The increased ventilatory response to exercise in pregnancy reflects alterations in the respiratory control systems ventilatory recruitment threshold for CO2

We tested the hypothesis that the magnitude of the pregnancy-induced increase in exercise hyperpnea is predictable based on the level at which PaCO2 is regulated at rest. We performed a detailed retrospective analysis of previous data from 25 healthy young women who performed exercise and rebreathing tests in the third trimester (TM3; 36.5 ± 0.2 weeks gestation; mean ± SEM) and again 20.4 ± 1.7 weeks post-partum (PP). At rest, arterialized venous blood was obtained for the estimation of PaCO2, [H+] and [HCO3−]; and serum progesterone ([P4]) and 17β-estradiol ([E2]) concentrations. Duffin's modified hyperoxic rebreathing procedure was used to evaluate changes in central ventilatory chemoreflex control characteristics at rest. Breath-by-breath ventilatory and gas exchange variables were measured at rest and during symptom-limited incremental cycle exercise tests. At rest in TM3 compared with PP: PaCO2, [H+], [HCO3−] and the central chemoreflex ventilatory recruitment threshold for PCO2 (VRTCO2) decreased, while ventilation (V˙E), [P4], [E2] and central chemoreflex sensitivity (V˙ES) increased (all p ≤ 0.001). The slope of the linear relation between V˙E and V˙CO2 during exercise was significantly higher in TM3 vs. PP (31.2 ± 0.6 vs. 27.5 ± 0.5, p < 0.001). The magnitude of this change in the V˙E-V˙CO2 slope correlated significantly with concurrent reductions in each of the VRTCO2 (R2 = 0.619, p < 0.001), PaCO2 (R2 = 0.203, p = 0.024) and [HCO3−] (R2 = 0.189, p = 0.030); and was independent (p > 0.05) of changes in [P4], [E2] and V˙ES. In conclusion, the increased ventilatory response to exercise in pregnancy can be explained, in large part, by reductions in the respiratory control system's resting PCO2 equilibrium point as manifest primarily by reductions in the VRTCO2.