The respiratory and cerebrovascular reactivity to changes in the partial pressure of arterial carbon dioxide (PaCO₂) are important mechanisms which keep CO₂ or pH homeostasis remarkably constant in the brain. It remains unclear, however, how cerebrovascular CO₂ reactivity might influence respiratory chemoreflex. The purpose of the present study was therefore to examine the interaction between onset responses of the respiratory chemoreflex and middle cerebral artery mean blood velocity (MCA V_mean) to hypercapnia (5.0% CO₂, 40% O₂ balanced with N₂) at rest and during dynamic exercise (VO₂, ~1.0 L/min). Each onset response was evaluated using a single exponential regression model consisting of the response time latency (CO₂-response delay; t₀) and time constant (). At rest, both t₀ and data indicated that the MCA V_mean onset response was faster than that of the ventilatory (V_E) response (P<0.001). In contrast, during exercise, t₀ of V_E and MCA V_mean onset responses were decreased. In addition, despite the enhanced PaCO₂ response to CO₂ administration (P=0.014), of MCA V_mean tended to increase during exercise (P=0.054) whereas of V_E was decreased (P=0.015). These findings indicate that: 1) at rest, faster washout of CO₂ via cerebral vasodilation results in a reduced activation of the central chemoreflex and subsequent reduced V_E onset response; 2) during exercise, despite higher rates of increasing PaCO₂, the lack of change in the onset response of CBF and reduced washout of CO₂ may act to augment the V_E onset response.