It has been proposed that chronic intermittent hypoxia (CIH) contributes to generate hypertension in patients with obstructive sleep apnea syndrome and animal models, due to an enhanced sympathetic outflow. A possible contributing mechanism to the CIH-induced hypertension is a potentiation of carotid body (CB) chemosensory responses to hypoxia, but early changes that precede the CIH-induced hypertension are not completely known. Since the variability of heart rate (HRV) has been used as an index of autonomic influences on cardiovascular system, we studied the effects of short and long-term CIH exposure on HRV in animals with or without hypertension. In cats exposed to CIH (PO2 similar to 75 Torr, 10 times/hr during 8 hr) for 4 days, the ventilatory response to acute hypoxia was potentiated, the arterial pressure remained unchanged, but the HRV power spectrum showed a shift towards the low frequency band. Exposure of rats to CIH (PO2 similar to 37.5 Torr, 12 times/hr during 8 hr) for 12 days enhanced the ventilatory response to acute hypoxia, but did not increase the arterial pressure. After 21 days of CIH, we found a significant increase of arterial pressure and a shift of the HRV power spectrum towards the low frequency band. Thus, our results support the idea that hypertension induced by long-term CIH was preceded by alterations in the autonomic balance of HRV, associated with an enhance CB chemoreflex sensitivity to hypoxia. Therefore, few days of CIH are enough to enhance the CB reactivity to hypoxia, which contribute to the augmented ventilatory response to hypoxia, and to the early alterations in the autonomic balance of HRV.