Recent systematic reviews and meta-analyses have reported on the concerning prevalence of symptoms of urinary incontinence during a wide range of physical activities, with prevalence reaching 44% among females who perform activities such as running [1]. One in two women will limit and restrict the intensity of their physical activity because of urinary tract symptoms and this can have deleterious health implications [2]. It is imperative that we better understand the specific pathophysiology of athletic incontinence in general, and urine leakage during running in particular, to help women maintain or improve their physical and mental health. 

Multifactorial mechanisms such as neuromuscular damage and structural damage to the urethra, bladder neck, and the levator ani muscles (PFMs) as well as their associated connective tissues [3] likely contribute to the pathophysiology of urinary incontinence—however, only a handful of studies have compared the morphology and function of these tissues between athletes with and without symptoms of athletic incontinence, and these have reported conflicting results. The aim of this study was to investigate differences in pelvic floor morphology and function between female runners who do and do not regularly experience running-induced stress urinary incontinence (RI-SUI), with a view to understanding its pathophysiology, and ultimately improving how it is prevented and managed.

This was a cross-sectional, observational case-control study which received approval from the local institutional research ethics board. Women aged 18 years and over with no known risk factors related to physical activity (PAR-Q+), who run at least 5 km in under 50 minutes, twice per week and more than 10km a week, and who have done so for at least one year, were recruited into two cohorts: runners who regularly (≥ 1 per month) experience RI-SUI and those who do not. An a priori power calculation estimated that a minimum of 16 women per group would be necessary to detect between-group differences. Runners were excluded if they reported a history of urogenital surgery, symptoms of energy deficiency as determined by the Low Energy Availability in Females Questionnaire (LEAF-Q), dyspareunia, any neurologic disorder, were pregnant or had delivered a baby within the previous year. All eligible females provided demographic information and were asked to complete several questionnaires (ICIQ-FLUTS, ICIQ-BS, ICIQ-Vaginal Symptoms, IPAQ-LF). 

The morphology of the urethra and PFMs was assessed using 2D and 3D (GE Voluson S6 system; General Electric, Toronto, Canada) B-mode ultrasound imaging. Static 3D volumes of the length of the urethra were collected using an endoprobe at the level of the meatus and then, in a standardized standing position, using a curvilinear probe placed transperineally, static 3D volumes and dynamic volumes (4D) were acquired while the participant performed a maximum effort Valsalva maneuver (MVM). 2D ultrasound videos were then recorded during MVM, and maximal voluntary contraction (MVC) efforts of the PFMs. Next, still in standing, participants were instrumented with an intravaginal dynamometer and were asked to perform a MVC against a dynamometric anteroposterior diameter of 35mm. In supine, passive forces were recorded while the anteroposterior diameter of the dynamometer arms moved from 15mm to 40mm at a constant speed of 50mm/s. Pelvic floor muscle elongation was held for 7 seconds at the maximum (40mm) diameter before the arms return to their initial position. Three repetitions of each task were performed for both dynamometry and ultrasound imaging. Measures of PFM function acquired through dynamometry included baseline force, relative peak force, rate of force development achieved during MVC, and static endurance measured as the time before the peak force achieved during the MVC decreased by 35%. Passive tissue forces measured during elongation included baseline force, relative peak resistance to passive stretch, rate of force development (stiffness) during passive elongation, and the stress relaxation coefficient (SRc). All outcomes were tested for normality using the Shapiro-Wilks test, and Independent t-tests or Mann-Whitney U were used as appropriate to test group differences on all study outcomes. Cohen’s d effect sizes were calculated for each outcome.

Twenty runners were included in the control group (i.e. continent runners), and nineteen experienced running-induced SUI (RI-SUI) (i.e., SUI during running ≥ 1/month). The groups were similar in terms of demographic outcomes; however, the controls were slightly younger than the cases (mean=36.2 years SD=7.9; mean=43.9 SD=10.6, respectively (p≤0.01)). The ICIQ-FLUTS total score was significantly higher in participants who experienced SUI during running, which was driven by the results from the Urinary Incontinence subscale (mean=1.7/20 SD=2.0; mean=5.8/20 SD=2.3, respectively (p≤0.001)).

The rate of force development during the MVC was significantly higher in participants reporting RI-SUI (p≤0.05) and conversely, significantly lower during passive elongation (stiffness) of the PFMs (p≤0.05) compared to continent runners. Concurrently, the extent of bladder neck elevation between rest and maximum voluntary activation was significantly higher among those with RI-SUI compared to those without (p≤0.05). Although not significant, small to moderate effect sizes were observed for other outcomes—active force outcomes measured during MVC tended to be higher in runners with RI-SUI (relative peak force, endurance), while relative peak force measured during passive tissue elongation tended to be lower. The cross-sectional area of the urethral wall and the area of the levator hiatus tended to be larger in runners with RI-SUI compared to those without, while their bladder necks tended to sit more caudally.

The results of this study point to adaptations in the pelvic floor among those with RI-SUI that were not observed among runners with the same running exposure but without RI-SUI. In particular, those with RI-SUI showed better PFM contractile function including improved power (i.e., higher rate of force development) and greater lift of the bladder neck during PFM MVC concurrent with greater thickness of the urethral wall, which may reflect hypertrophy of the striated urethral sphincter. Conversely, those with RI-SUI demonstrated less effective passive support of their pelvic tissues, reflected by lower stiffness during passive elongation of the paravaginal tissues, and lower bladder neck height at rest. Because the runners with and without RI-SUI had similar running experience and volume, these adaptations do not appear to be solely related to the cumulative load imposed by running on the pelvic support structures. While we cannot be confident that the improvement in PFM contractile abilities are compensatory to the loss of passive support, we hypothesize that this is the case. The next steps for this research are  to investigate the impact of an acute bout of running on the active and passive properties of the female pelvic floor and to quantify and compare the extent of pelvic floor loading experienced during running by runners with RI-SUI to those measured in runners without RI-SUI.

The robust methodology used in this study adds to our understanding of the pathophysiology surrounding athletic incontinence. The significant changes and moderate effect sizes found in the active and passive pelvic floor tissue properties suggest that runners with RI-SUI demonstrate enhanced PFM function and impaired pelvic organ support.

T. Pires, P. Pires, H. Moreira, and R. Viana, “Prevalence of urinary incontinence in high-impact sport athletes: a systematic review and meta-analysis,” J. Hum. Kinet., vol. 73, no. 1, pp. 279–288, 2020.
J. G. Dakic, J. Hay-Smith, J. Cook, K.-Y. Lin, M. Calo, and H. Frawley, “Effect of Pelvic Floor Symptoms on Women’s Participation in Exercise: A Mixed-Methods Systematic Review With Meta-analysis.,” J. Orthop. Sports Phys. Ther., vol. 51, no. 7, pp. 345–361, 2021, doi: https://dx.doi.org/10.2519/jospt.2021.10200.
K. Falah-Hassani, J. Reeves, R. Shiri, D. Hickling, and L. McLean, “The pathophysiology of stress urinary incontinence: a systematic review and meta-analysis,” Int. Urogynecol. J., vol. 32, no. 3, pp. 501–552, 2021.

Continence 7S1 (2023) 100992
DOI: 10.1016/j.cont.2023.100992