Keywords

6.1 Introduction

Pregnancy and childbirth bring along several changes to a woman’s body, especially to the musculoskeletal system. Pregnancy represents a window of opportunity for the adoption of an active and healthy lifestyle, but it is also a risk period for musculoskeletal disorders, impairments, and other discomforts. This chapter addresses the evidence-based knowledge on the most prevalent pelvic floor muscle dysfunction (urinary incontinence), diastasis recti abdominis, pregnancy-related low back pain and/or pelvic girdle pain, since these factors are reported to have a negative effect on daily activities. The chapter also provides recommendations for treatment of such disorders and guidance on how to recover functional capacity.

6.2 The Pelvic Floor

The urethra, bladder, vagina, uterus, and bowel situated within the pelvis are given structural support by pelvic floor structures arranged into a superficial and a deep layer of muscles and connective tissue (ligaments and fascia) [1]. In addition to pelvic organ support, the pelvic floor maintains continence, permitting urination, defecation, intercourse, and vaginal birth [1].

The superficial layer of the pelvic floor includes the perineal muscles (ischiocavernosus, bulbospongiosus, and transversus perinei superficialis), and the deep layer includes the levator ani (LA) muscle [1]. These pelvic floor layers in addition to the urethral and anal sphincter system (external and internal sphincter muscles and vascular elements within the submucosa) play a significant role in maintaining pelvic organ support and continence [1,2,3].

The pelvic floor muscles (PFM) interact with the supportive ligaments and fasciae in order to maintain support of the pelvic organs and protect the pelvic floor connective tissue from excessive loads [3,4,5]. The function of this supportive system is illustrated by the “boat in dry dock theory” by Norton [5], where the PFM act as water in the dock floating the boat (pelvic organs) unloading the mooring (ligaments and fasciae) holding the boat in place. If the water is removed (loss of pelvic floor muscle tone), the moorings (pelvic ligaments and fasciae) are placed under excessive strain.

A voluntary PFM contraction can best be described as an inward lift and squeeze around the urethra, vagina, and rectum [6, 7]. During a voluntary PFM contraction, the medial portion of the LA muscle interacts with the endopelvic fasciae and compresses the urethra against adjacent tissues, which creates increased urethral pressure and stabilization of the urethra and bladder neck [2, 3].

The normal baseline activity of the PFM keeps the pelvic openings closed and keeps the pelvic floor elevated in a cranial direction [4, 8]. In situations where abdominal pressure increases, during physical exertions such as coughing, laughing, high-impact activities, etc., a simultaneous well-timed PFM contraction will counteract the increased abdominal pressure by increased structural support and compression of the urethra [2,3,4, 9]. The PFM is supposed to react automatically when the abdominal pressure increases. The pelvic floor works like a “firm trampoline” giving a quick response when loads are put onto it [10].

Together with the urethral sphincter muscles, the PFM play an important role for maintaining urinary continence [2,3,4, 9]. The mechanical supportive potential of the PFM is demonstrated by Miller et al. [11]. By perineal ultrasound assessment, they found that a voluntary contraction of the PFM prior to and during a cough (a maneuver called the “Knack”) resulted in a significant reduced displacement of the bladder neck [11]. Use of the “Knack” maneuver has also shown to significantly reduce urine loss among women with SUI [12, 13].

6.2.1 Pelvic Floor Dysfunction and Risk Factors

The understanding of the development of pelvic floor muscle dysfunction is far from complete. Rather than a single factor, the most common types of pelvic floor dysfunction (UI, fecal incontinence, and pelvic organ prolapse) probably have a complex list of risk factors [14,15,16]. Factors that may lead to the development of pelvic floor impairment and dysfunction in women can according to Bump and Norton [14] be classified into the following four categories:

  • Predisposing factors: e.g., gender, racial, neurologic, anatomic, collagen, muscular, cultural, and environmental.

  • Inciting factors: e.g., childbirth, nerve damage, muscle damage, radiation, tissue disruption, and radical surgery.

  • Promoting factors: e.g., constipation, occupation, recreation, obesity, surgery, lung disease, smoking, menstrual cycle, infection, medication, and menopause.

