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Onset responses of ventilation and cerebral blood flow to hypercapnia in humans: rest and exercise

¹Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas; ²Department of Physiology, University of Otago, Dunedin, New Zealand; ³Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, and ⁴Morinomiya University of Medical Sciences, Osaka, Japan

Submitted 26 September 2008 ; accepted in final form 30 December 2008

The respiratory and cerebrovascular reactivity to changes in arterial PCO₂ () is an important mechanism that maintains CO₂ or pH homeostasis in the brain. It remains unclear, however, how cerebrovascular CO₂ 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% CO₂-40% O₂-balance N₂) at rest and during dynamic exercise (1.0 l/min O₂ consumption). 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, t₀ and data indicated that the MCA V_mean onset response was faster than the ventilatory (E) response (P < 0.001). In contrast, during exercise, t₀ of E and MCA V_mean onset responses were decreased. In addition, despite the enhanced response to CO₂ administration (P = 0.014), of MCA V_mean tended to increase during exercise (P = 0.054), whereas of E 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 E onset response, and 2) during exercise, despite higher rates of increasing , the lack of change in the onset response of cerebral blood flow and reduced washout of CO₂ may act to augment the E onset response.

chemoreflex; breathing; cerebral perfusion

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