Introduction and hypothesis: Obstetrical external anal sphincter (EAS) injury and subsequent dysfunction are leading risk factors for female fecal incontinence (FI). Limited knowledge of the EAS structure–function relationship hinders treatment optimization. We directly measured functionally relevant intrinsic parameters of human EAS and tested whether vaginal delivery alters the EAS structure–function relationship. Methods: Major predictors of in vivo EAS function were compared between specimens procured from vaginally nulliparous (VN, n = 5) and vaginally parous (VP, n = 7) cadaveric donors: operational sarcomere length (Ls), which dictates force–length relationship; physiological cross-sectional area (PCSA), which determines isometric force-generating capacity; fiber length (Lfn), responsible for muscle excursion and contractile velocity; and muscle stiffness. Data were analyzed using unpaired and paired t tests, α < 0.05. Results are presented as mean ± SEM. Results: The VN and VP (median parity 3) groups were similar in age and BMI. No gross anatomical defects were identified. EAS Ls (2.36 ± 0.05 μm) was shorter than the optimal Lso (2.7 μm), at which contractile force is maximal, P = 0.0001. Stiffness was lower at Ls than Lso (5.4 ± 14 kPa/μm vs 35.3 ± 12 kPa/μm, P < 0.0001). This structural design allows active and passive tension to increase with EAS stretching. EAS relatively long Lfn (106 ± 24.8 mm) permits rapid contraction without decreased force, whereas intermediate PCSA (1.3 ± 0.3 cm2) is conducive to maintaining resting tone. All parameters were similar between groups. Conclusions: This first direct examination of human EAS underscores how EAS intrinsic design matches its intended function. Knowledge of the EAS structure–function relationship is important for understanding the pathogenesis of FI and the optimization of treatments for EAS dysfunction.
Bibliographical noteFunding Information:
Funding This study was funded by the Society of Urodynamics, Female Pelvic Medicine, and Urogenital Reconstruction Research Foundation Grant for the Study of Overactive Bladder and Fecal Incontinence, and NICHD R03HDO75994 and K12HD001259 grants.
The authors would like to thank The University of Minnesota?s Anatomy Bequest Program and the individuals who donated their bodies for the advancement of education and research. This study was funded by the Society of Urodynamics, Female Pelvic Medicine, and Urogenital Reconstruction Research Foundation Grant for the Study of Overactive Bladder and Fecal Incontinence, and NICHD R03HDO75994 and K12HD001259 grants.
© 2017, The International Urogynecological Association.
- External anal sphincter
- Fecal incontinence
- Muscle architecture