  • Decompensating factors: e.g., aging, dementia, debility, disease, environment, and medication.

DeLancey et al. [16] integrate factors affecting pelvic floor dysfunction into an “Integrated Lifespan Model,” in which pelvic floor function is plotted into three major life phases: (1) development of functional reserve during growth, influenced by predisposing factors, e.g., genetic constitution; (2) amount of injury and potential recovery occurring during and after childbirth; and (3) deterioration occurring with advancing age. Throughout the lifespan a decline of the functional reserve of the pelvic floor may be accelerated by other factors, e.g., obesity and chronic coughing, medications, and dementia.

Knowledge about the various risk factors and their relative importance in relation to type of pelvic floor dysfunction is essential for primary and secondary prevention strategies [14, 16].

6.2.2 Urinary Incontinence

UI has been defined by the International Continence Society as “the complaint of any involuntary leakage of urine” and can further be classified into subtypes with the following definitions [17]:

  • Stress urinary incontinence (SUI): “the complaint of involuntary leakage on effort or exertion, or on sneezing or coughing.”

  • Urge urinary incontinence (UUI): “the complaint of involuntary leakage accompanied by or immediately proceeded by urgency.”

  • Mixed urinary incontinence (MUI): “the complaint of involuntary leakage associated with urgency and also with exertion, effort, sneezing, or coughing.”

6.2.2.1 Prevalence

A systematic literature review by Hunskaar et al. [18], including 36 epidemiological studies from 17 countries, showed a prevalence of any UI within the range 5–69% among the general female population. However, most of these studies showed a UI prevalence within the range 25–45% [18]. A wide range in UI prevalence might be explained by differences in the population studied, definition of UI, type of UI, and assessment of UI [19,20,21]. According to an updated review on UI prevalence by Milsom et al. [22], recent epidemiological studies report estimates on UI prevalence that are within the prevalence range reported by Hunskaar et al. [18]. The most common type of UI reported by young and middle-aged women is SUI, while older women are more likely to report MUI and UUI [18, 22].

6.2.2.2 Prevalence During Pregnancy

Studies of prevalence of UI during pregnancy have shown period prevalence within the range 32–64% for any type of UI and 40–59% for the combination SUI/MUI [18, 22]. Higher period prevalence has been reported in parous than in nulliparous women [23,24,25,26,27]. The largest prospective population-based study included in the review by Milsom et al. [22] is the study published by Wesnes et al. [27]. This study was part of the Norwegian Mother and Child Cohort Study. Results showed that prevalence of UI increased from 15% before pregnancy to 48% at gestational week 30 for nulliparous women and from 35% before pregnancy to 67% at gestational week 30 for parous women. SUI was the most common type of UI with figures showing an increase from 9% before pregnancy to 31% at gestational week 30 for nulliparous women and from 24% to 42% for parous women.

6.2.2.3 Prevalence After Childbirth

The estimation of postpartum UI is, according to Milsom et al. [22], challenged by study heterogeneity (study design and method, definition of UI, and sample studied). In their review they therefore chose to summarize data from 22 studies on primiparous women enrolled at larger hospitals serving a defined population. The range of UI prevalence (any type) in primiparous women during the first year postpartum, regardless of delivery mode, was 15–30%. According to Milsom et al. [22], the included studies showed consistently higher UI prevalence in women who delivered vaginally than in women who delivered by caesarean section, with the exception of one study [28].

6.2.3 Etiology and Pathophysiology of Urinary Incontinence

UI also occurs in women who never have gone through pregnancy and childbirth. However, pregnancy and childbirth are considered main etiological factors for the development of UI [29]. Connective tissue, peripheral nerves, and muscular structures are already during pregnancy subjected to hormonal, anatomical, and morphological changes. During vaginal delivery, the abovementioned structures are forcibly stretched and compressed. This may initiate changed tissue properties, which may contribute to altered pelvic floor function and increased risk of UI [29]. The picture of possible causative factors and the pathophysiology of UI are complex, some factors are studied more than others, and the importance of factors associated by the pregnancy itself versus factors associated childbirth is still under discussion [29].

