Longitudinal study of cerebral blood flow regulation during exercise in pregnancy.

Cerebrovascular adaptation to pregnancy is poorly understood. We sought to assess cerebrovascular regulation in response to visual stimulation, hypercapnia and exercise across the three trimesters of pregnancy. Using transcranial Doppler (TCD) ultrasound, middle and posterior cerebral artery mean blood velocities (MCAvmean and PCAvmean) were measured continuously at rest and in response to (1) visual stimulation to assess neurovascular coupling (NVC); (2) a modified Duffin hyperoxic CO2 rebreathe test, and (3) an incremental cycling exercise test to volitional fatigue in non-pregnant (n = 26; NP) and pregnant women (first trimester [n = 13; TM1], second trimester [n = 21; TM2], and third trimester [n = 20; TM3]) in total 47 women. At rest, MCAvmean and PETCO2 were lower in TM2 compared to NP. PCAvmean was lower in TM2 but not TM1 or TM3 compared to NP. Cerebrovascular reactivity in MCAvmean and PCAvmean during the hypercapnic rebreathing test was not different between pregnant and non-pregnant women. MCAvmean continued to increase over the second half of the exercise test in TM2 and TM3, while it decreased in NP due to differences in ΔPETCO2 between groups. Pregnant women experienced a delayed decrease in MCAvmean in response to maximal exercise compared to non-pregnant controls which was explained by CO2 reactivity and PETCO2 level.

Maternal cardioautonomic responses during and following exercise throughout pregnancy.

Blood pressure regulation during pregnancy is poorly understood. Cardiovagal baroreflex gain (BRG) is an important contributor to blood pressure regulation through its influence on heart rate. Heart rate fluctuations occur in response to various physiological stimuli and can be measured using heart rate variability (HRV). It is unclear how these mechanisms operate during pregnancy, particularly with regard to exercise. We examined BRG and HRV prior to, during, and following prenatal exercise. Forty-three pregnant (n = 10 first trimester (TM1), n = 17 second trimester (TM2), n = 16 third trimester (TM3)) and 20 nonpregnant (NP) women underwent an incremental peak exercise test. Beat-by-beat blood pressure (photoplethysmography) and heart rate (lead II electrocardiogram) were measured throughout. BRG (the slope of the relationship between fluctuations in systolic blood pressure and the R-R interval) and HRV (root mean square of the successive differences; RMSSD) were assessed at rest, during steady-state exercise (EX), and during active recovery. BRG decreased with gestation and was lower in the TM3 group than in the NP group (17.9 ± 6.9 ms/mm Hg vs 24.8 ± 7.4 ms/mm Hg, p = 0.017). BRG was reduced during EX in all groups. Resting HRV (RMSSD) also decreased with gestation and was lower in the TM3 group than in the NP group (29 ± 17 ms vs 48 ± 20 ms, p < 0.001). RMSSD was blunted during EX in all groups compared with rest. During active recovery, RMSSD was further blunted compared with EX in the NP group but not during pregnancy (TM1, TM2, and TM3). Compared with the nonpregnant controls, the pregnant women had lower BRG and HRV at rest, but comparable cardioautonomic control during both exercise and active recovery following peak exercise.

Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.

Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation. We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls. Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001). Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls. Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04). However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006). Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation. These data indicate that the third trimester of normotensive pregnancy is associated with reductions in neurovascular transduction, which result in the dissociation of sympathetic outflow from hemodynamic outcomes, even during cold pressor-induced sympathoexcitation.