Low back pain is a leading cause of disability and work absence, significantly impacting both individuals and society economically (Manchikanti et al., 2014). Epidemiological surveys indicate that 70%–80% of adults have experienced low back pain, establishing it as a global public health issue (Chen et al., 2022). The majority of these patients (approximately 84%) suffer from non-specific low back pain (NLBP), characterized by pain not attributable to a specific pathological cause. When this pain persists for more than 3 months, it is termed chronic non-specific low back pain (CNLBP) (Chou et al., 2007; Maher et al., 2017). Although some patients exhibit conditions like disc degeneration, lumbar disc herniation, and spinal stenosis, these conditions often do not correlate strongly with symptoms and can be present in asymptomatic individuals. Research suggests that chronic strain on the muscles and fascia of the lower back might play a crucial role in the development of CNLBP (Ouyang et al., 2013; Lemes et al., 2021). Studies have identified key pathological changes in the lumbar muscles of CNLBP patients, such as muscle fiber atrophy, degeneration, and increased fat content (Goubert et al., 2016; Seyedhoseinpoor et al., 2022). Physical examinations often reveal stiff muscles, painful nodules, and cord-like changes. However, there is a lack of objective, quantitative evaluation criteria for chronic muscle and fascia strain. Conventional imaging techniques do not reveal the mechanical properties of muscles and fascia in CNLBP, such as elasticity or tension. Moreover, the impact of muscle fiber structure changes on muscle biomechanical properties and function remains unclear (Noonan and Brown, 2021). Therefore, studying the mechanical properties of muscles and fascia, including elasticity or stiffness, could enhance our understanding of muscle fiber alterations and their relationship to both normal and impaired muscle function.

The erector spinae (ES) and multifidus (MF) muscles are crucial paraspinal muscles and core stabilizers of the lumbar spine. Current studies indicate that patients with chronic low back pain often exhibit degenerative changes in these muscles, such as atrophy and fatty infiltration (Goubert et al., 2017). Additionally, delayed pre-activation and impaired coordination control of these muscles contribute to decreased spinal stability (Zhang et al., 2021; Cheng et al., 2023). However, the physiological mechanisms underlying these phenomena, particularly the link between MF degeneration and spinal disorders, remain insufficiently explored. The thoracolumbar fascia (TLF) has also been identified as a potential source of CNLBP (Willard et al., 2012). The TLF, along with muscles and the spine, forms an extensive muscle-fascia complex system that stabilizes the thoracolumbosacral spine region and facilitates tension transmission between structures (Bojairami and Driscoll, 2022). Histological studies have shown the presence of injury-free nerve endings in the TLF and suggest that long-term muscle fatigue due to poor posture and weight-bearing can lead to microinjuries and inflammation (Sinhorim et al., 2021; Kondrup et al., 2022). These microinjuries and associated inflammation in the TLF might contribute to pain and appear to cause morphological changes in patients with chronic low back pain (Hoheisel and Mense, 2015). However, the exact relationship between these changes and the etiology of pain remains unclear.

Since Ophir et al. (Ophir et al., 1991) first used strain elastography (SE) to measure muscle stiffness in vitro in 1991, ultrasound elastography has enabled the study of the mechanical properties of individual muscles. However, traditional SE relies on applying pressure to the tissue with the ultrasound probe, causing tissue deformation and providing relative stiffness measurements. This quasi-static technique is heavily dependent on the examiner’s applied pressure, which can affect the accuracy of the results. Shear wave elastography (SWE), an emerging technology, overcomes this limitation by quantifying tissue stiffness through the measurement of shear wave propagation speed induced by ultrasound, without relying on manual pressure from the examiner (Taljanovic et al., 2017). SWE is non-invasive, provides real-time, dynamic quantitative data on soft tissue biomechanics, and generates qualitative elastography maps that visually depict tissue stiffness changes (Klauser et al., 2014). Additionally, SWE can differentiate between different tissue layers, making it particularly useful in complex structures such as the fascia and muscles of the lower back, where it allows for precise targeting and measurement of deep muscle shear modulus. Recent studies have demonstrated that SWE has high reliability and validity in assessing the elasticity of lumbar muscles and fascia (Moreau et al., 2016; Koppenhaver et al., 2018; Chen et al., 2020).