6.2.3.1 Pregnancy

Prospective observational studies have shown increased prevalence of UI from the first trimester to the second and further into the third trimester [26, 30, 31]. One hypothesis of increased prevalence during pregnancy is linked to increased bladder pressure due to the growing uterus and weight of the fetus, and another is linked to hormonal changes altering the viscoelastic properties [26]. In the observational study by Hvidman et al. [26], the authors suggest that UI may not be provoked by the onset of pregnancy but by its progressive concentration of pregnancy hormones which may lead to local tissue changes. They found no association between UI and the birth weight of the child and state less support for the theory linking UI to increased pressure on the bladder caused by weight of the fetus. Studies have shown an association between UI and maternal obesity both during pregnancy [27] and after childbirth [32,33,34], which could be caused by increased intra-abdominal pressure and increased bladder pressure [35].

The PFM is considered to play a significant role in the continence control system [2,3,4, 9], and urine loss may be linked to impaired PFM function, e.g., weak PFM. Several observational studies have demonstrated significantly higher PFM strength in continent women than in women having UI [36,37,38,39,40,41,42,43], while some studies did not find such difference [44, 45]. Two of the abovementioned studies were on pregnant women [36, 40, 43]. In addition to significantly higher PFM strength, Mørkved et al. [40] also report a significantly thicker PFM among the continent pregnant women.

UI during pregnancy is transient in some women but may become long-lasting in others. Prospective observational studies have shown that antenatal UI may increase the risk of postpartum UI [34, 46,47,48].

6.2.3.2 Childbirth

Parity seems to be an increased risk factor for UI [15, 24, 31, 49,50,51]. In a cross-sectional study of 27,900 women, Rortveit et al. [50] report a relative risk (RR) of UI of 2.2 (95% CI, 1.8–2.6) for primiparous women and 3.3 (95% CI, 2.4–4.4) for grand multiparous women. Altman et al. [48] included 304 primiparous women and followed them 10 years prospectively. They found vaginal delivery to be independently associated with a significant long-term increase in SUI and UUI, regardless of maternal age and number of deliveries. This is supported by Viktrup et al. [34] following 241 primiparous women 12 years after their first delivery.

The protective effects of caesarean section have been and still are much debated. In a systematic review by Press et al. [52], the prevalence of postpartum SUI after caesarean section was compared with vaginal delivery. Based on data from six cross-sectional studies, caesarean section reduced the risk of postpartum SUI from 16% to 10% (OR 0.56; 95% CI, 0.45–0.68), while data from 12 cohort studies gave a reduction from 22% to 10% (OR 0.48; 95% CI, 0.39–0.58). However, risk of severe SUI and UUI did not differ by mode of birth.

6.2.3.3 Bladder Neck and Urethral Hypermobility

Impaired structural support of the urethra may cause increased bladder neck mobility and reduced compression of the urethra which again may lead to UI [3]. Peschers et al. [53] investigated change in bladder neck mobility, during the Valsalva maneuver, from late pregnancy to 6–10 weeks postpartum. They found increased mobility in women who delivered vaginally (p < 0.001) but found no such change in women with elective caesarean section (p = 0.28). Their findings are supported by Meyer et al. [54] and Dietz et al. [55].

Meyer et al. [56] found significantly higher bladder mobility, during the Valsalva maneuver, in women with SUI (mean parity 2.4, SD 0.8) when compared to nulliparous continent women. However, the association between increased bladder neck mobility and SUI may not solely be explained by vaginal childbirth. King and Freeman [57] followed nulliparous pregnant women with no preexisting UI from gestational week 15–17 to 10–14 weeks postpartum. They found that primiparous women with SUI postpartum had significantly greater antenatal bladder neck mobility than continent counterparts, which could be explained by a predisposed weak connective tissue, aggravated by pregnancy hormones and collagen remodeling [57, 58].

