Menopause. It’s the plague of middle-aged women everywhere. Hot-flashes when it’s 32ºF outside, using three pairs of pajamas before dawn secondary to night sweats, and not to mention irritating vaginal dryness. But possibly one of the most embarrassing experiences that affect many menopausal women is stress urinary incontinence (SUI).

How Common is It?
Although SUI has been shown to increase with age and is often associated with menopause, there is conflicting research in finding a correlation with hormonal changes and SUI. Some studies have found that SUI increases in the “midlife,” while urinary urgency and frequency increases with older adults. Several researchers continue to postulate that estrogen may play a role in the mechanisms of urinary incontinence.¹

The prevalence of SUI—defined by the International Continence Society as “The involuntary loss of urine which is a social or hygienic problem and objectively demonstrable”²—is highly variable in the current research, as it is studied in many age groups, populations, and has used several definitions of SUI in creating inclusion criteria. Studies specific to menopause often explore not only SUI, but also urinary urgency/frequency, nocturia, dysuria, and other bladder dysfunctions. These bladder dysfunctions have shown to occur in more than 25% of postmenopausal in the United States, the Netherlands and Britain³ with some studies reporting a SUI prevalence as high as 75% at the age of 45.⁴ Along with the research, PTs are seeing a high volume of perimenopausal women in the clinic seeking treatment for SUI.

Most women’s health therapy education focuses on the neuromuscular and musculoskeletal aspects of pelvic floor rehabilitation, yet the biochemistry of menopause is not taught in detail. However, the science of hormones and hormonal changes plays a large role in understanding and fine-tuning physical therapy treatment for perimenopausal women. Familiarity with various hormone replacements and the cellular changes affecting menopausal women is essential in creating innovative treatments for all bladder and pelvic dysfunctions.

The 1-2-3’s of Estrogen
Prior to understanding SUI during menopause, one must have a basic knowledge of hormones. To simplify the rocket science of hormonal changes and replacement, I will give only a brief overview of estrogen. One of the most eye-opening introductions to the basic science of hormones was presented at the conference “More Pelvic Floor Dysfunctions—Level III” by Hollis Herman and is the source for the following information:

As menopause is defined by not menstruating for 1 year, estrogen changes are essential to understand. First, estrogen comes in three forms: Estrone (E1), 17 Beta Estradiol (E2), and Estriol (E3). Estriol (E3) is the “pregnancy” estrogen as it is produced by the placenta and is not found in nonpregnant women. Prior to menopause, 17 Beta Estradiol (E2) is our predominant natural estrogen and is produced in the ovaries. This estrogen has more than 400 functions in your body and loss of (E2) can lead to changes in the skin, decreased lubrication, sleeplessness, and many other changes, including bladder problems. Common Estradiol (E2) replacements that may be seen in the clinic include Vivelle, the Estring, Estrace tablets or cream, Climera, and the Estraderm patch.

After menopause, Estrone (E1) is the predominant estrogen. This estrogen is made in the fat (and has been shown at levels 40% higher in obese women), liver, brain, bone marrow, and skin. In obese women, estrone has been linked with a high risk of breast and endometrial cancer. Although this estrogen can help produce 17 Beta Estradiol (E2), it needs a functioning ovary to do so. Commercial estrone includes the very popular Premarin (equine estrogen from a pregnant mare), Prempro, Estratest, and many others. As PTs, we are in no way qualified to advise any type of hormone therapy, but knowledge of common estrogen-replacement therapy and the functions of estrogen (especially 17 Beta Estradiol (E2)) can give us a clearer picture as to why our perimenopausal patients are suffering from urinary changes.⁵

SUI Treatment Options
Interestingly, estrogen replacement has not been shown to be an effective treatment specifically for SUI.^1,3 Some researchers have even found that hormone replacement therapy (HRT) increased the risk of urinary incontinence. Estrogen plus Progestin replacement increased the risk of weekly SUI by 16% and weekly urge incontinence by 12% within 4 months of beginning treatment.⁶ Congugated equine estrogen alone and added to medroxyprogesterone acetate worsened the symptoms in women who already experienced urinary incontinence and increased the risk of incontinence in continent women.⁷

While evidence-based treatments of electromyography biofeedback and pelvic floor exercise are effective in the treatment for SUI,^8,9 the available literature has shown in several studies that some medications, plus pelvic floor exercises, equals the best results in decreasing SUI. One researcher found that combination therapy with Estriol plus pelvic floor muscle exercises were effective for mild SUI (for up to 18 months).¹⁰ A recent article in the Journal of Urology claimed that Duloxetine (a serotonin and noradrenaline reuptake inhibitor, which targets the distal urethral sphincter) and pelvic floor muscle training resulted in the most effective treatment and should be used as a first-line treatment.¹¹ Clinically, it would be interesting to see if your patients who take a certain brand of antidepressant have better outcomes with their treatment.