Pirri et al. (2023) explored the morphological changes in the TLF using ultrasound imaging, revealing that, compared to individuals without LBP, patients with CNLBP exhibited significantly reduced anisotropy levels and increased thickness in the TLF. These structural changes, which they termed “frozen back,” were hypothesized to be linked to a decrease in the sliding ability between fascial layers. Immunohistochemical examination of TLF samples from two patients with chronic low back pain by Willard et al. (Willard et al., 2012) demonstrated that the density of myofibroblasts in these patients was comparable to that observed in patients with frozen shoulder, and they described this condition as “frozen lumbar.” Ranger et al. (Ranger et al., 2016) further investigated the relationship between TLF structure and low back pain, showing that shortened TLF length was closely associated with more severe low back pain. Additionally, changes in the morphology and function of the paraspinal muscles, such as muscle fiber atrophy, degeneration, and fatty infiltration, have been identified as key contributing factors in CNLBP (Goubert et al., 2016; Goubert et al., 2017). Since muscles possess viscoelastic properties, when muscle tissue is replaced by fat or other scar connective tissues, their viscoelasticity is inevitably affected. As these physical properties change, the ability of the tissue to transmit mechanical waves is also impacted (Amir et al., 2022). Therefore, this study aims to assess changes in the stiffness of lumbar fascia and muscles in CNLBP patients using SWE and explore the relationship between these changes and pain severity as well as functional disability. We hypothesize that lumbar fascia and muscle stiffness is higher in CNLBP patients compared to individuals without LBP, and that this increased stiffness is significantly correlated with pain intensity and functional disability.

This study assessed differences in bilateral TLF, ES, and MF stiffness between subjects with CNLBP and healthy controls. Additionally, it examined the correlation between fascial and muscle stiffness and pain and dysfunction within the CNLBP group. Our findings indicate that TLF, ES, and MF stiffness were significantly higher in patients with CNLBP compared to those without low back pain. There was a positive correlation between increased stiffness and pain levels, which supports previous hypotheses. A significant positive correlation was found between increased stiffness and both pain severity and functional impairment index in certain measurement areas. Moreover, we observed a higher correlation between muscle and fascial stiffness and pain levels in the L_4-5 region compared to L_1-2. This may be attributed to the anatomical and functional characteristics of the lumbar spine. The load on the lumbar spine increases progressively from top to bottom. The L_4-5 segment, located in the lower lumbar region, serves as a key junction for supporting body weight and transmitting forces. This increased mechanical load makes it more susceptible to degenerative changes in the joints and surrounding soft tissues. Additionally, the L_4-5 segment is a critical point for spinal mobility, with significantly greater range of motion than the upper lumbar segments, facilitating complex movements such as flexion, extension, lateral bending, and rotation (Sabnis et al., 2018). Due to the higher frequency of movement, the L_4-5 segment is more prone to chronic damage to the muscles, ligaments, and joints from repeated mechanical stress (Basques et al., 2017). Moreover, studies have shown that the L_4-5 segment is a high-risk area for degenerative lumbar diseases, such as disc herniation, spinal stenosis, and osteoarthritis (Kurowski and Kubo, 1986; Liu et al., 2017). These long-term degenerative changes further increase the risk of injury to the surrounding fascia and muscles.

In this study, we found that the stiffness of the TLF was significantly increased in CNLBP patients, and there was a strong positive correlation between increased stiffness and pain and functional impairment, particularly in the L_4-5 region. Several factors may contribute to these changes. First, prolonged mechanical stress and load are key factors. Chronic low back pain patients often experience sustained mechanical load on the fascia due to poor posture or repetitive stress, leading to fascia hypertrophy and fibrosis (Ramsook and Malanga, 2012). Second, fibrosis is a pathological change induced by chronic inflammation, where prolonged inflammation promotes the proliferation of fibrous tissue, reducing fascia elasticity and increasing stiffness (Kondrup et al., 2022). The decreased ability of the fascia layers to glide may also be a contributing factor to increased fascia stiffness, as the loss of elasticity restricts normal kinematic function, thereby affecting lumbar flexibility. Moreover, the myofascial system is critical for cushioning and force transmission in the human body. Unlike the rigid bones that act as pressure-resistant structures, these tissues rely on their tensile properties to function properly. When tissues lose their normal physiological elasticity, embedded receptors may remain active even at rest. In this non-physiological state, any muscle contraction or stretch may be transmitted through myofascial connections to neighboring tissues, leading to excessive sensory input (Sinhorim et al., 2021; Ushida et al., 2022). Fascial tissues, particularly the TLF, are rich in sensory nerve endings and innervation and may contain high-threshold mechanoreceptors (Suarez-Rodriguez et al., 2022). Wilke et al. (Wilke et al., 2017) pointed out that the mechanoreceptors densely distributed in fascia respond to applied pressure, leading to reduced sympathetic tone and changes in local tissue viscosity when stimulated. Previous studies have shown that pain often spreads outward from the initially affected area (Mosabbir, 2022). As other muscles compensate for the dysfunction, this compensation can result in overload, further expanding the impact of pain and dysfunction and causing discomfort over a broader range.

