p<0.001). These changes in oxidative profile and capillarity suggest that exposure to chronic hypoxia in utero programmes the development and differentiation profile of skeletal muscle fibres in the EDL, possibly to optimize oxygen consumption and delivery. Since eNOS protein does not increase despite the increase in C:F it may be that eNOS expression within cells is decreased. Angiogenesis is a tightly regulated system, and this developmental programming may have long-term effects on muscle performance in adult life.