The contribution of automatic drives to breathing at rest, relative to beha
vioural drives such as 'wakefulness', has been a subject of debate. We meas
ured the combined central and peripheral chemoreflex contribution to restin
g ventilation using a modified rebreathing method that included a prior hyp
erventilation and addition of oxygen to maintain isoxia at a P-ET,P-O2 (end
-tidal partial pressure of oxygen) of 100 mmHg. During rebreathing, ventila
tion was unrelated to P-ET,P-CO2 (end-tidal partial pressure of carbon diox
ide) in the hypocapnic range, but after a threshold P-ET,P-CO2 was exceeded
, ventilation increased linearly with P-ET,P-CO2. We considered the sub-thr
eshold ventilation to be an estimate of the behavioural drives to breathe (
mean +/- S.E.M. = 3.1 +/- 0.5 1 min(-1)), and compared it to ventilation at
rest (mean +/- S.E.M. = 9.1 +/- 0.7 1 min(-1)). The difference was signifi
cant (Student's paired t test, P < 0.001). We also considered the threshold
P-CO2 observed during rebreathing to be an estimate of the chemoreflex thr
eshold at rest (mean +/- S.E.M. = 42.0 +/- 0.5 mmHg), However, P-ET,P-CO2 d
uring rebreathing estimates mixed venous or tissue P-CO2, whereas the resti
ng P-ET,P-CO2 during resting breathing estimates P-a,P-CO2 (arterial partia
l pressure of carbon dioxide). The chemoreflex threshold measured during re
breathing was therefore reduced by the difference in P-ET,P-CO2 at rest and
at the start of rebreathing (the plateau estimates the mixed venous P-CO2
at rest) in order to make comparisons. The corrected chemoreflex thresholds
(mean +/- S.E.M. = 26.0 +/- 0.9 mmHg) were significantly less (paired Stud
ent's t test, P < 0.001) than the resting P-ET,P-CO2 values (mean +/- S.E.M
. = 34.3 +/- 0.5 mmHg). We conclude that both the behavioural and chemorefl
ex drives contribute to resting ventilation.