Additionally, as a crucial component of the superficial stabilizing muscle group, the ES plays a vital role in maintaining the stability of the spine and pelvis (Daggfeldt et al., 2000; Howarth et al., 2013). Due to its superficial location and ease of measurement, surface electromyography (sEMG) and B-mode ultrasonography are the most commonly used methods for assessing ES function. sEMG provides valuable information on neuromuscular electrical activity; however, its accuracy can be easily influenced by external factors and it does not reflect the biomechanical properties of the tissue. Consistent findings from sEMG studies suggest that ES activation levels are typically high, with a tendency for delayed activation (Becker et al., 2018; Sakai et al., 2019). B-mode ultrasound assesses muscle contraction by comparing muscle thickness or cross-sectional area at rest and during contraction (Cheung et al., 2020). However, significant errors may arise when the muscle cannot be assumed to be ‘at rest,’ such as in cases of muscle spasm or postural tension. The MF, located at the deepest level of the spinal region, has the largest attachment area among the paravertebral muscles and is rich in sensory receptors, playing a key role in spinal stability (Hofste et al., 2020). Research indicates that MF contributes to two-thirds of spinal stiffness during movement (Ward et al., 2009). Mechanical overload, prolonged immobilization, and sports injuries can lead to degenerative changes in the MF, including atrophy and fatty infiltration, resulting in delayed pre-activation, impaired coordination, and reduced control (Goubert et al., 2016). Numerous studies have linked MF degeneration and functional abnormalities to various spinal disorders, including chronic low back pain and degenerative lumbar spinal stenosis (Goubert et al., 2017; Faur et al., 2019). However, the relationship between morphological changes in the lumbar MF and lumbar spine function in CNLBP patients remains unclear. A cross-sectional study found a significant negative correlation between the severity of MF fatty infiltration and lumbar flexion mobility (Hildebrandt et al., 2017). In contrast, Rezazadeh et al. (Rezazadeh et al., 2019) reported no association between changes in MF cross-sectional area and dysfunction indices in CNLBP patients. Given these conflicting findings, a comprehensive assessment of lumbar function and pain in CNLBP patients is essential. Exploring MF changes from a biomechanical perspective may offer deeper insights into its role in CNLBP and inform more effective treatment strategies.

Based on SWE imaging, this study found that the stiffness of the ES and MF muscles was significantly higher in certain regions of CNLBP patients compared to those without low back pain, and this was correlated with pain and functional impairment. Chronic low back pain often triggers a “protective muscle contraction” mechanism, where the ES and MF muscles remain in a state of continuous contraction to limit excessive spinal motion and prevent further injury (Larsen et al., 2018). Moreover, reflexive control of spinal movement depends on sensory-motor mechanisms regulated by mechanoreceptor input. These afferent nerves are present in various spinal tissues, including paraspinal muscles, interspinal muscles, interspinous ligaments, thoracolumbar fascia, intervertebral discs, and facet joint capsules (Ebenbichler et al., 2001; Holm et al., 2002). The afferent nerves in the discs and joint capsules have high mechanical thresholds and are only activated under severe loading conditions, while those in muscles, ligaments, and fascia can be activated at lower thresholds and have proprioceptive functions (Yamashita et al., 1993; Sekine et al., 2001). Zuriaga et al. (Sanchez-Zuriaga et al., 2010) found that prolonged spinal flexion impairs sensory-motor control mechanisms and reduces the protective function of back muscles over the spine. This effect is attributed to time-dependent “creep” in soft tissues rather than muscle fatigue, which aligns with the findings of (Shin et al., 2009). Static posture, mechanical overload, and sports injuries can lead to delayed pre-activation of paraspinal muscles, altering lumbar load distribution and subsequently impairing coordination and control (Haddas et al., 2016). Nociceptors transmit neural impulses via Aδ and C fibers to the dorsal horn of the spinal cord, projecting to higher centers and triggering reflexive activity that produces pain. Concurrently, this reflex activity increases the excitability of α and γ motor neurons in the corresponding segments, enhancing the stretch reflex, which leads to muscle spasms, increased tension, and greater stiffness (Freddolini et al., 2014; Sessler et al., 2021; Creighton et al., 2023). Prolonged noxious stimulation of the lumbar muscles in CNLBP patients reduces the firing frequency of motor neurons, affecting the recruitment rate of sarcomeres, reducing the number of active thick filaments, and decreasing lumbar muscle contractility, which reflexively inhibits normal muscle activity (Russo et al., 2018; Noonan and Brown, 2021). These changes significantly reduce lumbar muscle involvement, disrupt spinal stability and vertebral balance, and create a vicious cycle that contributes to the development of low back pain.

