Clavicular air sac pressure, arterial blood gases and pH, and rectal temperature were measured in treadmill-exercised cockerels breathing air, 10% O2 in N2 or a mixture of 10% O2/3% CO2 in N2. Air sac pressures were used to estimate changes in the rate and the relative depth of breathing. In air-breathing conditions exercise took place at two intensities corresponding to treadmill speeds of 3.2 and 5.0 km h-1, respectively. Rectal temperature increased by 0.5 degrees C but there was no sign of thermal hyperventilation and arterial PCO2 remained constant. Increased ventilation was mainly brought about by changes in respiratory rate, with relatively small increases in depth. During exercise at 3.2 km h-1 inhalation of 10% O2 in N2 produced a 35% increase in ventilation and breathing became faster and shallower. Arterial PCO2 fell by 3-4 Torr, apparently as a result of lung hyperventilation. Addition of 3% CO2 to the hypoxic gas restored normal arterial PCO2 and reversed the trend to polypneic breathing. However, it failed to produce an exact matching of respiratory characteristics with those observed during isocapnic exercise hyperpnea. It is concluded that rapid, shallow breathing during hypocapnic hypoxia in running birds serves as a mechanism to minimize lung hyperventilation and CO2 washout. This reflex, which may stem from the intrapulmonary CO2 receptors, occurs in the face of a severe hypoxic challenge. Failure to match respiratory characteristics during isocapnic hypoxia and isocapnic exercise may be due to an inhibitory effect of the inhaled CO2 on these receptors.