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 Pa CO2 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 (TM(3); 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 Pa CO2, [H(+)] and [HCO(3)(-)]; and serum progesterone ([P(4)]) and 17beta-estradiol ([E(2)]) 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 TM(3) compared with PP: Pa CO2, [H(+)], [HCO(3)(-)] and the central chemoreflex ventilatory recruitment threshold for Pa CO2 (VRT CO2) decreased, while ventilation (V E), [P(4)], [E(2)] and central chemoreflex sensitivity (V ES) increased (all p<or=0.001). The slope of the linear relation between V E and V CO2 during exercise was significantly higher in TM(3) vs. PP (31.2+/-0.6 vs. 27.5+/-0.5, p<0.001). The magnitude of this change in the VE-V CO2 slope correlated significantly with concurrent reductions in each of the VRT CO2 (R(2)=0.619, p<0.001), Pa CO2 (R(2)=0.203, p=0.024) and [HCO(3)(-)] (R(2)=0.189, p=0.030); and was independent (p>0.05) of changes in [P(4)], [E(2)] 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 Pa CO2 equilibrium point as manifest primarily by reductions in the VRT CO2.