The use of SWE in musculoskeletal applications, particularly for assessing muscular tissues, has been rapidly increasing since 2010 when initial studies demonstrated plausible changes in muscle stiffness using this technology (Shinohara et al., 2010). A previous study employed strain ultrasonography to evaluate muscle stiffness in the low back muscles, focusing solely on the MF. This study found no significant difference in lumbar MF stiffness between patients with low back pain and healthy subjects in the prone position (Chan et al., 2012). However, quantitative measurement of muscle stiffness using strain-based imaging methods poses challenges. The accuracy of these methods depends heavily on the compression control exerted by the assessor on the probe, and they do not provide absolute values. In contrast, SWE offers quantitative measurements that are less dependent on the assessment technique, resulting in more accurate and reliable results. SWE is increasingly recognized as the best method for estimating individual muscle strength and can quantify localized changes in muscle damage, such as myofascial trigger points (Hug et al., 2015). The validity and reliability of SWE for assessing the TLF, ES, and MF are well-established, but most studies have focused on asymptomatic subjects (Koppenhaver et al., 2018; Chen et al., 2020). Only two similar studies on low back pain have been found, and their outcomes are inconsistent. Masaki et al. reported significantly higher MF stiffness in patients with LBP compared to individuals without LBP, with no significant difference in ES stiffness. However, this study included only nine patients, which could impact the reliability of the results (Masaki et al., 2017). Another study found that both ES and MF stiffness were significantly higher in LBP patients than in asymptomatic controls, with a positive correlation between stiffness, pain, and dysfunction (Koppenhaver et al., 2020). Additionally, neither study differentiated between NLBP and specific low back pain, which includes lumbar spine disorders and may present differently. In our study, we specifically identified patients with CNLBP and aimed to assess the stiffness of muscles and fascia in multiple lower back areas. To our knowledge, this is the first study to compare TLF stiffness between CNLBP patients and asymptomatic subjects and to correlate it with clinical symptoms.

Quantifying the elasticity index of muscles and fascia in patients with CNLBP and analyzing its correlation with clinical symptoms from a biomechanical perspective not only helps clarify the predisposing factors of tissue pain and injury but also aids in understanding the integrity of the body’s tissue structure. This approach provides valuable insights for diagnosing low back pain and assessing the efficacy of treatment interventions. The stiffness of lumbar muscles and fascia may serve as a crucial diagnostic or prognostic factor for CNLBP, offering a potential metric for evaluating the condition’s progression and response to treatment.

This study presents several limitations that warrant consideration. First, the cause of the increased lumbar fascial or muscle stiffness observed in patients with CNLBP remains uncertain whether it stems from overuse, muscle spasm, or another factor. In future studies, SWE combined with electromyography could be used to evaluate the stiffness characteristics of lumbar fascia and muscles under different postures or contraction states. Second, the mechanisms underlying pain generation and adaptation are complex. Given that this study is cross-sectional, the correlational conclusions drawn from it should be interpreted with caution. Future research could benefit from longitudinal studies that assess changes in fascial and muscle stiffness before and after specific interventions using SWE. Thirdly, the study’s participants were all recruited from the same geographical area and primarily consisted of young to middle-aged adults between 20 and 35 years. Therefore, caution should be exercised when extrapolating these findings to other demographic groups, as the results may not be generalizable to older adults or populations from different regions.

In patients with CNLBP, the stiffness of the TLF, ES, and MF is generally higher than in individuals without low back pain. However, this increased stiffness is not consistently observed across all detection areas. Additionally, higher stiffness may be associated with pain and dysfunction, with this relationship being more pronounced in the TLF.