Acute ethanol depresses respiration, but little is known about chronic ethanol exposure during gestation and breathing, while the deleterious effects of ethanol on CNS development have been clearly described. In a recent study we demonstrated that pre‐ and postnatal ethanol exposure induced low minute ventilation in juvenile rats. The present study analysed in juvenile rats the respiratory response to hypoxiain vivoby plethysmography and the phrenic (Phr) nerve response to ischaemiain situ. Glycinergic neurotransmission was assessedin situwith strychnine application and [3H]strychnine binding experiments performed in the medulla. After chronic ethanol exposure, hyperventilation during hypoxia was bluntedin vivo.In situPhr nerve response to ischaemia was also impaired, while gasping activity occurred earlier and recovery was delayed. Strychnine applicationsin situ(0.05–0.5 μm) demonstrated a higher sensitivity of expiratory duration in ethanol‐exposed animals compared to control animals. Moreover, [3H]strychnine binding density was increased after ethanol and was associated with higher affinity. Furthermore, 0.2 μmstrychnine in ethanol‐exposed animals restored the low basal Phr nerve frequency, but also the Phr nerve response to ischaemia and the time to recovery, while gasping activity appeared even earlier with a higher frequency. Polycythaemia was present after ethanol exposure whereas lung and heart weights were not altered. We conclude that chronic ethanol exposure during rat brain development (i) induced polycythaemia to compensate for low minute ventilation at rest; (ii) impaired the respiratory network adaptive response to low oxygen because of an increase in central glycinergic tonic inhibitions, and (iii) did not affect gasping mechanisms. We suggest that ethanol exposure during early life can be a risk factor for the newborn respiratory adaptive mechanisms to a low oxygen environment.