Evidence-Based: Physical Therapy Pelvic Floor


There are several important clinical correlates of urethral
muscular anatomy. Perhaps the most important is
that SUI is caused by problems with the urethral sphincter
mechanism as well as with urethral support.
Although this is a relatively new concept, the supporting
scientific evidence is strong.

The usual argument for urethral support playing an
important role in SUI is that urethral support operations
cure SUI without changing urethral function. Unfortunately,
this logic is just as flawed as suggesting that
obesity is caused by an enlarged stomach because gastric
stapling surgery, which makes the stomach smaller, is
effective in alleviating obesity. The fact that urethral
support operations cure SUI does not implicate urethral
hypermobility as the cause of SUI.

Most studies have shown not only that there is substantial
variation in resting urethral closure pressures in
normal women compared with those with SUI, but also
that the severity of SUI correlates quite well with resting
urethral closure pressure.

Loss of urethral closure pressure probably results
from age-related deterioration of the urethral musculature
as well as from neurologic injury (Hilton & Stanton
1983, Smith et al 1989a, b, Snooks et al 1986). For example,
the total number of striated muscle fibres within
the ventral wall of the urethra has been found to
decrease seven-fold as women progress from 15 to 80
years of age, with an average loss of 2% per year.

Because the mean fibre diameter does not change
significantly with age, the cross-sectional area of striated
muscle in the ventral wall decreases significantly with
age; however, nulliparous women seemed relatively
protected (Perucchini et al 2002b). This 65% age-related
loss in the number of striated muscle fibres found in
vitro is consistent with the 54% age-related loss in
closure pressure found in vivo by Rud et al 1980, suggesting
that it may be a contributing factor. However,
prospective studies are needed to directly correlate the
loss in the number of striated muscle fibres with a loss
in closure pressure in vivo.

It is noteworthy that in our in-vitro study, thinning
of the striated muscle layers was particularly evident in
the proximal vesical neck and along the dorsal wall of
the urethra in older women (Perucchini et al 2002b). The
concomitant seven-fold age-related loss of nerve fibres
in these same striated urogenital sphincters
directly correlated with the loss in striated muscle fibres
in the same tissues (Pandit et al 2000); and the
correlation supports the hypothesis of a neurogenic
source for SUI and helps to explain why faulty innervation
could affect continence.

We believe that the ability of pelvic floor exercise to
compensate for this age-related loss in sphincter striated
muscle may be limited under certain situations. Healthy
striated muscle can increase its strength by about 30%
after an intensive 8–12 week progressive resistance
training intervention. For example suppose an older woman had a maximum
resting urethral closure pressure of 100 cmH2O when
she was young but it is now 30 cmH2O due to loss of
striated sphincter muscle fibres. If she successfully
increases her urethral striated muscle strength by 30%
through an exercise intervention and there is a one-to one
correspondence between urethral muscle strength
and resting closure pressure, she will only be able to
increase her resting closure pressure by 30%, from
30 cmH2O to 39 cmH2O, an increment less than onetenth
of the 100 cmH2O increase in intravesical pressure
that occurs during a hard cough. It remains to be determined
whether pelvic floor muscle exercise is as effective
in alleviating SUI in women with low resting
urethral pressures as it can be in women with higher
resting pressures, especially for women participating in
activities with large transient increases in abdominal


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