We hypothesized that active expiration following chronic intermittent hypoxia (CIH) exposure is dependent on alterations in the electrophysiological properties of expiratory neurones in the Bötzinger Complex (BötC), in which are an important part of the complex respiratory network. Using simultaneous recordings of respiratory nerves and whole cell path-clamp of respiratory neurones of ventrolateral medulla, we evaluated the mechanisms underlining CIH-induced active expiration in juvenile rats. In CIH rats, the decrease in the frequency discharge of post-inspiratory (post-I) neurons reduced the post-I activity of cervical vagus nerve. As consequence, the firing frequency of augmenting-expiratory neurones (aug-E) and the abdominal activity in the second half expiration (active expiration) were enhanced in CIH rats. However, CIH produced changes in the input resistance and excitability, independent of synaptic transmission, only in BötC post-I neurones. These changes were due to increased potassium-mediated leak current in post-I neurones, with no changes in the currents mediated by calcium-activated large conductance potassium channels or low voltage-activated calcium channels. In addition, the increase in the potassium-mediated leak current in response to acute hypoxia (10% O2) was higher in post-I neurons from CIH than control rats. With these precise electrophysiological approaches, we are describing the mechanisms underlying active expiration in CIH rats, which critically depend on changes of ionic currents in BötC post-I neurones. Possible implications of changes in the post-I neurones electrophysiological properties in the respiratory control of upper airway resistance and in the sympathetic over activity and hypertension in CIH rats will be also discussed.