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Stress urinary incontinence in women—An overuse syndrome
) Medical Hypotheses I
1 M.&al tlpl&s~ (1993) Y. 381s3fl2 oL.qImlc3mupuKLtd1993
Stress Urinary Incontinence in Women-An Syndrome
Overuse
M.J6iWIK The Department of Gynecology 15-062 Bialystok, Poland
and Septic Obstetrics, Medical Academy, Bialystok,
Ul,
Warszawska 15,
Abstract-The levator ani muscles in women are overloaded by constant supporting abdominal contents, and counteracting rises of abdominal pressure at the level of the urethra. The excessive load leads to a decrease in their type II fibers. This results in stress urinary incontinence due to loss of the fibers responsible for additional compression of the urethra at strain.
Introduction
Clinical background
According to the criteria of the International Continence Society (l), stress urinary incontinence (SUI) in women is described as an involuntary loss of urine via urethra in the absence of bladder detrusor muscle contraction. The main feature of this troublesome and frequent disorder is decreased urethral pressure at strain and/or at rest. Normally, rises in abdominal pressure generate a reflex contraction of the levator ani muscles exerting then an additional external compression of urethral walls, and thus preventing passive leakage of urine. From a physiological standpoint (2), the levatores a&-typical skeletal muscles-contain fibers of two types: type I-white slow-twitch fibers, capable of longer but weak contractions, and type II-red fasttwitch fibers recruited at higher work loads, able to maintain contraction for a very short time. The presence of both types of fibers has been histologically contirmed in these muscles (3). Their functional specialization has been suggested (4, 5). Type II fibers seem to be fitted for counteracting urination in stress conditions.
In contrast to quadrupeds, the pelvic floor in Hominoidea achieved a horizontal position (6) and began to play the main role in supporting pelveo-abdominal contents. Evidence of a state of constant active contraction of the levatores ani has been demonstrated (7, 8). This is a unique situation for skeletal muscle. Skeletal muscles are not structurally prepared to exert prolonged excessive work. Such a condition results in an increase of the type I fibers content, i.e. in a decrease of fast-twitch fibers’ quantity, as observed by Gollnick et al (9) in human soleus muscle. A decrease of the type II fibers in the levatores ani in SUI was observed by several authors (4,5, 10). If we take into consideration the fact that SUI patients often have a history of pain located somewhere in the region of the urethra in the absence of symptoms of intlammation and positive urine cultures, one can suspect an overuse syndrome. As defined originally by Dennet and Fry (1 l), the syndrome is ‘a musculoskeletal disorder character&d by pain, tenderness, and often functional loss in muscle groups and ligaments subjected to heavy or unaccustomed use’. Complaints of
Date received25 January 1993 Date accepted 1 March 1993
381
382
MEDICAL BYFQlHE%g
pain given by SUI patients are very likely to be of muscular origin and conform to a recent theory of occupational myalagia (12). Conclusions Taking it all together, as SUI is not observed in the animal world, it is possible that with assumption of erect posture in humans the pelvic contents and abdominal viscera began to exert an excessive pressure on the pelvic floor mobilising the levatores ani to too intensive work. This promotes in some women a progressive overuse deficit of the type II fibers which leads directly to SUI.
4.
5.
6. 7* s. 9.
References 10. Abrams P, Blaivas J G. Stanton S L, Anderson J T. The standardisation of temtinology of lower urinary tract function. Stand J Urn1 Nephrol (Suppl) 114: 5, 1988. Sjiisviim M jingquist K-A, Bylund A-C. Frid6r-1J, Gustavsson L. Scherst6n T. Morphcsnetric analyses of human muscle fiber types. Muscle and Nerve, 1982; 5: 538. Gosling J A. Dixon J S, Critchley H 0 D, ‘lbompsco S-A. A
11. 12.
comparative study of the human external sphincter and periurethml levator ani muscles. Br J Ural 1981; 53: 35. Koelbl H, Strassegger H, Riss P A, Gruber H. Morphologic and functional aspects of pelvic floor muscles in patients with pelvic relaxation and genuine stress incontinence Obstetrics and Gynecology 1989; 74: 789. Gilpin S A, Gosling J A, Smith A R B, Warrell D W. The pathogenesis of genitourinary prolapse and stress incontinence of urine. A histological and histochemical study. Br J Obstet Gynaecol 1989; 96: 15. Abitbol MM. Evolution of the ischial spine of the pelvic floor in the Hominoidea. Am J Phys Anthropol 1988; 75: 53. Parks A G, Porter N H. Melzak J. Experimental study of the nflex mechanism controlling the muscles of the pelvic floor. Dis Colon Rectum 1962; 5: 407. Porter N H. A physiological study of the pelvic floor in rectal prolapse. AM R ColJ Surg EngJ 1962; 31: 379. Gollnick P D, Armstrong R B, Saubert IV C W. Piehl K. Saltin B. Enzyme activity and fiber composition in skeletal muscle of untrained and trained men. J Appl Physiol 1972; 33: 3 12. Dixon P J, Christmas T J, Chapple C R. Stress incontinence due to pelvic floor muscle involvement in limb-girdle muscular dystrophy. Br J Ural 1990, 65: 653. Dennett X. Fry H R H. Overuse syndrome: a muscle biopsy study. Lancet 1988; 1: 905. Edwards R H T. Hypotheses of peripheral and central mechanisms underlying occupational muscle pain and injury. Eur J Appl Physiol 1988; 57: 275.
