Chronic exposure to intermittent hypoxia (CIH) introduces significant neural plasticity in the respiratory and sympathetic networks. As a consequence, substantial changes in the mechanisms controlling respiratory and sympathetic activities can be observed in rats exposed to CIH. These include exaggerated respiratory and sympathetic chemoreflex responses, enhanced respiratory long-term facilitation and baseline sympathetic overactivity. The latter has been pointed out as an important factor contributing to the development of arterial hypertension in rats submitted to CIH. In our studies, we have been exploring the hypothesis that the enhanced sympathetic drive following CIH exposure is, at least in part, dependent on alterations in the respiratory network and its interaction with the sympathetic nervous system. We found that juvenile rats exposed to 10 days of CIH exhibited a pattern of active expiration with recruitment of abdominal muscles during late expiratory phase (late-E) in conditions of normoxia/normocapnia. Correlated with the emergence of late-E bursts in abdominal activity, we verified that sympathetic nerve of CIH rats also displayed novel bursts of activity during late-E, which were eliminated with the reduction of the central respiratory drive with hypocapnia. The abdominal and sympathetic late-E activities of CIH rats were recorded in the absence of peripheral feedback information and were associated with changes in the neuronal activity of expiratory neurons of ventral surface of medulla. Altogether, our data suggest that strengthened interactions between expiratory and sympathetic neurons contribute to elevate baseline sympathetic activity of CIH rats. These observations put forward the central respiratory-sympathetc coupling mechanisms as a novel player for the development of neurogenic hypertension.