At the level of the skeletal muscles, a reduction in force production occurs at menopause, but the underlying mechanisms are still unknown. Research published by Kadi et al examined the fast- and slow-twitch muscle fibers in rats following ovary removal. They divided the rats into groups who exercised, had estrogen (17 Beta Estradiol (E2)) treatment, or both (plus a control group). It is noteworthy to say that the researchers were looking at the extensor digitorum longus (fast twitch) and the soleus (slow twitch). All of the rats with the ovary removal (with no exercise or HRT) exhibited a change in the myosin heavy chain isoforms from fast to slow in both the digitorum longus and the soleus. When the group of rats with the ovary removal were allowed to exercise (running) but had no estrogen replacement, the fast-twitch muscle continued to change to slow-twitch fibers, but the slow-twitch fibers do not change form. In the combination (estrogen plus exercise) group, no changes were found in the fast- or slow-twitch fibers.¹² Further studies are needed to find if this translates in a clinical setting.

Despite the low estrogen concentration, there is evidence that middle-aged women can improve their muscle performance by physical training.¹³ But is it possible that a lack of fast-twitch fibers may be the reason why some patients (not taking HRT) improve only to a certain point, yet continue to have difficulty if they are “caught off guard” by a quick sneeze or cough?

Menopausal Changes of the Urethral Sphincter
In addition to a decrease in fast-twitch fibers, the urethral sphincter may also be affected by postmenopausal atrophy.¹⁴ Theoretically, slight changes in the structures surrounding the urethra could significantly affect continence. In healthy 22-year-old females, pressure in the urethra increased 240 (+/-30 ms) before the bladder with a valsalva maneuver or coughing.⁵ There is increased maximum intraurethral pressure and increased urethral length (functional and absolute) when a healthy female transitions from supine to a standing position. These changes are thought to be compensatory mechanisms to maintain continence as they counteract the simultaneous increase in the pressure of the bladder.¹⁶

Histologically, women with SUI have been found to have decreased skeletal muscle and increased connective tissue/fibrosis in the urethral sphincter.¹⁷ Hormone replacement of 17 Beta-Estradiol has been shown to significantly increase muscle fibers and decrease collagen fibers in both the detrusor (bladder) muscle and the urethra in a study performed on rats.¹⁸ Multiple studies have looked at the breakdown of collagen as a cause of stress incontinence and have found that women with SUI have degeneration of collagen fibers.^19-25 A question yet to be answered is: Can pelvic-muscle exercises alone targeting the urethra reverse or help maintain the integrity of existing collagen structures, increase muscle fibers, and eliminate incontinence?

Clinical Application
As there is currently no “gold standard” protocol set for SUI during menopause, research is needed to look specifically at different pelvic exercise protocols for premenopausal, perimenopausal, and postmenopausal women. Keeping in mind that the literature does show a menopause-related decrease in urethral function and fast-twitch fibers, patients may benefit from working on muscular and postural patterns to promote fast recruitment of the urethral sphincter prior to functional activities that increase intra-abdominal pressure. As clinicians, we should be aware of the HRT taken by our clients while continuing to perform evidence-based treatments for SUI.

Robin Christenson, MPT, is a women’s health PT who has much experience with women who are premenopausal, perimenopausal, and postmenopausal. She owns and operates a women’s health physical therapy clinic, Womanology Inc, in Newport Beach, Calif.

References
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2. Abrams P, Blaivas JG, Stanton SL, Anderson JT. The standardization of terminology of the lower urinary tract function. Br J Obstet Gynaecol. 1990:97 Suppl 6:1–16.

3. Coope, J. Hormonal and non-hormonal interventions for menopausal symptoms. Maturitas. 1996;23:159–168.

4. Hørding U, Pedersen KH, Sidenius K, Hedegaard L. Urinary incontinence in 45-year-old women. An epidemiological survey. Scand J Urol Nephrol. 1986;20:183–186.

5. Herman H. More pelvic floor dysfunction topics. Paper presented at: the American Physical Therapy Association Section on Women’s Health Lecture; January 9–11, 2004; Jacksonville, Fla.

6. Steinauer JE, Waetjen LE, Vittinghoff E, et al. Postmenopausal hormone therapy: does it cause incontinence? Obstet Gynecol. 2005 Nov;106(5 Pt 1):940–945.