1 M.&al tlpl&s~ (1993) Y. 381s3fl2 oL.qImlc3mupuKLtd1993
Stress Urinary Incontinence in Women-An Syndrome
Overuse
M.J6iWIK The Department of Gynecology 15-062 Bialystok, Poland
and Septic Obstetrics, Medical Academy, Bialystok,
Ul,
Warszawska 15,
Abstract-The levator ani muscles in women are overloaded by constant supporting abdominal contents, and counteracting rises of abdominal pressure at the level of the urethra. The excessive load leads to a decrease in their type II fibers. This results in stress urinary incontinence due to loss of the fibers responsible for additional compression of the urethra at strain.
Introduction
Clinical background
According to the criteria of the International Continence Society (l), stress urinary incontinence (SUI) in women is described as an involuntary loss of urine via urethra in the absence of bladder detrusor muscle contraction. The main feature of this troublesome and frequent disorder is decreased urethral pressure at strain and/or at rest. Normally, rises in abdominal pressure generate a reflex contraction of the levator ani muscles exerting then an additional external compression of urethral walls, and thus preventing passive leakage of urine. From a physiological standpoint (2), the levatores a&-typical skeletal muscles-contain fibers of two types: type I-white slow-twitch fibers, capable of longer but weak contractions, and type II-red fasttwitch fibers recruited at higher work loads, able to maintain contraction for a very short time. The presence of both types of fibers has been histologically contirmed in these muscles (3). Their functional specialization has been suggested (4, 5). Type II fibers seem to be fitted for counteracting urination in stress conditions.
In contrast to quadrupeds, the pelvic floor in Hominoidea achieved a horizontal position (6) and began to play the main role in supporting pelveo-abdominal contents. Evidence of a state of constant active contraction of the levatores ani has been demonstrated (7, 8). This is a unique situation for skeletal muscle. Skeletal muscles are not structurally prepared to exert prolonged excessive work. Such a condition results in an increase of the type I fibers content, i.e. in a decrease of fast-twitch fibers’ quantity, as observed by Gollnick et al (9) in human soleus muscle. A decrease of the type II fibers in the levatores ani in SUI was observed by several authors (4,5, 10). If we take into consideration the fact that SUI patients often have a history of pain located somewhere in the region of the urethra in the absence of symptoms of intlammation and positive urine cultures, one can suspect an overuse syndrome. As defined originally by Dennet and Fry (1 l), the syndrome is ‘a musculoskeletal disorder character&d by pain, tenderness, and often functional loss in muscle groups and ligaments subjected to heavy or unaccustomed use’. Complaints of
Date received25 January 1993 Date accepted 1 March 1993
381
382
MEDICAL BYFQlHE%g
pain given by SUI patients are very likely to be of muscular origin and conform to a recent theory of occupational myalagia (12). Conclusions Taking it all together, as SUI is not observed in the animal world, it is possible that with assumption of erect posture in humans the pelvic contents and abdominal viscera began to exert an excessive pressure on the pelvic floor mobilising the levatores ani to too intensive work. This promotes in some women a progressive overuse deficit of the type II fibers which leads directly to SUI.
4.
5.
6. 7* s. 9.
References 10. Abrams P, Blaivas J G. Stanton S L, Anderson J T. The standardisation of temtinology of lower urinary tract function. Stand J Urn1 Nephrol (Suppl) 114: 5, 1988. Sjiisviim M jingquist K-A, Bylund A-C. Frid6r-1J, Gustavsson L. Scherst6n T. Morphcsnetric analyses of human muscle fiber types. Muscle and Nerve, 1982; 5: 538. Gosling J A. Dixon J S, Critchley H 0 D, ‘lbompsco S-A. A
11. 12.
comparative study of the human external sphincter and periurethml levator ani muscles. Br J Ural 1981; 53: 35. Koelbl H, Strassegger H, Riss P A, Gruber H. Morphologic and functional aspects of pelvic floor muscles in patients with pelvic relaxation and genuine stress incontinence Obstetrics and Gynecology 1989; 74: 789. Gilpin S A, Gosling J A, Smith A R B, Warrell D W. The pathogenesis of genitourinary prolapse and stress incontinence of urine. A histological and histochemical study. Br J Obstet Gynaecol 1989; 96: 15. Abitbol MM. Evolution of the ischial spine of the pelvic floor in the Hominoidea. Am J Phys Anthropol 1988; 75: 53. Parks A G, Porter N H. Melzak J. Experimental study of the nflex mechanism controlling the muscles of the pelvic floor. Dis Colon Rectum 1962; 5: 407. Porter N H. A physiological study of the pelvic floor in rectal prolapse. AM R ColJ Surg EngJ 1962; 31: 379. Gollnick P D, Armstrong R B, Saubert IV C W. Piehl K. Saltin B. Enzyme activity and fiber composition in skeletal muscle of untrained and trained men. J Appl Physiol 1972; 33: 3 12. Dixon P J, Christmas T J, Chapple C R. Stress incontinence due to pelvic floor muscle involvement in limb-girdle muscular dystrophy. Br J Ural 1990, 65: 653. Dennett X. Fry H R H. Overuse syndrome: a muscle biopsy study. Lancet 1988; 1: 905. Edwards R H T. Hypotheses of peripheral and central mechanisms underlying occupational muscle pain and injury. Eur J Appl Physiol 1988; 57: 275.