Despite a dearth of evidence on their effectiveness, hypopressive exercises (HE) have been embraced by some clinicians as an intervention for pelvic floor disorders.  As originally described by Caufriez [1], the theoretical aim of HEs is to decrease intra-abdominal pressure (IAP) while concurrently and reflexively increasing the activation of the pelvic floor muscles (PFMs). Yet we could not find empirical evidence of these phenomena. Further, in HE training, emphasis is placed on the use of specific hypopressive postures (HPs) for optimal effect [1], yet the rationale for this is also unclear. The objectives of this study were to determine (1) if the performance of an HE causes transient changes in IAP, electromyographic (EMG) activation of the levator ani muscles (LAMs) and the external anal sphincter (EAS), and/or motion of urogenital structures visualized on ultrasound imaging, and (2) the effect of an HP on these same outcomes.

This cross-sectional, observational study received approval from the local institutional research ethics board and all participants provided written informed consent prior to engaging in any study activities. Healthy females, naïve to HEs, were recruited from the local community. Participants were excluded if they were <18 years old, were in menopause, experienced chronic or recurrent pelvic pain, had a history of pelvic surgery, or were pregnant or < six months postpartum. Participants attended an initial training session where they learned from a certified Hypopressive trainer how to perform HEs in supine and standing in two HPs (Demeter and Athenas, respectively), a follow-up training session one week later to ensure the exercises were being performed correctly, and a data collection session one week after that. 
The primary outcomes were transient changes observed in IAP, EMG amplitude of the LAMs and EAS, and pelvic morphology [levator plate length (LPL), bladder neck height (BNH) and levator plate angle (LPA)] observed on 2D transperineal ultrasound imaging (USI), acquired during the HEs. 
At the data collection session, LAMs strength and stiffness were recorded using a custom intravaginal dynamometer. Electrodes were then located intravaginally over the LAMs (differential suction electrode) and on the skin surface overlying the EAS, interfaced with Delsys D.E. 2.1 preamplifiers and a Bagnoli-8 EMG amplifier system (Delsys Inc, Boston, USA). An IAP sensor [2] was inserted into the posterior fornix of the vagina. Participants first performed three maximum voluntary contractions (MVCs) of their PFMs (maximal effort squeeze and lift). Next, in random order, they performed three repetitions of the HE maneuver with and without the HP in supine and standing. All outcomes [(EMG, IAP and transperineal USI videos (GE Voluson S6; RAB6-D 4D convex curvilinear probe, GE, Toronto, Canada)] were acquired synchronously throughout these tasks. 
EMG data had any offset removed, were full-wave rectified, and were smoothed using a 4th order, dual-pass low-pass Butterworth filter (cut-off 6 Hz). The peak of the EMG signal during each HE task was normalized to the highest peak achieved during the PFM MVCs.
Outcome data were tested for normality (Shapiro-Wilk test). Student t-tests were used to determine whether there were changes in IAP, EMG amplitude or pelvic morphology during the HEs performed in supine or standing in conjunction with the corresponding HP. Separate two-way repeated-measures analysis of variance (RM-ANOVA) models and non-parametric Friedman’s ANOVAs were used to determine if there were differences in outcomes between positions (supine vs standing) or postures (HP vs no HP) or interactions between position and posture. An adjusted α=0.05/10 was set for all hypothesis testing to account for multiple outcomes. Despite some non-normal variables, there were no differences in the outcomes of hypothesis testing between parametric and nonparametric analyses, and the histograms and Q-Q plots suggested pseudonormality; all outcomes are therefore presented using parametric analyses for consistency. 
The sample size was determined apriori based on pilot (n=7) IAP and EMG data acquired to address objective 1. IAP was lower (supine: 13.47±14.82 cmH20; standing 18.90±14.90 cmH20) and LAM EMG was higher (supine: 9.6±6.2 uV; standing 5.5 ±3.7 uV) during the HE compared to rest. To achieve power=0.80 (α=0.05), the required minimum sample size was n=9 for a reduction in IAP and n=12 for activation of the LAMs. A moderate effect size (d=0.50) was assumed for the effect of the HP, requiring a sample size of n=30 to reach statistical significance.

Thirty-six participants [age= 34 (6) years, body mass index= 25 (5) kg/m2, n=15 nulliparous, n=19 continent of urine], completed the training and attended the data collection session (Figure 1). The mean LAM MVC force was 3.8 (2.7) N and LAM stiffness was 6.0 (2.2) N/mm.
All study outcomes are presented in Table 1. To address objective 1, we considered only data collected when the HE was performed along with the HP.  There was no significant change in IAP during the HE in supine [d=0.07, p=0.70] or in standing [d=0.34, p=0.07]. In supine, LAM activation was 44(35)%MVC, (d=1.24, p<0.001) while in standing it was 50(44)%MVC (d=1.12, p<0.001). In supine EAS activation was 27(24)%MVC (d =1.15, p<0.001) while in standing it was 27(27)%MVC (d=0.99, p<0.001). Some transient changes in pelvic morphology were observed: the LPL shortened (supine d=0.84, p<0.001; standing d=0.56, p=0.002) and the LPA (supine d=0.90, p<0.001; standing d=0.61, p<0.001) and BNH (supine d=0.49, p=0.006; standing d=0.31, p=0.074) increased during the HE. 
There was no interaction between body position (supine vs standing) and the use of the HP, and no main effect of body position or the HP on any outcomes; all effect sizes were small (Table 1).

The theory put forth by Caufriez is not supported. The IAP did not change during the HE maneuver performed either in supine or in standing. While the HE did cause significant activation of the PFMs, the underlying mechanism for this contraction is not clear. Caufriez stated that during the HE, a reduction in IAP causes reflex activation of the type 1 muscle fibres of the PFMs and abdominal muscles. Yet because the IAP did not change during the HE, this theory is not supported. Because the abdominal and PFMs often contract together [3], the activation of the LAMs and EAS during the HE may be mediated by the abdominal muscle activation required to perform the HE maneuver. As would be expected, activation of the PFMs was accompanied by reduction in the LPL and increase in the LPA. 
The HP does not appear to enhance the reduction of IAP nor the activation of the PFMs during a HE, nor is there an effect of body position (supine/standing) on these outcomes. 
The extent of activation of the PFMs observed during the HE was 50% MVC and lower, thus preferential activation of the slow twitch muscle fibres is supported. However, at this activation level, HEs are unlikely to induce a training effect that is superior to targeted, intentional PFM training, which is known to be effective for the management of urinary incontinence and pelvic organ prolapse.

HEs do not cause a significant change in IAP when performed by females naïve to HEs after two training sessions and two weeks of practice. The PFMs are active during HEs, reaching 50% LAM MVC, but the effect is not enhanced by the HPs (Demeter and Athenas) tested in this study.

Caufriez, M. Gymnastique abdominale hypopressive. Brussels: Ed. Bruxelles, 1997.
Niederauer, de Gennaro, J., Nygaard, I., Petelenz, T., & Hitchcock, R. (2017). Development of a novel intra-abdominal pressure transducer for large scale clinical studies. Biomedical Microdevices, 19(4), 80–10. https://doi.org/10.1007/s10544-017-0211-2
Madill, S. J., & McLean, L. (2008). Quantification of abdominal and pelvic floor muscle synergies in response to voluntary pelvic floor muscle contractions. Journal of Electromyography and Kinesiology, 18(6), 955–964. https://doi.org/10.1016/j.jelekin.2007.05.001

Continence 12S (2024) 101555
DOI: 10.1016/j.cont.2024.101555