The contribution of automatic drives to breathing at rest, relative to behavioural drives such as 'wakefulness', has been a subject of debate. We measured the combined central and peripheral chemoreflex contribution to resting ventilation using a modified rebreathing method that included a prior hyperventilation and addition of oxygen to maintain isoxia at a PET,O2 (end-tidal partial pressure of oxygen) of 100 mmHg. During rebreathing, ventilation was unrelated to PET,CO2 (end-tidal partial pressure of carbon dioxide) in the hypocapnic range, but after a threshold PET,CO2 was exceeded, ventilation increased linearly with PET,CO2. We considered the sub-threshold ventilation to be an estimate of the behavioural drives to breathe (mean ± S.E.M. = 3.1 ± 0.5 l min-1), and compared it to ventilation at rest (mean ± S.E.M. = 9.1 ± 0.7 l min-1). The difference was significant (Student's paired t test, P < 0.001). We also considered the threshold PCO2 observed during rebreathing to be an estimate of the chemoreflex threshold at rest (mean ± S.E.M. = 42.0 ± 0.5 mmHg). However, PET,CO2 during rebreathing estimates mixed venous or tissue PCO2, whereas the resting PET,CO2 during resting breathing estimates Pa,CO2 (arterial partial pressure of carbon dioxide). The chemoreflex threshold measured during rebreathing was therefore reduced by the difference in PET,CO2 at rest and at the start of rebreathing (the plateau estimates the mixed venous PCO2 at rest) in order to make comparisons. The corrected chemoreflex thresholds (mean ± S.E.M. = 26.0 ± 0.9 mmHg) were significantly less (paired Student's t test, P < 0.001) than the resting PET,CO2 values (mean ± S.E.M. = 34.3 ± 0.5 mmHg). We conclude that both the behavioural and chemoreflex drives contribute to resting ventilation. Experimental Physiology (2001) 86.1, 109-116.