Document Detail


Interaction between the ventilatory and cerebrovascular responses to hypo- and hypercapnia at rest and during exercise.
MedLine Citation:
PMID:  18635644     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cerebrovascular reactivity to changes in the partial pressure of arterial carbon dioxide (P(a,CO(2))) 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 CO(2). 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 CO(2) reactivity, these two subsystems of the respiratory chemoreflex system and cerebral CO(2) reactivity were evaluated (n = 7) by the administration of CO(2) 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,CO(2))-minute ventilation (VE) relation shifted to higher VE and P(a,CO(2)) 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 CO(2) 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 CO(2) homeostasis in the brain during exercise.
Authors:
Shigehiko Ogoh; Naoyuki Hayashi; Masashi Inagaki; Philip N Ainslie; Tadayoshi Miyamoto
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-07-17
Journal Detail:
Title:  The Journal of physiology     Volume:  586     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2008 Sep 
Date Detail:
Created Date:  2008-09-03     Completed Date:  2008-12-18     Revised Date:  2013-06-05    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  4327-38     Citation Subset:  IM    
Affiliation:
Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA. sogoh@hsc.unt.edu
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MeSH Terms
Descriptor/Qualifier:
Brain / blood supply*
Exercise / physiology*
Humans
Hypercapnia / metabolism*
Hypocapnia
Male
Oxygen / metabolism
Young Adult
Chemical
Reg. No./Substance:
7782-44-7/Oxygen
Comments/Corrections

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