Abstract

Human pregnancy is characterized by significant and progressive changes in ventilation and acid-base status. However, the mechanisms that underlie these changes are poorly understood but may be due, at least in part, to the effects of pregnancy on the central chemoreflex control of breathing. PURPOSE This study used a modified carbon dioxide (CO2) rebreathing procedure to examine the effects of pregnancy on the central chemoreflex control of breathing during wakefulness. METHODS Pregnant (n = 11) and non-pregnant (n = 11) subjects were matched for age and height. Pregnant subjects were tested between 34 and 38 weeks of gestation (36 ± 0.67 wk). Non-pregnant subjects were tested in the mid-luteal phase of their menstrual cycle (24.70 ± 0.68 days). During rebreathing trials, subjects hyperventilated to reduce the end-tidal CO2 tension (PETCO2) below 25 mmHg and were then switched to a rebreathing bag containing a normocapnic-hyperoxic gas mixture. During the trial, PETCO2 increased while the end-tidal oxygen tension was maintained at a constant hyperoxic level. The point at which ventilation began to rise as PETCO2 increased was identified as the central chemoreflex ventilatory recruitment threshold (VRT). Ventilation below the VRT (i.e., behavioural drives) was measured and the slope (i.e., central chemoreflex sensitivity) of the ventilatory response above the VRT was determined. RESULTS The VRT for CO2 was significantly lower in pregnant vs. non-pregnant subjects (40.5 ± 0.8 vs. 45.8 ± 0.7 mmHg, p<0.001). Ventilation measured below the VRT for CO2 was significantly greater in pregnant than non-pregnant women (14.8 ± 1.1 vs. 9.3 ± 1.6 l/min, p<0.05). Similarly, central chemoreflex sensitivity was markedly higher in pregnant compared to non-pregnant subjects (5.07 ± 0.74 vs. 3.16 ± 0.29 l/min/mmHg, p<0.05). CONCLUSIONS: These data support the hypothesis that pregnancy significantly 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 the central chemoreflex control of breathing and may explain, at least in part, the high prevalence of breathlessness at rest and during exercise in healthy pregnant women.

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