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This Article Full Text Full Text (PDF) All Versions of this Article: 586/17/4327    most recent jphysiol.2008.157073v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Ogoh, S. Articles by Miyamoto, T. PubMed PubMed Citation Articles by Ogoh, S. Articles by Miyamoto, T. Related Collections Integrative

¹ Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX, USA
² Institute of Health Science, Kyushu University, Hakata, Japan
³ Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan
⁴ Department of Physiology, University of Otago, Dunedin, New Zealand
⁵ Morinomiya University of Medical Sciences, Osaka, Japan

Cerebrovascular reactivity to changes in the partial pressure of arterial carbon dioxide (P_a,CO2) via limiting changes in brain [H⁺] modulates ventilatory control. It remains unclear, however, how exercise-induced alterations in respiratory chemoreflex might influence cerebral blood flow (CBF), in particular the cerebrovascular reactivity to CO₂. The respiratory chemoreflex system controlling ventilation consists of two subsystems: the central controller (controlling element), and peripheral plant (controlled element). In order to examine the effect of exercise-induced alterations in ventilatory chemoreflex on cerebrovascular CO₂ reactivity, these two subsystems of the respiratory chemoreflex system and cerebral CO₂ reactivity were evaluated (n = 7) by the administration of CO₂ as well as by voluntary hypo- and hyperventilation at rest and during steady-state exercise. During exercise, in the central controller, the regression line for the P_a,CO2–minute ventilation relation shifted to higher and P_a,CO2 with no change in gain (P = 0.84). The functional curve of the peripheral plant also reset rightward and upward during exercise. However, from rest to exercise, gain of the peripheral plant decreased, especially during the hypercapnic condition (–4.1 ± 0.8 to –2.0 ± 0.2 mmHg l^–1 min^–1, P = 0.01). Therefore, under hypercapnia, total respiratory loop gain was markedly reduced during exercise (–8.0 ± 2.3 to –3.5 ± 1.0 U, P = 0.02). In contrast, cerebrovascular CO₂ reactivity at each condition, especially to hypercapnia, was increased during exercise (2.4 ± 0.2 to 2.8 ± 0.2% mmHg^–1, P = 0.03). These findings indicate that, despite an attenuated chemoreflex system controlling ventilation, elevations in cerebrovascular reactivity might help maintain CO₂ homeostasis in the brain during exercise.

(Received 17 May 2008; accepted after revision 10 July 2008; first published online 17 July 2008)
Corresponding author S. Ogoh: Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA.  Email: sogoh{at}hsc.unt.edu