We tested the hypothesis that preventing the poikilocapnic response to high intensity exercise would increase the ventilatory response to exercise. We measured ventilatory variables in 10 healthy men during incremental cycling with and without inspired CO(2) (randomised order). Inspired CO(2) elevated resting ventilation (V(E)), tidal volume (V(T)), PETCO₂ and PETO₂ by 5 ± 5 L/min, 0.3 ± 0.2 L, 6 ± 3 mm Hg and 11 ± 7 mm Hg, respectively (P<0.05); resting breathing frequency (f), expired CO(2) (VCO₂) and O(2) consumption (VO₂) remained similar (P>0.05). During high intensity exercise, inspired CO(2) elevated PETCO₂ by 7 ± 2, 10 ± 4 and 11 ± 4 mm Hg at 80%, 90% and 100% VO₂ max, respectively (P<0.01), while PETCO₂ remained unchanged (P>0.05). During high intensity exercise, inspired CO(2) elevated VT by 0.2 ± 0.3 L at 80%, 90% and 100% VO₂ max, respectively (P<0.05), while no differences were observed in V(E), f, VO₂, or power output (P>0.05). These data suggest a progressively diminishing role of CO(2) chemoreception in the control of ventilation during maximal incremental exercise.