We had reported previously [Szdzuy, K., Mortola, J.P., 2007b. Ventilatory chemosensitivity of the 1-day-old chicken hatchling after embryonic hypoxia. Am. J. Physiol. (Regul. Integr. Comp. Physiol.) 293, R1640-R1649] that hypoxia during incubation blunted ventilatory chemosensitivity in the hatchling. Because the carotid bodies become functional in the last portion of incubation, we asked whether these last days were the critical period for the effects of hypoxia on the development of ventilatory chemosensitivity. White Leghorn chicken eggs were incubated at 38 degrees C either in 21% O(2) (Controls) or in 15% O(2) for the whole 3-week incubation (HxTot) or for only the 1st (Hx1), 2nd (Hx2) or 3rd week of incubation (Hx3). Hatching time had a delay of half a day in HxTot, and was normal in the other groups. Body weight was similar in all hatchlings. Oxygen consumption ( [Formula: see text] ) and pulmonary ventilation (V e) were measured at about 20 h post-hatching. Ventilatory chemosensitivity was evaluated from the degree of hyperpnea (increase in V e) and hyperventilation (increase in [Formula: see text] ) during acute hypoxia (15 and 10% O(2), 20 min each) and acute hypercapnia (2 and 4% CO(2), 20 min each). The responses to hypoxia were similarly decreased in HxTot and in Hx3 compared to controls, and were normal in the other experimental groups; those to hypercapnia were blunted only in HxTot. The results are in agreement with the idea that prenatal hypoxia blunts V e chemosensitivity by interfering with the normal development of the carotid bodies.