A sustained elevation in ventilation upon recovery from a bout of intermittent hypoxia, known as ventilatory long-term facilitation (vLTF) has previously been shown in a range of animal species and humans during sleep 1,2,5,6,7. However, it has only recently been possible to reproduce vLTF in awake humans. Harris et al. 2006 were the first to elicit vLTF in awake humans, but at the same time demonstrating that there was a requirement for a concomitant elevation in CO2 3. Although this finding has been reproduced in humans under conditions of sustained elevation in CO2 4,8, it remains to be determined which location(s) in the human body intermittent hypoxia affects in mediating vLTF. The logical location would be the carotid chemoreceptors as they are the primary oxygen sensing sites in the human body but currently no evidence to support this exists. Participants completed two trials in a randomized cross over design. During trial 1 participants were exposed to an intermittent hypoxia protocol almost identical to that of Harris et al. 2006. End-tidal partial pressure of CO2 (PETCO2) was elevated 4 mmHg above each participant’s normal levels and this was sustained throughout the study. The intermittent hypoxia protocol consisted of 8 episodes of 4 minutes hypoxia (PETO2= 50mmHg) interspersed with 4 minutes of euoxia (PETO2= 100mmHg). During the periods preceding and following intermittent hypoxia (baseline and recovery phases, respectively) participants were exposed to 100% O2 for 1-minute periods, in order to silence the carotid chemoreceptors and thus allowing their contribution in mediating vLTF to be evaluated. Trial 2 served as a control trial and it was identical to trial 1 except that participants were not exposed to intermittent hypoxia but breathed a gas mixture that resulted in elevating each participant’s PETCO2 by 4 mmHg and maintaining PETO2 at 100 mmHg. In trial 1 minute ventilation increased from a baseline value before intermittent hypoxia of 22.34 ± 2.76 l/min to 29.79 ± 2.79 l/min at the end of recovery. The same comparison in trial 2 revealed a similar response with minute ventilation increasing from a baseline value of 23.87 ± 1.82 l/min to 29.94 ± 3.98 at the end of recovery. The influence of exposing participants to 100% inspired O2 was also similar between the two trials. In trial 1 minute ventilation decreased at baseline by 1.75 ± 0.45 l/min due to inspiration of 100% O2, and by 1.99 ± 0.4 l/min following intermittent hypoxia. In trial 2 the respective values were 2.20 ± 1.53 vs. 3.41 ± 1.76 l/min, respectively. These results suggest that intermittent hypoxia-induced vLTF in awake humans as previously shown under hypercapnic conditions may not be mediated by the intermittent hypoxia, but may in fact be a product of ventilatory drift due to sustained hypercapnia.