Cardio-respiratory parameters and air sac and blood gases were measured in the unrestrained, unanesthetized duck during exposure to normobaric (PB = 746 Torr) or hypobaric (PB = 253 Torr) normoxia (PIO2 = 143 Torr) and hypoxia (PIO2 = 41.5 Torr). Compared with normobaria at the same PIO2, hypobaria caused a statistically significant increase in ventilation during both normoxia and hypoxia, resulting in elevated PO2 and diminished PCO2 in the caudal thoracic and clavicular air sac, and in increased PaO2 and decreased PaCO2. Similarly, lactic acid production was elevated in hypobaria, and the resulting decrease in arterial pH may be responsible for the increase in ventilation. Despite these changes, there was no evidence for altered gas exchange efficiency during hypobaria. This suggests that no significant diffusion limitation is present in the air capillary gas phase in normobaria, that could have been diminished with hypobaria. It also suggests that the aerodynamic valving efficiency, present during inspiration at the level of the medioventral bronchi, is not affected by hypobaria. Although the mechanisms underlying the increased lactic acid production and ventilation are not understood, they may exert an advantageous effect on high altitude tolerance of the bird.