Sustained prenatal hypoxia decreases the growth and metabolic rate of the embryo and causes a blunted hypoxic ventilatory response (HVR) in the newborn. The most likely interpretation is that the sustained hypoxic stimulation may interfere with the normal prenatal development of the chemoreceptors. However, we wanted to consider the possibility that the prolonged hypoxic hypometabolism may be a contributing factor. Chicken embryos were incubated at 35 degrees C (Cold group, N=14), which is known to lower the embryonic oxygen consumption ((V)over dot(O2)) by similar to 30% throughout incubation, or at 37.5 degrees C (Controls, N=16). Cold incubation delayed hatching by similar to 2 days. The 1-day old hatchlings had normal pulmonary ventilation ((V)over dot(E)), measured by the barometric technique, and oxygen consumption ((V)over dot(O2)), simultaneously measured by an open flow methodology. During acute hypoxia (similar to 15% or similar to 11% O-2) the hyperventilation (increase in (V)over dot(E)/(V)over dot(O2)), the hyperpnea and the hypometabolism were almost identical between the two groups of hatchlings. We conclude that a sustained decrease in metabolic rate during the embryonic period by itself does not carry obvious consequences on the newborn's resting (V)over dot(E) and HVR. (C) 2013 Elsevier B.V. All rights reserved.