Submitted on December 23, 2004
Accepted on January 24, 2005
Effects of Human Pregnancy on the Ventilatory Chemoreflex Response to Carbon Dioxide
Dennis Jensen1, Larry A Wolfe2*, Lubomira Slatkovska1, Katherine A Webb3, Gregory A. L Davies4, and Denis E O'Donnell5
1 School of Physical and Health Education, Queen's University, Kingston General Hospital, Kingston, ON, Canada
2 School of Physical and Health Education, Queen's University, Kingston General Hospital, Kingston, ON, Canada; Physiology, Queen's University, Kingston General Hospital, Kingston, ON, Canada
3 Division of Respirology and Critical Care, Queen's University, Kingston General Hospital, Kingston, ON, Canada
4 Obstetrics and Gynaecology, Queen's University, Kingston General Hospital, Kingston, ON, Canada
5 Physiology, Queen's University, Kingston General Hospital, Kingston, ON, Canada; Medicine, Queen's University, Kingston General Hospital, Kingston, ON, Canada; Division of Respirology and Critical Care, Queen's University, Kingston General Hospital, Kingston, ON, Canada
* To whom correspondence should be addressed. E-mail: wolfel{at}post.queensu.ca.
This study examined the effects of human pregnancy on the central chemoreflex control of breathing. Subjects were two groups (n =11) of pregnant (PG, gestational age, 36.5 ± 0.4 wk) and non-pregnant control subjects (CG), equated for mean age, body height, pre-pregnant body mass, parity and aerobic fitness. All subjects performed a hyperoxic-CO2 rebreathing procedure that 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 (PETCO2) increased while end-tidal PO2 was maintained at a constant hyperoxic level. The point at which ventilation (VE) began to rise as PETCO2 increased was identified as the central chemoreflex ventilatory recruitment threshold for CO2 (VRTCO2). VE below (basal VE) and above (central chemoreflex sensitivity) the VRTCO2 was determined. The VRTCO2 was significantly lower in the PG vs. CG (40.5 ± 0.8 vs. 45.8 ± 1.6 l.min-1) and both basal VE (14.8 ± 1.1 vs. 9.3 ± 1.6 l.min-1) 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 PaCO2 with VE basal, central chemoreflex sensitivity and VRTCO2 and for VRTCO2 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 non-chemoreflex drives to breathe.