A study on bladder neck mobility and tissue stiffness was performed by Howard et al. [59]. Results from their study showed that primiparous women with SUI displayed similar bladder neck mobility during a cough and during a Valsalva maneuver (p = 0.49), while significantly less mobility was displayed during a cough than during the Valsalva both for continent nulliparous women (p = 0.001) and for continent primiparous women (0.002). When controlling for abdominal pressures, their calculations showed that nulliparous women displayed a significantly greater pelvic floor stiffness during a cough than the continent and incontinent primiparous women (p = 0.001).

6.2.3.4 Neural Denervation

Neuromuscular impairment is associated with the development of incontinence. Smith et al. [60] found that terminal branches of the pudendal nerve had a delayed conduction both to the striated urethral muscle and to the PFM in women with SUI when compared to continent women. Such denervation seems to be related to parity and vaginal childbirth [61,62,63,64]. In a biomechanical study by Lien et al. [65], lengthening of pudendal nerve branches was simulated by using a 3D computer model. The results from this study showed that the inferior rectal branch of the pudendal nerve may exhibit a strain of 35%. Pudendal nerve neuropathy appears to be associated with both a long second stage and high birth weight [63, 66, 67]. Such neural impairment may alter the muscle morphology. In a study by Gilpin et al. [68], biopsy samples from women with SUI showed a significant higher number of muscle fibers with pathological damage when compared to biopsy samples from continent women.

6.2.3.5 Weakening of the Pelvic Floor Muscles

Vaginal delivery is considered as a main risk factor for weakening of the PFM [63, 66, 69,70,71,72,73,74]. Due to the extensive stretching of muscle fibers and the likelihood of muscle denervation, it is not surprising that vaginal delivery may lead to reduced vaginal resting pressure and impaired PFM strength and endurance and that caesarean section may protect the PFM. A PubMed search gave seven studies [36, 54, 75,76,77,78,79] investigating change in PFM strength from pregnancy to shortly after childbirth in relation to mode of delivery. Except from one study [77], the other six studies showed a significant reduction in PFM strength after vaginal delivery, but no significant decline after caesarean section.

6.2.4 Levator Ani Muscle Defects

Vaginal delivery may stretch and load beyond the physiological properties of the PFM, which may lead to muscle fiber tearing and reduced contractile force. The biomechanical study by Lien et al. [80] showed that muscle fibers, of the most medial part of the LA muscle, might be stretched up to three times their resting length as the fetal head is crowning. Their findings showing a pronounced stretch and deformation of the medial part of the LA muscle are confirmed by Hoyte et al. [81] and Parente et al. [82].

During recent years, technical advancement within magnetic resonance and ultrasound imaging has enabled diagnosis of defects of the LA muscle [83]. Major defects of the LA muscle are often defined as an abnormal insertion of this muscle toward the pubic bone, visually seen as a complete loss of visible muscle attachment at this specific site either unilaterally or bilaterally [69, 72, 83]. Imaging studies have shown that major LA muscle defects among primiparous women delivering vaginally could appear in 20–36% of the women [69, 84]. The use of forceps [70] and length of the second stage [70, 85] are associated with major LA muscle defects, whereas the importance of fetal head circumference and high fetal birth weight seems to be less clear [84,85,86].

Decreased strength is one of the most common symptoms following muscle tears within sport injuries [87]. Hence, decreased PFM strength in women with major LA muscle defects is expected but has been sparsely investigated. A PubMed search revealed five observational studies [88,89,90,91,92] in which PFM strength in women with and without LA muscle defects was assessed. Results from all five studies showed significantly reduced PFM strength in women with LA muscle defects when compared to women without such defects. Dynamometer was used for assessment of PFM strength in two of these five studies [88, 91], digital palpation in one study [89], transperineal ultrasound in one [90], and manometer in one [92]. These studies did also differ in age and parity of the women included.

Major LA muscle defects have shown a marked effect on hiatal dimensions [93,94,95] and pelvic organ support [95] which in turn could be explanatory factors for pelvic floor dysfunction. Major defect of the LA muscle has been linked to pelvic organ prolapse in particular [83, 88, 96, 97], while the link between LA muscle defects and UI is debated. Two studies [69, 84] report a significant association between LA muscle defects and SUI in the postpartum period. However, contradictory findings are reported for the link between LA muscle defects and SUI in studies on women with mixed parity and mean age >50 years [86, 98, 99].

