What causes women to develop weak pelvic floor muscles, particularly during childbirth, menopause, or with certain medical conditions?

Why Women Develop Weak Pelvic Floor Muscles

Women develop weak pelvic floor muscles primarily through mechanical injury during vaginal childbirth, where soft tissues must stretch to more than 3 times their original length, causing levator ani muscle avulsion, perineal body disruption, and pelvic muscle fiber separation—injuries that occur in up to 19% of primiparous women and carry a 7.3 odds ratio for developing prolapse later in life. 1, 2

Primary Mechanisms of Pelvic Floor Weakness

Childbirth-Related Mechanical Injury

Vaginal delivery causes direct structural damage through extreme tissue stretching:

• The pelvic floor, anal canal, and bladder/urethral support structures must stretch considerably during vaginal birth, resulting in levator ani muscle injury and avulsion 1
• Even without visible perineal tears, ultrasound reveals separation or disruption of pelvic muscle fibers in many women 1
• This overstretching—not compression or neuropathy—is the primary mechanism responsible for muscle tears visible on imaging 2
• Women with levator ani avulsion face significantly greater risks of symptomatic prolapse 1

Instrumental delivery amplifies tissue damage:

• Forceps delivery, despite protecting the fetus, associates with substantially greater maternal tissue damage and levator injury risk 1, 2
• Vacuum delivery associates with reduced levator damage compared to forceps 2
• Occiput posterior birth position increases injury risk 2

Time-dependent injury progression:

• Both intrinsic and extrinsic susceptibility factors increase with labor duration 1
• Prolonged first or second stages of labor increase intervention likelihood and subsequent injury risk 1

Measurable Functional Decline

Pelvic floor muscle strength drops significantly after vaginal delivery:

• Normal vaginal delivery reduces muscle strength by 20.1 hPa (95% CI: 16.2-24.1) at 6-12 weeks postpartum 3
• Instrumental vaginal delivery reduces strength by 31.4 hPa (95% CI: 7.4-55.2) 3
• Acute cesarean section results in significantly less reduction at only 5.2 hPa (95% CI: -6.6-17.0) 3
• Women with at least one vaginal delivery show significantly higher rates of low peak pressure (<20 cm H₂O) compared to cesarean-only deliveries (243 of 588 vs 107 of 555, p<0.001) 4

Low pelvic floor muscle strength predicts disorder development:

• Among women with vaginal delivery history, peak pressure <20 cm H₂O associates with shorter time to stress incontinence (time ratio 0.67,95% CI: 0.50-0.90), overactive bladder (time ratio 0.67,95% CI: 0.51-0.86), and pelvic organ prolapse (time ratio 0.76,95% CI: 0.65-0.88) 4
• No such association exists among cesarean-only deliveries 4

Secondary Contributing Factors

Hormonal Changes During Menopause

Estrogen deficiency negatively impacts pelvic floor integrity:

• Aging, structural changes, and estrogen deficiency have documented negative impacts on the pelvic floor 5
• Hypoestrogenism causes genitourinary menopause syndrome affecting vulvo-vaginal structures, urethra, and bladder 1
• Menopause represents an established risk factor for pelvic floor dysfunction 6

Chronic Mechanical Stress

Sustained increases in intra-abdominal pressure weaken pelvic floor over time:

• Chronic straining during defecation contributes to pelvic floor dysfunction 6, 7
• Conditions causing chronic increased intra-abdominal pressure (chronic cough, heavy lifting, obesity) lead to chronic overstraining 6, 5
• Obesity independently increases pelvic floor dysfunction risk 6

Pregnancy-Related Changes

Pregnancy itself initiates structural alterations:

• Softening of the symphysis pubis and sacroiliac joints during pregnancy leads to longer-term symphyseal or pelvic girdle pain 1
• Tissue laxity develops over the longer term, progressing to pelvic organ prolapse or incontinence 1

Additional Risk Factors

Demographic and obstetric characteristics modify injury risk:

• Advanced age at delivery increases levator injury risk 6, 2
• Vaginal multiparity compounds risk 6
• Birthweight >4000g increases injury likelihood 2
• Long second stage of labor elevates risk 2

Clinical Consequences

These injuries result in tissue laxity and functional impairment:

• Enlarged urogenital hiatus precedes prolapse development 2
• Levator injury appears in 55% of women with prolapse later in life, with odds ratio of 7.3 compared to women with normal support 2
• Approximately 25-33% of postmenopausal women develop pelvic organ prolapse 8, 6
• Lifetime risk of requiring surgical intervention by age 80 reaches 11%, with 29% reoperation rate 8

Critical Clinical Pitfall

Knowledge deficits prevent early intervention:

• On a 0-10 scale, peripartum women rate their pelvic floor knowledge at only 4.38 (SD 2.71) and postmenopausal women at 4.92 (SD 2.72) 9
• 75% of peripartum women and 68% of postmenopausal women feel insufficiently informed 9
• Insufficient knowledge about pelvic floor dysfunction represents the largest barrier to seeking care 9