Hormonal changes during pregnancy prepare the soft tissues (including the pelvic floor) for birth. Already in the first trimester, the corpus luteum secretes relaxin, which is indirectly involved in the breakdown of elastin and changes in collagen in the tissues. Elastin gives tissues resilience and elasticity so that they can return to their original shape after stretching, while collagen is essential for tissue stability. When elastin is damaged (e.g., by overstretching during normal labor), it can rebuild, but its original properties are not fully restored. The breakdown of collagen alters the mechanical properties of the pelvic floor ligaments, weakening their support function and causing pelvic floor dysfunction. Of course, it should not be forgotten that hormones affect not only the reproductive system and the pelvic floor, but the whole body – an increased level of progesterone causes relaxation of the ligaments of the peripheral joints, which leads to their instability (which during pregnancy is a preparation for childbirth) (1).

When hormone levels increase, such as during pregnancy, fascial tissue becomes more elastic: in the studies by Fede et al. (2), after the administration of β-estradiol to the sample, collagen-I decreased from 5.2 to 1.9%, while collagen III and fibrillin increased (from 2.4 to 6.7% and from 0.5 to 3.6%, respectively). This change in extracellular matrix composition allows tissues to adapt during pregnancy, similar to the ovulation period, where the same trend of changes in ECM is observed: collagen-I decreases from 5.2 to 1.9%, collagen III increases from 2.4 to 6.8%, and fibrillin increases from 0.5 to 3%. Stiffer fascia can help stabilize the sacroiliac joint and lower spine, while looser fascia can cause pelvic or lumbar pain typical of pregnancy. Interestingly, the development of joint pain during pregnancy in 35 first-trimester women was not associated with increased joint laxity but with markedly elevated levels of estradiol and progesterone. Similarly, fluctuations in estradiol levels have been associated with joint pain, stiffness, and depressed mood during menopause (2).

Understanding how disrupted sex hormones can affect fascial tissue is an important step in understanding gender differences in the development of myofascial pain and helps physicians diagnose and treat their patients. Sex hormone receptors are present on fascial fibroblasts, with expression decreasing in postmenopausal women as hormone levels decrease. Fascia cells may also modulate the synthesis of extracellular matrix components in response to hormone levels: When β-estradiol levels are low, fascial tissue accumulates collagen I (from 5.2% of the control sample to 8.4%), with concomitant decreases in collagen III (from 2.4% to 1.5%) and elastin fibers (from 0.5% to 0.2%). As a result, tissues become less flexible and stiff, which is usually the case during menopause. When hormone levels are high, as is common during the peak of ovulation or during pregnancy, the opposite is true: the level of collagen III increases to 6.8% during ovulation and 6.7% during pregnancy, as does that of fibrillin-1 (from 0.2% at menopause to 3.6% during pregnancy), and collagen-I decreases to 1.9%. The result is softer, more supple tissue (3).

The presence of relaxin receptor 1 (RXFP1) and estrogen alpha receptor (ERα) in deep fascia also varies throughout life and is lower postmenopausally than premenopausally. These findings may explain some of the clinical differences found in women of different age groups and why women have different fascial muscle problems and postmenopausal myofascial pain. The effects of hormonal changes on deep fascia during the menstrual cycle were analyzed using ultrasound technology and elastography. Statistically significant differences were found between women using hormonal contraceptives and women not using them: The thoracolumbar fascia was thicker in the non-users, and the maximum and mean stiffness of the wide thigh fascia was higher (p = 0.01 and 0.0095, respectively). Other authors have shown that changes in plantar fascia flexibility during the menstrual cycle may influence postural sway and tremor and lead to potential fall risk (3).

Increased soft tissue stiffness and restricted movement may be due to focal areas of persistent muscle contraction or connective tissue adhesions that locally restrict movement. Patients may also have generalized hypermobility but overlapping local hypomobility in areas of scarring or adhesions due to macro- or microtrauma. Thus, the pathogenetic mechanisms of myofascial pain may be different in hypermobile and hypomobile tissues. Clearly, more research is needed to investigate the role of fascial mobility (decreased or increased) in musculoskeletal pain. More knowledge in this area could not only improve the quality of life of patients with inherited and acquired connective tissue disorders, but also highlight the role of fascial mobility and fascia in musculoskeletal pain (4).

How does this translate to physical therapy for women and what should be considered when planning therapy?

We rely on the basics:

• Tissue stretching promotes relief of inflammation (which has been studied both in vivo and in vitro).
• Manual therapy prevents fibrosis (regardless of the underlying mechanism, fibrotic changes in muscle have a significant impact on tissue dynamics and the ability to generate force) of myofascial tissue caused by its overuse.
• Resistance training is essential to reverse the changes in adipose tissue in painful chronic conditions (adipose tissue is a potential source of pro-inflammatory cytokines and has been linked to a number of musculoskeletal conditions).
• Activating muscles to contract is sufficient to reverse early muscle atrophy.
• Whole-body exercise (general improvement) can prevent inflammatory changes in the muscles of the back, for example, in low back pain (5).

Martyna Kasper-Jędrzejewska

References:

1. Tim S, Mazur-Bialy AI. The Most Common Functional Disorders and Factors Affecting Female Pelvic Floor. Life Basel Switz. 14 grudzień 2021;11(12):1397.
2. Fede C, Pirri C, Fan C, Albertin G, Porzionato A, Macchi V, i in. Sensitivity of the fasciae to sex hormone levels: Modulation of collagen-I, collagen-III and fibrillin production. PLoS ONE [Internet]. 26 wrzesień 2019 [cytowane 16 czerwiec 2020];14(9). Dostępne na: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6762168/
3. Myofascial pain in females and personalized care: The key role played by sex hormones – Fede – 2022 – European Journal of Pain – Wiley Online Library [Internet]. [cytowane 4 lipiec 2022]. Dostępne na: https://onlinelibrary.wiley.com/doi/10.1002/ejp.1920
4. Langevin HM. Fascia Mobility, Proprioception, and Myofascial Pain. Life Basel Switz. 8 lipiec 2021;11(7):668.
5. Zügel M, Maganaris CN, Wilke J, Jurkat-Rott K, Klingler W, Wearing SC, i in. Fascial tissue research in sports medicine: from molecules to tissue adaptation, injury and diagnostics: consensus statement. Br J Sports Med. grudzień 2018;52(23):1497.