Low back pain (LBP) is a leading cause of disability, accounting for nearly 70% of musculoskeletal disorders (Vos et al., 2012). However, the underlying pathoanatomy of the majority of LBP cases is not clearly understood (Deyo and Weinstein, 2001), and few biomarkers are available for diagnosing and/or monitoring the prevalence of LBP (Duthey, 2013).

Previous research has focused on the changes in tissue properties of LBP patients relative to control subjects. Changes within the cross-sectional area of spine-stabilizing lumbar tissues – i.e. multifidus (MF), erector spinae (ES), quadratus lumborum (QL), psoas major (PM) – have been hypothesized to contribute to and/or indicate LBP within patients (Danneels et al., 2000). Such studies have used imaging modalities, including magnetic resonance imaging (MRI) (Barker et al., 2004, D’hooge et al., 2012, Fortin et al., 2015, Goubert et al., 2017, Hides et al., 1995, Kader et al., 2000, Kjaer et al., 2007, Niemeläinen et al., 2011, Paalanne et al., 2011, Ploumis et al., 2011, Wan et al., 2015), computed tomography (Danneels et al., 2000, Kamaz et al., 2007) and ultrasound imaging (Hides et al., 1994, Wallwork et al., 2009). While the MF has demonstrated atrophy within LBP patients (Danneels et al., 2000, Kader et al., 2000, Kamaz et al., 2007, Ploumis et al., 2011, Wallwork et al., 2009, Wan et al., 2015), studies investigating atrophy within the ES (D’hooge et al., 2012, Goubert et al., 2017, Niemeläinen et al., 2011, Ploumis et al., 2011, Wan et al., 2015), QL (Kamaz et al., 2007, Ploumis et al., 2011), and PM (D’hooge et al., 2012, Kamaz et al., 2007, Ploumis et al., 2011) in LBP patients yielded inconsistent results. Likewise, the fatty infiltration (FI) of lumbar soft tissues may be a greater indicator of muscle atrophy (D’hooge et al., 2012, Fortin et al., 2015), with LBP patients indicating increased FI (D’hooge et al., 2012, Goubert et al., 2017, Kjaer et al., 2007). The thoracolumbar fascia (TLF), a soft tissue that contributes to force transmission within the lumbar musculoskeletal system, has demonstrated hypertrophy within LBP patients (Langevin et al., 2009, Larivière et al., 2020).

Morphological changes to the soft tissues within LBP patients may indicate a stress allocation bias within the lumbar spine. As soft tissue performance is regulated by external trigger mechanisms whereby tissues to convert mechanical stimuli (e.g. stress) into biochemical signals (e.g. electrical, metabolic, and hormonal signals for skeletal muscle), altered mechanotransduction would affect both the active and passive components for muscles. Within tissues without contractile components (e.g. tendons and ligaments), such remodeling would be considered to passively affect tissues through modification to the extracellular matrix. In tissues experiencing elevated stress, tissues may undergo positive tissue remodeling, leading to increased tissue cross-section, strength, and rigidity. Conversely, stimuli-deficient tissues will undergo atrophy, leading to a reduction in tissue rigidity This allocation bias may ultimately lead to physiological stress shielding. Described by Driscoll and Blyum (2011), stress shielding occurs when tissues with increased rigidity withstand the majority of stress induced by physiological motion, preventing weaker tissues from receiving normal loading. In turn, the stimuli-deficient tissues undergo degenerative tissue remodeling, leading to atrophy and reduced rigidity. To perform the desired physiological motion, alternative tissues may be activated, leading to further irregularities in stress distributions and tissue activation. Ultimately, these tissues may become trapped in a degenerative remodelling cycle unless interrupted by an appropriate clinical intervention (Driscoll and Blyum, 2011).

Previous clinical studies have correlated morphological variation within lumbar soft tissues of LBP patients. In silico studies investigating these changes in material properties as a consequence of LBP yielded elevated loading skewed towards the TLF rather than the lumbar muscles that aid in spinal stability (Newell and Driscoll, 2021a, Newell and Driscoll, 2021b). As such, this skewed stress distribution suggests that the TLF may be preventing the MF and ES from receiving normal loading and laying the foundation for physiological stress shielding (Newell and Driscoll, 2021a, Newell and Driscoll, 2021b). Thus, this study hypothesizes that the TLF and lumbar muscle morphology of LBP patients will exhibit hypertrophy and atrophy, respectively, relative to healthy subjects. Therefore, this study seeks to investigate changes within the total and functional cross-sectional areas (tCSA, fCSA), and FI of healthy and LBP subjects’ lumbar soft tissues to evaluate the potential for physiological stress shielding within the lumbar spine of LBP patients.