6.2.5 Muscle Injury Regeneration

The healing process of a torn muscle has three phases: (1) the destruction phase, (2) the repair phase, and (3) the remodeling phase [87, 100, 101]. In the destruction phase, the rupture is followed by necrosis and formation of a hematoma. In the repair phase, a phagocytosis of necrotized tissue takes place, followed by proliferation of skeletal muscle satellite cells which induce regeneration of myofibrils. Along with this is formation of scar tissue and revascularization of the injured area initiated. During the remodeling phase, a further maturation of the regenerated myofibrils is implemented together with remodeling of the scar tissue, followed by recovery to functional capacity [87, 100, 101].

6.2.5.1 Treatment Principles for Skeletal Muscle Injuries

Recommendations for treatment of muscle injuries and how to recover functional capacity are most often based on theoretical framework from epidemiological studies, clinical practice, and findings from experimental research [102]. Early mobilization is a standard treatment after muscle injury within sports medicine, and training is believed to be important in speeding up tissue healing (repair and remodeling). This approach is supported by experimental studies showing that early mobilization after a muscle injury may facilitate the following: more rapid capillary ingrowths, improved parallel orientation of the regenerating myofibrils, and improved tensile properties [87, 100, 101, 103].

6.3 Diastasis Recti Abdominis

Pregnancy and childbirth bring along several changes to a woman’s body, especially to the musculoskeletal system [104]. The most obvious change is related to the growth of the fetus and the stretching of the abdominal muscles, which may influence the mother’s posture and balance [104]. Today there is a strong focus on the pregnant woman’s appearance, especially through social media. Webpages and apps recommend how women should stay thin and get back into shape and “a flat tummy” at an early stage of the postpartum period. Using the search terms “diastasis recti” and “exercise,” 278,000 hits were obtained on Google. In addition, there are easily available advices on how to get rid of what is named “the mum’s belly” (e.g., www.mammamage.se, www.breakingmuscle.com, www.befitmom.com, www.babybellybelt.com, tummyzip.com). A systematic review of the scientific literature has found none or very weak evidence behind any of these advices [105].

A strong focus on an area of the body that is naturally changed during pregnancy and after childbirth and that may recover by itself over time maybe a risk factor for development of an unhealthy attitude toward exercise, appearance, body shape, and image, and new mothers may become dissatisfied with their bodies and especially their abdomen. On the other hand, pregnancy and childbirth are risk periods for the development of obesity and musculoskeletal complaints such as low back and pelvic girdle pain [106] and pelvic floor dysfunctions including urinary and anal incontinence and pelvic organ prolapse [107]. A possible link between these conditions and injuries and weakness of the abdominal muscles has been postulated [108].

Diastasis recti abdominis (DRA) is defined as an impairment with midline separation of the two rectus abdominis muscles along the linea alba. The condition affects a significant number of women during the antenatal and postnatal period [109]. Prevalence rates (with and without protrusion/hernia) during pregnancy vary between 27% and 100% in the second and third trimesters [110, 111]. Postpartum, the prevalence rates of DRA vary between 30% and 68% [112, 113]. In a longitudinal study of 300 first-time pregnant women at Akershus University Hospital in Norway, Sperstad et al. [114] found that prevalence rates changed from 33% at gestational week 21 to 60%, 45.4%, and 32.6% at 6 weeks, 6 months, and 12 months postpartum, respectively. However, DRA has been found to be common in middle-aged women [115] and may also be present in men [116]. Whether strong abdominal muscles can prevent or are a risk factor for development of the condition is not known. To date there are no prevalence studies or assessments of this condition among recreational exercisers and elite athletes [104].

