Obstructive sleep apnoea (OSA) patients have increased risk of cardiovascular and respiratory disease including hypertension, arrhythmia and breathing instability. A key feature of OSA is exposure to chronic intermittent hypoxia (CIH). Carotid body (CB) hyperactivity caused by CIH is central to the development of pathology. However, the mechanisms underpinning CB hyperactivity in response to CIH remain incompletely characterised. We hypothesise that the rise in serum catecholamines in response to CIH could be a key driver of CB hyperactivity. This study examined the effect of chronic administration of a beta blocker (propranolol) on baseline and hypoxic ventilation, before and after exposure to CIH. A total of 33 male Wistar rats (11-13 weeks) were split into four groups (Control (N) n=10, Propranolol (PN) n=8, Chronic Intermittent Hypoxia (CIH) n=7, CIH + Propranolol (CIHP) n=8). The CIH paradigm consisted of 8 cycles hr-1, 8 hours day-1, 5% O2 nadir, for 3 weeks. Propranolol was added to the drinking water (40 mg/kg body weight/day). Ventilation was recorded using whole body plethysmography on conscious rats. The protocol consisted of 5 min baseline ventilation followed by 5 min hypoxia (10% O2). Propranolol modified the breathing pattern in normoxia and hypoxia by significantly increasing tidal volume (21% O2: N 4.3±0.2 vs PN 5.3±0.2 ml/kg, P<0.05; 10% O2: N 5.8±0.1 vs PN 7.0±0.3 ml/kg P<0.05) and reducing respiratory frequency (21% O2: N 96±2 vs PN 80±3 bpm, P<0.05; 10% O2: N 146±6 vs PN 128±5 bpm P=0.1), without altering overall minute ventilation. Propranolol did not significantly impact on the elevation in tidal volume, respiratory frequency or minute ventilation induced by hypoxia. Following CIH, there was an approximately 20% increase in minute ventilation in normoxia (P<0.05) and a trend towards an increase in hypoxia (P=0.09). CIH also significantly increased the inspiratory duty cycle and the Inspiratory:Expiratory time ratio. A similar effect of propranolol on breathing pattern was observed after CIH, as evidenced by a 30% increase in tidal volume and a 10% reduction in respiratory frequency without an overall change in minute ventilation. Following CIH, propranolol did not significantly impact on the elevation in tidal volume, respiratory frequency or minute ventilation induced by hypoxia. These results suggest that propranolol induces a change in the pattern of ventilation before and after CIH, characterised by a switch towards slower and deeper breathing. This change in pattern is predicted to cause an increase in alveolar ventilation. A role for the CB in mediating these effects is questionable as the hypoxic ventilatory response was not significantly modified by propranolol before or after CIH. Future experiments are required to directly measure CB activity following propranolol treatment before and after CIH.