The female pelvic floor consists of fascias, ligaments, and the pelvic floor muscles (PFM). The PFM form the base of the abdominal cavity on which the pelvic organs rest and where the urethra, vagina, and rectum pass through. The area surrounding the three openings of the pelvic floor in women (the levator hiatus) is the largest hernia port in the body.¹,² The PFM comprise three layers of muscles with the different muscles having different origins, insertions, and fiber directions. There is continuous muscle activity of the PFM, except just before and during voiding and defecation.³ If we were able to contract each muscle of the pelvic floor separately, each muscle would have a different function. However, a voluntary contraction of the PFM implies a mass contraction observed as a squeeze around the openings and a lift of the pelvic floor in a forward and inward (cranial) direction.⁴ Unfortunately, several studies have found that more than 30% of women with urge incontinence (UI) are not able to contract the PFM at their first consultation, even after thorough individual instruction.⁵ The most common errors are to contract other outer pelvic muscles such as hip adductor, gluteal muscles, and abdominal muscles instead of or in addition to the PFM.⁵,⁶ In addition, Bump et al.⁷ found that 25% were straining instead of performing a squeeze or inward lift of the pelvic floor. They also found that among women who were able to contract, only 49% were doing a contraction of enough intensity to influence the urethral closure pressure. To be effective in treatment of UI, it is essential that the women can perform a correct contraction and with adequate strength to make a difference.

In an intact and well-functioning pelvic floor, the connective tissue of the ligaments and facias and the PFM act together to counteract the impact of any increase in intra-abdominal pressure and ground reaction forces, keeping the pelvic organs in place with little downward movements and little or no opening of the levator hiatus area and/or the urethra.¹,² This is an automatic function, and for women with a well-functioning pelvic floor and no symptoms, there is no need to think about voluntarily contracting the PFM.

If, for some reason, this entity is not working adequately, for example, due to inherited morphologic factors or acquired factors, pelvic floor dysfunctions may occur.¹,²,³ Pelvic floor dysfunctions include UI, anal incontinence, pelvic organ prolapse (POP), sensory and emptying abnormalities of the lower urinary tract, defecatory dysfunction, sexual dysfunction, and chronic pain syndromes.² DeLancey et al.² described the integrated lifespan model where they used a graphical tool to integrate pelvic floor function related to pelvic floor disorders in three major phases. These phases are development of functional reserve during an individual’s growth; variations in the amount of injury and potential recovery that occur during and after vaginal birth; and deterioration occurring with advancing age. This chapter focuses on PFM training (PFMT) in treatment of stress urinary incontinence (SUI), overactive bladder (OAB) symptoms, and POP.

The PFM are the only muscles in the body with an anatomical location surrounding the levator hiatus and the three pelvic openings in women. Bø et al.⁸ described a possible mechanism for how voluntary contraction of the PFM and strength training over time may positively affect PFM function and prevent and treat UI. A single voluntary contraction of the PFM increases urethral closure pressure⁹; causes simultaneous co-contraction of the urethral sphincter¹⁰; and reduces the levator hiatus area by 25%, from a resting area of 20 cm² (95% confidence interval [CI] 17 to 23) to 15 cm² (95% CI 13 to 17). The muscle length shortens 21%, from 12.5 cm (95% CI 11.1 to 13.8) to 9.7 cm (95% CI 8.7
to 10.7),¹¹ and lifts the pelvic floor higher up in the pelvis, stabilizing the pelvic floor.⁸ One effective approach, known as “the Knack,” is to practice precontraction/co-contraction of the PFM during situations where such contractions are needed to prevent loss of urine.¹² However, it is unknown whether this approach leads to automatic precontraction/co-contraction of the PFM during such situations.

An assessor-blinded randomized controlled trial (RCT) in 109 women with POP and comorbidities such as UI and anal incontinence found that 6 months of PFMT caused permanent morphologic improvements of the pelvic floor. These morphologic changes included elevation of the bladder neck and rectal ampulla by approximately 0.5 cm, narrowing of the hiatal area by 6%, greater muscle thickness by 16%, and reduced muscle length by 4%.¹³ In that trial, there was less opening of the hiatal area and less increase in muscle length during straining in the PFMT group, which may indicate automatic function and increased PFM stiffness.¹³ Moreover, several randomized trials have found that women who have trained the PFM have significantly less incontinence during running and jumping (without voluntary contraction) than controls, indicating a positive effect on automatic function.¹⁴ Hence, there are rationales related to anatomy, biomechanics, and exercise physiology that support PFMT in the treatment of UI and POP.⁸,¹⁴

As the cause of urinary urge incontinence (UUI) in nonneurogenic patients is unknown, the rationale for PFMT in the group of patients with OAB is not as clear as for SUI. However, a voluntary contraction of the PFM has been shown to inhibit the urge to void, detrusor contraction, and urinary leakage.¹⁵ To date, there is no knowledge about how strong this voluntary contraction needs to be to influence urethral closure pressure. It is also unknown whether PFMT over time is needed in addition to the immediate effect of the voluntary contraction during urge to void to treat UUI and other symptoms of OAB.