DRA is diagnosed by measuring the distance between the median borders of the two rectus abdominis, inter-rectus distance (IRD), and measurement methods in use are palpation with fingerbreadths, caliper, or ultrasound [117]. Palpation is the most commonly used method in clinical practice [118] and has an intra- and inter-tester ICC of 0.7 and 0.5, respectively [119]. However, ultrasound has been found to have the best intra- and inter-tester reliability with ICC > 0.9 [120]. To date there is no consensus on where to measure IRD along the linea alba (frequently used locations are 4.5 cm above the umbilicus, at the umbilicus, and 4.5 cm below the umbilicus) or the cutoff point for diagnosing the condition [117]. A commonly used cutoff point is two fingerbreadths on palpation [117]. Candido et al. [121] have classified severity of the diastasis as mild (2.5–3.5 cm or visible protrusion with diastasis less than 2.5 cm), moderate (3.5–5 cm), and substantial (>5 cm).

The etiology and risk factors for DRA are not clear [122]. Fernandes da Mota et al. [123] found that neither age, BMI, weight gain during pregnancy, hypermobility, birth weight, abdominal circumference at gestational week 35, nor exercise level before and during pregnancy was a risk factor for diastasis 6 months postpartum. This was in agreement with results of Sperstad et al. [114] comparing women with and without diastasis 12 months postpartum. Spitznagle et al. [115] found higher prevalence of DRA in older multiparous women, while Candido et al. [121] did not find any relationship with parity. None of the abovementioned studies found any relationship with mode of delivery (vaginal versus caesarean section) and diastasis.

6.3.1 Consequences of Diastasis Recti Abdominis

It has been postulated that DRA, in addition to being a cosmetic concern for many women, may reduce low back and pelvic stability, cause low back and pelvic girdle pain and be related to pelvic floor dysfunctions such as urinary incontinence, anal incontinence, and pelvic organ prolapse [115, 124]. However, to date there is scant scientific knowledge on this topic. An association between DRA and abdominal muscle strength has not yet been substantiated with strong evidence. In a longitudinal small study following six women from gestational week 14 to 8 weeks postpartum, Gilleard and Brown [125] found that women with IRD >3.5 cm measured with palpation had reduced curl-up “capacity.” This was supported by a study following 40 women postpartum, which found that postpartum women had weaker abdominal muscles than a control group [126]. However, at 6 months postpartum, there was no correlation between IRD and reduced abdominal muscle strength.

No strong link between DRA and low back pain has been found. Parker et al. [127] found that women at least 3 months postpartum with DRA had more abdominal and pelvic pain than women without. However, two other studies did not find any difference in prevalence of low back or pelvic girdle pain in primiparous women 6–12 months postpartum between women with and without DRA [111, 114]. Most of these studies included women with light and moderate diastasis. Hence, it is important to investigate the association between severe diastasis and low back and pelvic girdle pain.

6.4 Pregnancy-Related Low Back Pain and Pelvic Girdle Pain

Pregnancy-related low back pain (LBP) and/or pelvic girdle pain (PGP) is common across many countries, irrespective of socioeconomic factors [128,129,130,131], and is reported to have a negative effect on daily activities such as walking, lifting, climbing stairs, lying flat on the back, turning in bed, housework, exercise, employment, leisure, sexual life, hobbies, and personal relationships [132]. Women with LBP and PGP report a significantly lower health-related quality of life than that reported by healthy women, and a major factor affecting their quality of life is found to be lack of physical ability [133, 134]. PGP during pregnancy greatly affects a woman’s experience of her pregnancy, her roles in relationships, and her social context [135, 136]. These women are struggling with enduring pain that disturbs most aspects of their lives [135, 137], and the pain is perceived as an unpredictable and potentially disabling condition [138]. Whereas most women recover after delivery, a number of women continue living with disabling PGP. Postpartum PGP may influence women’s lives for months and years after delivery. Discouragement, isolation and loneliness may be part of a daily life with pain and limited physical activity [139].

