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This Article Full Text Full Text (PDF) All Versions of this Article: 288/5/R1369    most recent 00862.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Jensen, D. Articles by O'Donnell, D. E. Search for Related Content PubMed PubMed Citation Articles by Jensen, D. Articles by O'Donnell, D. E.

ENVIRONMENTAL, EXERCISE AND RESPIRATORY PHYSIOLOGY

Effects of human pregnancy on the ventilatory chemoreflex response to carbon dioxide

¹School of Physical and Health Education; Departments of ²Physiology, ³Obstetrics and Gynaecology, and ⁴Medicine; ⁵Division of Respirology and Critical Care, Queen's University, Kingston General Hospital, Kingston, Ontario, Canada

Submitted 23 December 2004 ; accepted in final form 24 January 2005

This study examined the effects of human pregnancy on the central chemoreflex control of breathing. Subjects were two groups (n = 11) of pregnant subjects (PG, gestational age, 36.5 ± 0.4 wk) and nonpregnant control subjects (CG), equated for mean age, body height, prepregnant body mass, parity, and aerobic fitness. All subjects performed a hyperoxic CO₂ rebreathing procedure, which includes prior hyperventilation and maintenance of iso-oxia. Resting blood gases and plasma progesterone and estradiol concentrations were measured. During rebreathing trials, end-tidal PCO₂ increased, whereas end-tidal PO₂ was maintained at a constant hyperoxic level. The point at which ventilation (E) began to rise as end-tidal PCO₂ increased was identified as the central chemoreflex ventilatory recruitment threshold for CO₂ (VRTCO₂). E levels below (basal E) and above (central chemoreflex sensitivity) the VRTCO₂ were determined. The VRTCO₂ was significantly lower in the PG vs. CG (40.5 ± 0.8 vs. 45.8 ± 1.6 Torr), and both basal E (14.8 ± 1.1 vs. 9.3 ± 1.6 l/min) and central chemoreflex sensitivity (5.07 ± 0.74 vs. 3.16 ± 0.29 l·min^–1·Torr^–1) were significantly higher in the PG vs. CG. Pooled data from the two groups showed significant correlations for resting arterial PCO₂ with basal E, central chemoreflex sensitivity, and the VRTCO₂. The VRTCO₂ was also correlated with progesterone and estradiol concentrations. These data support the hypothesis that pregnancy decreases the threshold and increases the sensitivity of the central chemoreflex response to CO₂. These changes may be due to the effects of gestational hormones on chemoreflex and/or nonchemoreflex drives to breathe.

human gestation; hyperoxia; chemoreflex sensitivity; ventilatory recruitment threshold