7. Hendrix SL, Cochrane BB, Nygaard IE et al. Effects of estrogen with and without Progestin on urinary incontinence. JAMA. 2005;293:935–948.

8. Hay-Smith EJ, Dumoulin C. Pelvic floor muscle training versus no treatment, or inactive control treatments, for urinary incontinence in women. Cochrane Database Syst Rev. 2006 Jan 25;(1):CD005654.

9. Neumann PB, Grimmer KA, Deenadayalan Y. Pelvic floor muscle training and adjunctive therapies for the treatment of stress urinary incontinence in women: a systematic review. BMC Women’s Health. 2006;6:11.

10. Ishiko O, Hirai K, Sumi T, Tatsuta I, Ogita S. Hormone replacement therapy plus pelvic floor muscle exercise for postmenopausal stress incontinence. A randomized, controlled trial. J Reprod Med. 2001;46: 213–220.

11. Ghoniem GM, Van Leeuwen JS, Elser DM, et al. A randomized controlled trial of Duloxetine alone, pelvic floor muscle training alone, combined treatment and no active treatment in women with stress urinary incontinence. J Urol. 2005;173:1647–1653.

12. Kadi F, Karlsson C, Larsson B, et al. The effects of physical activity and estrogen treatment on rat fast and slow skeletal muscles following ovariectomy. J Muscle Res Cell Motil. 2002;23:335–339.

13. Sipilä S, Poutamo J. Muscle Performance, sex hormones and training in peri-menopausal and post-menopausal women. Scand J Med Sci Sports. 2003;13: 19–25.

14.Fantl JA, Cardozo L, McClish DK. Estrogen therapy in the management of urinary incontinence in post-menopausal women: a meta-analysis. First report of the Hormones and Urogenital Therapy Committee. Obstet Gynecol. 1994;83:12–18.

15. Contantinou CE, Govan DE. Spatial distribution and timing of transmitted and reflexly generated urethral pressures in healthy women. J Urol. 1982;127:964–969.

16. Henriksson L, Ulmsten U, Andersson KE. The effect of changes of posture on the urethral closure pressure in healthy women. Scand J Urol Nephrol. 1977;11: 201–206.

17. Hale DS, Benson JT, Brubaker L, Heidkamp MC, Russel B. Histologic analysis of needle biopsy of urethral sphincter from women with normal and stress incontinence with comparison of electromyographic findings. Am J Obstet Gynecol. 1999;180(2 Pt. 1):342–348.

18. Sartori MG, Girao MJ, de Jesus Simoes M, Sartori JP, Baracat EC, Rodrigues de Lima G. Quantitaive evaluation of collagen and muscle fibers in the lower urinary tract of castrated and under-hormone replacement female rats. Clin Exp Obstet Gynecol. 2001;28:92–96.

19. Bergman A, Elia G, Cheung D, Perelman N, Nimni ME. Biomechanical composition of collagen in continent and stress urinary incontinent women. Gynecol Obstet Invest. 1994;37:48–51.

20. Chen B, Wen Y, Wang H, Polan ML. Differences in estrogen modulation of tissue inhibitor of matrix metalloproteinase-1 and matrix metalloproteinase-1 expression in cultured fibroblasts from continent and incontinent women. Am J Obstet Gynecol. 2003;189:59–65.

21. Chen BH, Wen Y, Li H, Polan ML. Collagen metabolism and turnover in women with stress urinary incontinence and pelvic pro-lapse. Int Urogynecol J Pelvic Floor Dysfunct. 2002;13:80–87.

22. Goepel C, Hefler L, Methfessel HD, Koelbl H. Periurethral connective tissue status of postmenopausal women with genital prolapse with and without stress incontinence. Acta Obstet Gynecol Scand. 2003;82:659–664.

23. Liapis A, Bakas P, Pafiti A, Frangos-Plemenos M, Arnoyannaki N, Creatsas G. Changes of collagen type III in female patients with genuine stress incontinence and pelvic floor prolapse. Eur J Obstet Gynecol Reprod Biol. 2001;97:76–79.

24. Radziszewski P, Borkowski A, Torz C, Bossowska A, Gonkowski S, Majewski M. Distribution of collagen type VII in connective tissues of postmenopausal stress-incontinent women. Gynecol Endocrinol. 2005;20: 121–126.

25. Ulmsten U, Ekman G, Giertz G, Malmstrom A. Different biomechanical composition of connective tissue in continent and stress incontinent women. Acta Obstet Gynecol Scand. 1987;66:455–457.