It is particularly well-known that the childbirths lead to the weakening of pelvic floor muscles (PFM) and pelvic nerve to the onset of stress urinary incontinence (SUI). A previous study demonstrated that simulated birth trauma with vaginal distention in rats induces urethral dysfunction and SUI1). In addition, lower urethral resistance was obtained in the rats whose pelvic nerve somatomotor branch (Smb) to pubococcygeus muscles (Pcm) were transected bilaterally2). Thus, PFM play important roles in lower urinary tract functions. Peripheral nerve injury causes denervation and causes a great variety of muscle changes such as atrophy. In the skeletal muscle, it is reported that a change in morphology and fiber type distribution occurs after nerve transection. However, it is unknown that nerve injury after childbirth occurs PFM compositions change. From the above, it is expected that nerve injury after childbirth will cause muscle atrophy of the PFM and change muscle fiber type distribution. The aim of this study is that morphological examination of pelvic floor muscle in transection of Smb in rats.

Seventeen female Sprague-Dawley rats (210-330g) were used in the present study. The animals were divided into 3 groups; (1) a control group (n=5), (2) 4-week after transected the Smb (1M group, n=6), and (3) 12-week after transected the Smb (3M group, n=6). In the1M and 3M groups, Smb transection was carried out under sodium pentobarbital anesthesia. One side Pcm used as sample muscles. A midline incision was made from the abdomen to the perineal vagina and harvest Pcm, and its wet weight was measured. We used the ATPase (pH10.2) and succinate dehydrogenase (SDH) activity to identify muscle fiber type (typeⅠ, typeⅡa, typeⅡb）distribution. One-way analysis of variance was performed to compare the data among 3 groups. P value of less than 0.05 was regarded to be statistically significant. The present study was conducted after being approved by Animal Study Facility Ethics Committee in our institute.

The Pcm wet weight was significantly lower in 1M group (p = 0.022) and 3M group (p = 0.015) than in control group (Fig 1). After 1 month of transection, the percentage of typeⅠfibers showed significantly decreased compared to the control group. The percentage of typeⅠ fibers decreased from 11.9 ± 3,4 % to 6.2 ± 2.0% (p = 0.022) (Fig 1, 2). TypeⅡa was not significantly different in each group. TypeⅡb showed 1M group significantly higher than 3M group.

To our knowledge, this is the first study to demonstrate that morphological changes of PFM in transection of Smb in rat model. We showed that Pcm weight was decreased significantly in 1 month after transection as compared to the control group. The previous study reported that skeletal muscle atrophy after denervation is considered to occur in 1 month. In our results revealed that the PFM atrophy was also observed at least 1 month after nerve damage. 

We found that the percentage of Pcm type I fibers significantly reduced 1month after nerve transection. The previous study investigating histological changes in lower extremity muscles have been shown that type I fibers decreased 1 month after nerve transection. This change could lead to reduced sustained muscle strength. PFM is known to be damaged due to pudendal nerve injury induced by vaginal delivery. The previous study showed that the Smb transection model induced SUI. It rational because it mimics what happen clinically. Also, we confirmed the PFM compositions change of Smb transection model. From the above, it is thought that the PFM compositions change is related to the cause of impaired urethral function. Smb transection model is validated for SUI.

The muscle fiber type distribution in Pcm of normal rats have mainly typeⅡfibers (88.1%). This result is consistent with previous study3). In humans, the ratio of typeⅠtoⅡfibers in PFM is approximately 3:2. Therefore, the percentage of typeⅠ/ typeⅡfibers of PFM differs between in humans and in rats. Further clinical studies will be necessary to confirm the changes of muscle fiber distributions induced by vaginal delivery in humans.

In conclusion, these findings suggest that childbirth is involved in PFM atrophy and degeneration and may contribute to the elucidation of the mechanism of SUI.

Am J Physiol Renal Physiol. 2017; 313(5): 1089-1096.
Am J Physiol Renal Physiol. 2007; 293(3): 920-926.
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