The prevalence rates of pregnancy-related LBP and PGP vary depending on the criteria used and mode of reporting, but are estimated to be about 50% during pregnancy [140]. Whereas LBP is usually defined as pain between the 12th rib and the gluteal fold, PGP is defined as pain experienced between the posterior iliac crest and the gluteal fold, particularly in the vicinity of the sacroiliac joints [106]. PGP generally arises in relation to pregnancy and is defined as pain in the pelvic musculoskeletal system that does not derive from gynecological and urological disorders. A diagnosis of PGP can be reached after the exclusion of lumbar causes, and the pain or functional impairments in relation to PGP must be reproducible by specific clinical tests [106]. Although similar and overlapping features may be ascribed to LBP and to PGP, it is argued that a distinction should be made [106, 140]. PGP has more impact on pain intensity and disability than LBP [141, 142]. Whereas the normal progression of LBP during pregnancy peaks between 12 and 30 weeks [143, 144], PGP increases progressively with advancing pregnancy [145]. Most probably about 20–25% of all pregnant women who suffer from PGP sufficiently seriously require medical help [106, 146]. Though the majority of women with PGP recover spontaneously soon after delivery, 3–7% report having serious problems from persistent PGP years after delivery [140, 147]. In the only study among elite athletes, 12.6% reported retrospectively that they experienced PGP 6 weeks postpartum and 9.7% experienced LBP. The prevalence increased to 19.4% for PGP and 29% for LBP at the time of completing the questionnaire 0–17 years after delivery [148].

The etiology and pathogenesis of PGP are unclear and probably multifactorial. Possible underlying causes include hormonal and biomechanical aspects, inadequate motor control, and stress on ligament structures [149]. PGP often occurs during the early stages of pregnancy [151], and the symptoms typically regress shortly after delivery [147]. A possible association between serum relaxin levels and PGP is debated [147, 150, 151]. The exact movements that occur in the pelvic joints have been traced [152, 153]. Recently, it was shown that the movement in the sacroiliac joints is small and almost undetectable by precise radiostereometric analysis [154]. Even though small, any increased motion in the pelvic joints may diminish the efficiency of load transfer and increase the shear forces across the joints. Increased shear forces has been suggested to be one factor for pain in women with PGP [106]. The self-locking mechanism of the sacroiliac joints with the principles of form and force closure, based on a theoretical model from anatomical and biomechanical studies, was introduced in 1997 by Snijders and co-workers [155]. Failure of the self-locking mechanism and load transfer through the pelvis has been suspected in patients with sacroiliac pain [156, 157], and asymmetric laxity of the sacroiliac joints has been shown to correlate with moderate to severe levels of symptoms in subjects with postpartum PGP [158].

The sacrospinous ligament and superficial sacroiliac joint structures, such as the long dorsal sacroiliac ligament, are a potential source of pain in PGP [159,160,161,162]. An impaired load transfer during activities may result in overload of the ligaments of the pelvis and hence have an influence on PGP [163, 164]. Frequent or sustained pain-provoking postures might influence the pelvic ligaments and in turn link to other symptoms. Changes in spinal curvature and posture may be caused by pregnancy. Both increased lumbar lordosis [165] and a tendency for lumbar kyphosis or a flattening of the lumbar spine is reported to be prevalent during pregnancy [166, 167].

There is some evidence that PGP is related to an altered pelvic mechanism and/or motor control [168]. PGP disorders have been associated with an alteration in the strategy for lumbopelvic stabilization with excessive as well as insufficient motor activation of the lumbopelvic and surrounding musculature [169]. Impaired motor control patterns may be a possible mechanism for ongoing pain and disability in patients with persistent PGP [170]. Attention has been paid to motor control of local muscles, especially the transverse abdominals [170, 171]. Also the pelvic floor muscles are considered to be an important part of the local muscle system, and Stuge and co-workers found significantly smaller levator hiatus area in women with PGP than in controls both at rest, during voluntary contraction, and during automatic contraction [172, 173].

Whereas the role of muscle function in LBP in the general population is debated, an association between reduced muscle function and the development of LBP and/or PGP in pregnant women is reported [174]. Indications exist that pregnant women with gluteus medius weakness are more likely to have LBP than those without this weakness [175]. In pregnant women with LBP and/or PGP, both lower levels of trunk muscle endurance and hip extension muscle strength [176] and increased muscle activity during the active straight leg raise test are reported [177]. Consequently, an association between muscle dysfunction and LBP and/or PGP during and after pregnancy may exist.