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.
Keywords: External anal sphincter; Fecal incontinence; Muscle architecture.