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pubmed:abstractText |
The respiratory and cerebrovascular reactivity to changes in arterial Pco(2) (Pa(CO(2))) is an important mechanism that maintains CO(2) or pH homeostasis in the brain. It remains unclear, however, how cerebrovascular CO(2) reactivity might influence the 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 (MCA) mean blood velocity (V(mean)) to hypercapnia (5.0% CO(2)-40% O(2)-balance N(2)) at rest and during dynamic exercise ( approximately 1.0 l/min O(2) consumption). Each onset response was evaluated using a single-exponential regression model consisting of the response time latency [CO(2)-response delay (t(0))] and time constant (tau). At rest, t(0) and tau data indicated that the MCA V(mean) onset response was faster than the ventilatory (Ve) response (P < 0.001). In contrast, during exercise, t(0) of Ve and MCA V(mean) onset responses were decreased. In addition, despite the enhanced Pa(CO(2)) response to CO(2) administration (P = 0.014), tau of MCA V(mean) tended to increase during exercise (P = 0.054), whereas tau of Ve decreased (P = 0.015). These findings indicate that 1) at rest, faster washout of CO(2) via cerebral vasodilation results in a reduced activation of the central chemoreflex and subsequent reduced Ve onset response, and 2) during exercise, despite higher rates of increasing Pa(CO(2)), the lack of change in the onset response of cerebral blood flow and reduced washout of CO(2) may act to augment the Ve onset response.
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