Our patients continue to hear about why chiropractors should always be the first source for chronic lower back pain, especially those who understand the fascial system. The way we understand fascia and how it functions is growing, especially in the massage, chiropractic sports communities and even in the physical therapy profession. Chiropractors, being they are physicians and many of us practice primary care for the musculoskeletal system have understood the way fascia works as an exoskeleton of sorts and controls how we move. It has its own nerve and blood supply and the muscles do not function without it. The growing knowledge of how back pain is caused by fascial dysfunction which often develops over years has allowed us to use methods such as myofascial release and instrument assisted soft tissue methods such as Graston technique to solve problems that often result in surgeries and other invasive treatments that often do more harm than help. I am always learning new methods and techniques such as fascial resetting that improves flexibility and reduces stiffness and pain. I usually try these new methods out on myself first to see how they work before showing others. Also, understanding that we cannot use one size fits all ideas on different people with different histories and body styles requires some thinking as different people have different dysfunctions causing their tightness and pain. It requires skill, experience and knowledge. This recent study based on this study published in the journal Biomechanics in 2025 helps us further understand these mechanisms. This is another reason that for chronic back pain, research suggests that you think chiropractic first and look for someone skilled in fascial release, something we have been practicing since the 1990’s being trained in Active Release Techniques and also utilizing other methods as well. Our holistic approach to back pain is safe, effective and can help you live a more productive pain free life. Book online or call today for an appointment. Chronic Low Back Pain Have Reduced Myofascial Force Transmission Between Latissimus Dorsi and Contralateral Gluteus Maximus Muscles Physio Meets Science published 7/14/2025 The human body’s myofascial system consists of connective tissues that enable mechanical force transmission not only within but also between muscles across joints and anatomical regions. Anatomical studies and cadaveric dissections have indicated potential myofascial continuity between the latissimus dorsi (LD) and contralateral gluteus maximus (GM) muscles via the thoracolumbar fascia (TLF), forming part of the so-called posterior oblique sling system [11,12]. Previous research suggested this interconnected system may facilitate force transmission across the trunk and pelvis and contribute to load transfer during gait and dynamic movement [1,7]. However, whether these transmission pathways are functionally relevant in vivo—particularly in pathological populations—remained unclear. Chronic low back pain (CLBP), which affects approximately 23% of the global population at some point in life [2], has been associated with impaired neuromuscular control and myofascial alterations [3,4,8]. Therefore, a brand-new study by Procópio and colleagues investigated whether myofascial force transmission between the LD and contralateral GM differs between individuals with CLBP and healthy controls (https://pubmed.ncbi.nlm.nih.gov/40616971/). Methods A total of 40 participants were included: 20 with clinically diagnosed chronic low back pain (CLBP group) and 20 age- and sex-matched healthy controls. Using ultrasound-based shear wave elastography (SWE), the researchers assessed passive tissue stiffness in the contralateral GM muscle during an isometric contraction of the LD muscle. Each subject lay prone while performing submaximal shoulder extension (activating the LD), and SWE was used to detect changes in the stiffness of the contralateral GM muscle, representing a proxy for myofascial force transmission (s. figure in comments). The primary outcome was the percent change in stiffness of the contralateral GM during LD contraction, compared between groups. Results In healthy controls, contraction of the LD muscle led to a significant increase in stiffness of the contralateral GM (mean increase: 12.7%, p < 0.001), indicating effective force transmission through the thoracolumbar fascial chain. In contrast, CLBP patients showed no significant change in contralateral GM stiffness (mean increase: 1.5%, p = 0.421). The between-group comparison revealed a statistically significant reduction in stiffness increase in the CLBP group compared to controls (p < 0.001). Discussion The results support the functional existence of a myofascial connection between the LD and contralateral GM via the TLF in healthy individuals, consistent with prior anatomical and modeling studies [5,11]. The observed impairment in the CLBP group aligns with research showing altered neuromuscular coordination, reduced fascial mobility, and increased connective tissue stiffness in individuals with chronic back pain [3,4,8]. These findings suggest that CLBP may disrupt long-range myofascial force chains, which could have implications for trunk and pelvic force transfer and locomotion efficiency. Such dysfunction may contribute to persistent motor control deficits and compensatory strategies commonly reported in CLBP populations [7,9,10]. Importantly, this study provides the first in vivo functional evidence—using shear wave elastography—of altered intermuscular force transmission in a chronic pain population. It strengthens the notion that the thoracolumbar fascia acts not just as a passive structure but as an active participant in force modulation and transmission across regions. However, we do not know whether this reduced myofascial force transmission is a cause, a consequence or an epiphenomenon of CLBP. Furthermore, there is no data to show which intervention is best suited to rehabilitate this reduced force transmission. Conclusion This study demonstrates that chronic low back pain is associated with reduced myofascial force transmission between the latissimus dorsi and contralateral gluteus maximus muscles. Thus, potential factors such as greater weakness [12], and decreased GM cross-sectional area [13] commonly observed in this population, reduced fascial gliding (3), the presence of fibrosis and adhesions in the thoracolumbar fascia, and alterations in neuromuscular control (3,4,11) may all contribute to impaired MFT in the pathway investigated. Illustration: https://pubmed.ncbi.nlm.nih.gov/30616942/ Key References (as cited in the study) 1. Barker, P. J., et al. (2007). Clinical Biomechanics, 22, 939–945. 2. Balagué, F., et al. (2012). Lancet, 379(9814), 482–491. 3. Langevin, H. M., et al. (2011). Spine, 36(13), E868–E876. 4. Langevin, H. M., & Sherman, K. J. (2007). Medical Hypotheses, 68(1), 74–80. 5. Vleeming, A., et al. (1995). Spine, 20(7), 753–760. 6. Willard, F. H., et al. (2012). Journal of Bodywork and Movement Therapies, 16(1), 66–73. 7. Wilke, J., et al. (2017). Journal of Anatomy, 231(6), 947–956. 8. Hodges, P. W., & Moseley, G. L. (2003). Manual Therapy, 8(4), 200–206. 9. Van Dieën, J. H., et al. (2003). Clinical Biomechanics, 18(7), 637–655. 10. Carvalhais, V. O. C., et al. (2013). Journal of Biomechanics 46 (5): 1003–7. 11. Huijing, P. A. (2009). European Journal of Applied Physiology, 108(3), 389–404. 12. Nadler, S.F., et al. (2000). Clin. J. Sport Med. 10, 89–97. 13. Amabile, A.H., et al. (2017). 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