Historically, exercise during pregnancy has been a cause of concern because it could potentially challenge the homeostasis of the maternal-fetal unit, and thus it might adversely affect the course and outcome of pregnancy.1,–,3 Particular caution should theoretically be placed on exercise performed during the last trimester of pregnancy, which is necessary for the maturation of the fetal lungs and other organs.

Several studies evaluated the effects of a single bout of dynamic, submaximal exercise (usually, cycle-ergometry at ≤80% age-predicted maximum heart rate (HR_max)) on the vascular resistance of the umbilical3,–,13 or fetal cerebral circulation in non-athletic, healthy women during the last trimester of uncomplicated pregnancy.4 13 They did not observe significant exercise-induced changes in umbilical perfusion,4,–,7 9,–,13 or even improvements due to decreased vascular resistance were reported.8 Two studies suggested fetal cerebral vasodilatation with maternal exercise.4 13 More discrepancies exist on the acute response of fetal HR (FHR) to late-pregnancy maternal exercise. Several studies reported significant increases in FHR6 12,–,14 or considerable individual variability in the FHR response,5 while others did not observe any change.4 11 A transient fetal impairment has been described at high exercise intensities (>90% HR_max), as described by FHR decrease and eventual fetal bradycardia.14

Potential sources of discrepancy between studies include, among others, differences in the duration or in the relative intensity of the acute exercise stimulus. Maternal physical activity habits during pregnancy could also modulate fetal cardiovascular response to a single stimulus. Whether regular physical activity performed over the pregnancy course influences the effects that an acute exercise bout performed at late pregnancy has on the umbilical circulation and on the fetal cardiovascular responses remains to be elucidated. This question is of clinical relevance, given the growing number of women who are engaging in regular exercise during the course of pregnancy. There is a need for strong evidence providing further support to the notion that healthy gravidae can safely engage in regular physical activity even at late gestation.15

The purpose of this study was to assess the effects of maternal physical activity levels on fetal cardiovascular responses to acute exercise during the third pregnancy trimester. For that purpose, we evaluated fetal cardiovascular responses to a single exercise bout in a group of physically active women (training) and in a group of sedentary women (control).

All the participants were informed about the aim and study protocol, and all provided written informed consent. The research protocol was reviewed and approved by the Research Ethics Committee of Hospital Severo Ochoa (Madrid, Spain). The study was performed following the ethical guidelines of the Declaration of Helsinki, last modified in 2000.

We performed the outcome measurements of the present study (see below) as a part of an ongoing randomised, controlled training trial. Healthy gravidae recruited in the same primary care medical centre, aged 25–35 years who were all sedentary (not exercising >20 min on >3 days per week), with singleton and uncomplicated gestation, and not at high risk for preterm delivery (no more than one previous preterm deliveries) were randomly assigned to either a training or a control group (n=80 each).

Women in the control group were asked to maintain their level of physical activity during the study period, and those in the intervention group were enrolled in three supervised training sessions per week from the start of the second trimester (weeks 12–13) to the end of pregnancy. Each exercise training session consisted of a warm-up period of about 8 min, followed by ∼20 min circuit training with toning and light resistance exercises (using barbells and low-to-medium resistance elastic bands) and finished with a cool-down period of about 8 min. Details of the exercise training protocol have been described by Barakat et al.15

Fifty-two randomly selected gravidae (n=26/group) volunteered to take part in the present study. They all underwent the same cycle-ergometer tests (see below) at the same time point of gestation (34 (1) weeks). After a 5 min acclimatization period, they pedalled during 20 min at moderate intensity, that is, eliciting a rate of perceived exertion value16 of 12–14 and at ∼60% of age-predicted maximum HR. Maternal HR and FHR were continuously monitored with a telemeter (Accurex Plus; Polar Electro Oy, Kempele, Finland) and an electronic monitor (Avalon Fetal FM 20; Philips Healthcare, Best, The Netherlands), respectively. Immediately before and after exercise, an experienced investigator (Hospital de Fuenlabrada, Madrid, Spain) performed Doppler flow measurements of the fetal middle cerebral (MCA) and umbilical arteries (UA) with a pulsed wave ultrasound recorder (Toshiba Nemio 20; Toshiba Information Systems, San Fernando de Henares, Spain). Details on Doppler examinations in the aforementioned fetal arteries are provided elsewhere.13 From blood flow velocity waveforms, we determined the pulsatility index of the MCA (MCA-PI) and UA (UA-PI), as well as the MCA-PI–to–UA-PI ratio, hereinafter called cerebroplacental ratio (CPR).17

We compared maternal characteristics between groups by unpaired Student t tests and χ² test. We performed a two-way (group and time) analysis of variance with repeated measures to compare fetal cardiovascular responses to exercise in the training and control groups. The significance level was set at p<0.05.

Maternal characteristics were similar between groups, yet resting HR was significantly lower in the training group compared with that of the controls, reflecting maternal training adaptation (table 1). The mean FHR increased throughout exercise in both groups (p<0.001 for time effect) in a similar fashion, that is, we did not observe a significant group or group×time interaction effect (fig 1A). The UA-PI increased and decreased with exercise in the control and training groups, respectively (p=0.026 for interaction effect), whereas the MCA-PI decreased similarly in both groups (fig 1B,C). The CPR also decreased in both groups with exercise, though less markedly in controls (p=0.028 for the interaction effect; fig 1D). The results did not change when the analyses were repeated after adjusting for maternal age, smoking status, occupational activity and parity.

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Figure 1

(A) Fetal heart rate at rest and during exercise in the training and control groups (values are mean (SD)). (B) Umbilical artery pulsatility index (PI), (C) fetal middle cerebral artery PI and (D) cerebroplacental ratio at pre-exercise and postexercise in the training and control groups. Values are mean and 95% CI.

Our findings corroborate that overall, acute maternal submaximal exercise has no deleterious effects on fetal cardiovascular responses despite inducing a physiological stimulus to the fetus (as reflected by increasing FHR with exercise). The CPR remained consistently18 within normal limits (>1.08) in all participants before or after exertion. This ratio reflects the fetal haemodynamics and cardiac output redistribution better than the MCA-PI or UA-PI alone and is a better predictor of fetal compromise, even when umbilical resistance is normal.19 Though overall maternal training status did not significantly influence the FHR or fetal haemodynamics during acute exercise, the UA-PI decreased with exercise only in the training group, suggesting a beneficial training adaptation, that is, decrease in the UA resistance with acute exercise. Further research could determine if attenuated release of norepinephrine levels as an adaptation to regular physical activity is responsible for the observed decrease in UA-PI with submaximal exercise.

The MCA-PI decreased similarly with exercise in both groups, likely reflecting fetal cerebral vasodilatation. Two studies also suggested fetal cerebral vasodilatation with maternal exercise, which in turn was thought to reflect slight fetal haemoglobin desaturation.4 13 Taken together, the present data and those of previous research4 13 indicate that the fetal cerebral circulation is well protected during maternal exercise at late pregnancy, at least if exercise intensity is low to moderate. This is an important consideration because cerebral metabolic requirements are increased during this phase of gestation.19

In summary, maternal submaximal dynamic exercise during the third pregnancy trimester does not adversely affect fetal haemodynamics. Overall, maternal training status does not influence fetal cardiovascular responses.