Background
Vaginal delivery and aging are key risk factors for pelvic floor muscle dysfunction, which is a critical component of pelvic floor disorders. However, alterations in the PFM intrinsic structure due to childbirth and aging that lead to muscle dysfunction remain elusive.
Objectives
To determine the impact of vaginal deliveries and aging on human cadaveric PFM architecture, the strongest predictor of active muscle function.
Study Design
Coccygeus, iliococcygeus and pubovisceralis were obtained from younger, ≤ 51 years, vaginally nulliparous (N=5) and vaginally parous (N=6), and older, >51 years, vaginally nulliparous (N=6) and vaginally parous (N=6) donors without history of PFDs. Architectural parameters, predictive of muscle’s excursion and force-generating capacity, were determined using validated methods. Intramuscular collagen content was quantified by hydroxyproline assay. Main effects of parity and aging and the interactions were determined using two-way ANOVA, with Tukey’s post-hoc testing with significance level of 0.05.
Results
The mean age of younger and older donors differed by ~40 years (P=0.001), but was similar between nulliparous and parous donors within each age group (P>0.9). Median parity was 2 (range 1–3) in younger and older vaginally parous groups, P=0.7. The main impact of parity was increased fiber length in the more proximal coccygeus (P=0.03), and iliococcygeus (P=0.04). Aging changes manifested as decreased physiological cross sectional area across all pelvic floor muscles, P<0.05, which substantially exceeded the age-related decline in muscle mass. Physiological cross sectional area was lower in younger vaginally parous, compared to younger vaginally nulliparous pelvic floor muscles, however the differences did not reach statistical significance. Pelvic floor muscles’ collagen content was not altered by parity, but increased dramatically with aging, P<0.05.
Conclusions
Increased fiber length in more proximal pelvic floor muscles likely represents an adaptive response to the chronically increased load placed on these muscles by the displaced apical structures, presumably as a consequence of vaginal delivery. In younger specimens, a consistent trend towards decrease in force generating capacity of all pelvic floor muscles in parous group suggests a potential mechanism for clinically identified pelvic floor muscle weakness in vaginally parous women. The substantial decrease in predicted muscle force production and fibrosis with aging represent likely mechanisms for the pelvic floor muscle dysfunction in older women.