Pregnancy lowers the baseline amplitude of respiratory sinus arrhythmia, but slow and deep breathing can raise it to the level seen in non-pregnant women during spontaneous breathing. The surprising part is how strongly breathing frequency matters. Gestational hypertension occurs in up to 15% of pregnancies and causes an increased risk of obstetric complications.

It is defined as high blood pressure presenting after 20 weeks of pregnancy, which was not present prior to pregnancy, and while pharmaceutical treatments exist, the only cure is to give birth. Since many women have an aversion to medication in pregnancy, pregnant women are highly motivated to adhere to and undertake non-pharmacological interventions.

Slow and deep breathing is recommended by the American Heart Association as an adjunctive treatment for hypertension in non-pregnant populations. A recent meta-analysis of studies on slow and deep breathing in primary hypertension found reductions of up to 5.26 millimetres of mercury for systolic blood pressure and 2.97 millimetres of mercury for diastolic blood pressure after daily practice.

Given that the aetiology of gestational hypertension has also been linked to high breathing frequencies and dysfunctional breathing, slow and deep breathing offers a potential effective treatment for uncomplicated gestational hypertension. Pregnancy itself induces a series of cardiovascular adaptations, which may subsequently change the acute response to slow and deep breathing compared with non-pregnant women.

During pregnancy, baseline cardiovascular measures such as heart rate, stroke volume and cardiac output are increased above non-pregnant levels, and these changes may influence the acute cardiovascular response to slow and deep breathing. The health benefits and reductions in blood pressure associated with slow and deep breathing are suggested to be related to diaphragmatic breathing, but during pregnancy the diaphragm is forced upwards by as much as five centimetres, which may limit its mobility and the ability to perform slow and deep breathing or achieve associated health benefits.

Before undertaking an intervention using slow and deep breathing as a treatment for gestational hypertension, there is a need to characterise the acute responses of pregnant women and whether they differ from non-pregnant women. A review of international guidance found that non-pharmacological interventions lacked evidence supporting potential benefits, leading to a lack of clear guidance in this area.

Normative and baseline data is needed before investigating slow and deep breathing with women who develop gestational hypertension. The aim of this study was to compare the acute cardiovascular responses of non-pregnant and pregnant women to slow and deep breathing at a range of breathing frequencies.

Forty-one women participated in the study: 23 healthy non-pregnant women and 18 healthy pregnant women. All participants were of reproductive age, defined by the World Health Organization as 15 to 49 years, and all pregnant women were over 20 weeks gestation.

All pregnant women were nulliparous and were carrying singleton pregnancies, while participants with cardiovascular or respiratory disease, smokers and women who vaped were excluded. All participants were normotensive at data collection, and the pregnant women submitted regular blood pressure measurements until birth to confirm they did not subsequently develop high blood pressure.

Participants completed five breathing conditions in a randomised order: spontaneous breathing, four, six and eight breaths per minute, and a dynamic frequency using an optimisation algorithm that maximised respiratory sinus arrhythmia. All breathing conditions were five minutes in duration, with a five-minute break of normal breathing between each measurement.

An app delivered the fixed breathing frequencies or used a novel, bespoke algorithm to deliver a personalised dynamic frequency. The algorithm maximised cardiovascular perturbations using the amplitude of respiratory sinus arrhythmia as the controlled variable. During each breathing condition, respiratory airflow, electrocardiogram and arterial blood pressure were monitored continuously.

Participants were seated in an upright position at an approximate angle of 60 degrees. Respired flow rate was measured continuously using a heated pneumotachograph connected to a flow measurement system while participants wore an oronasal mask.

After normality was confirmed, repeated measures analysis of variance with planned pairwise comparisons using Bonferroni corrections was used. Between-group comparisons between pregnant and non-pregnant women used independent-samples t-tests, with reported p values adjusted for repeated comparisons.

Spearman’s rank-order correlation analyses examined relationships between variables after the data violated normality assumptions, and the p value was set at 0.05 for all analyses. Data were collected from 41 participants, and six participants were excluded from the analysis: three because of technical errors in respiratory airflow measurement, two because they failed to adhere to the prescribed breathing condition, and one because the acquisition system failed to save the signal data.

Consequently, data analysis was performed. The amplitude of respiratory sinus arrhythmia was significantly lower for pregnant women than for non-pregnant women for all breathing conditions, with a p value below 0.001. Respiratory sinus arrhythmia during slow and deep breathing for pregnant women increased to a level similar to that observed during spontaneous breathing for non-pregnant women.

Respiratory sinus arrhythmia plateaued at six breaths per minute for both groups. The maximum amplitude during slow and deep breathing at six breaths per minute or fewer was 2.1 times higher than during spontaneous breathing for both groups, although it remained lower in absolute terms for pregnant women.

In the left-hand plot, the curves rise from spontaneous breathing toward the slow-breathing region, then show little additional increase at the lowest fixed frequency. The right-hand markers show the dynamic-frequency results separately, with error bars indicating substantial participant variability around each group mean.

The within-breath peak-valley amplitude of systolic and diastolic blood pressure was significantly greater during both inspiration and expiration for all slow and deep breathing conditions than during spontaneous breathing, with a p value below 0.001. This pattern was true for both pregnant and non-pregnant women.

The only significant difference in systolic blood pressure peak-valley amplitude between pregnant and non-pregnant groups was for the six-breaths-per-minute condition, with a p value of 0.001. Figure four shows blood-pressure oscillations as percentage changes relative to average pressure, separated by systolic and diastolic pressure and by inspiration or expiration.

Across the fixed-frequency conditions, the plotted amplitudes generally increase as breathing slows, with the largest values appearing around four breaths per minute; the authors report increases of up to four and a half times, or ten millimetres of mercury, compared with spontaneous breathing.

This matters because it quantifies how controlled breathing changes beat-to-beat cardiovascular dynamics in pregnant and non-pregnant women. Fifty-five percent of pregnant participants preferred the six-breaths-per-minute condition.

Another four participants chose six breaths per minute as their second preferred condition, where they had little preference between two conditions as their favourite. A total of 78% of participants chose six breaths per minute as their first or close second choice.

There was no correlation between preferred breathing frequency and gestational age, with a correlation of minus zero point thirteen and a p value of 0.623. This study characterises acute cardiovascular responses to slow and deep breathing, including inter-breath and intra-breath phase perturbations, while taking a Network Physiology approach.

It compares these acute cardiovascular responses in pregnant and non-pregnant women for the first time. Slow and deep breathing can increase respiratory sinus arrhythmia in pregnant women to levels similar to respiratory sinus arrhythmia during spontaneous breathing in non-pregnant participants, revealing the ability to return respiratory sinus arrhythmia to pre-pregnancy levels.

Haemodynamic changes in this study were measured non-invasively, so all cardiovascular variables are estimates of the true responses. The estimation of stroke volume using the Modelflow method has previously shown excellent agreement with stroke volume measured by Doppler ultrasound and when blood is withdrawn by phlebotomy.

Finapres blood pressure measures also correlate highly with auscultatory blood pressure measurements in normotensive participants, but the use of indirect measurement during slow and deep breathing still needs to be acknowledged. In these normotensive women, slow and deep breathing amplified cardiovascular oscillations in both groups, with RSA plateauing at six breaths per minute.

That makes four to six breaths per minute a useful range for future gestational-hypertension research, not yet a proven treatment.