Pelvic floor disorders negatively impact ~30% of women in the United States. Pelvic organ prolapse, a type of pelvic floor disorder characterized by the descent of abdominal organs from their normal positions, is caused by damage to pelvic floor muscles (PFMs). PFM injury contributing to prolapse is often due to childbirth, with computational studies estimating a greater than 300% strain of a PFM during vaginal fetal delivery. Previous studies on PFM damage have been done in non-pregnant rats, where long-term PFM dysfunction was shown to be triggered by sustained inflammation, long term muscle atrophy, and fibrosis. However, these studies fail to incorporate lactation as a variable, with studies suggesting that lactating individuals have a decreased regenerative capacity due to low estrogen levels. The interplay between immune response, lactation, and regeneration following maternal birth injury is not completely understood, requiring further research to design better regenerative therapies. I hypothesize that simulated birth injury in a biologically relevant pregnant rat model will depict a pro-inflammatory postpartum environment that delays regeneration and decreases muscle function in lactating rats compared to non-lactating rats. This talk will characterize long-term PFM pathophysiology in a simulated birth injury pregnant rat model. Future directions discussed will detail a multi-scale approach utilizing biomechanical testing and the potential for a minimally invasive extracellular matrix hydrogel.