Changes of trunk muscle stiffness in individuals with low back pain: a systematic review with meta-analysis

Low back pain (LBP) is considered one of the most prevalent and debilitating musculoskeletal conditions [1]. It affects the majority of the general population, although prevalence is the highest between the ages of 40 and 60 [2]. LBP frequently results in work absenteeism [3] and associated financial losses [4], which is a major socioeconomic burden. One of the major concerns is the development of chronic LBP and persistent symptoms. Notably, it is estimated that approximately one-third of acute LBP cases develop into chronic LBP [5]. The latter often leads to disability and reduced quality of life [6], thus having a negative impact on the individual’s psychological state [7].

The relatively high prevalence of chronic LBP and persistent symptoms (4.2 – 25.4 %) [8] may be related to changes in structural and neuromuscular properties associated with LBP. In fact, individuals with LBP often display atrophy of paraspinal muscles [9], decreased trunk muscle strength [10], endurance [11], and flexibility [12] as well as alterations in neuromuscular control [13, 14]. Furthermore, several authors have reported higher paraspinal muscle electromyographic (EMG) activity during standing [15] and walking [16]. It has been suggested that the increased muscle activity represents a spine splinting mechanism to increase trunk stiffness and protect the spine from abnormal loading and noxious stimuli [17]. However, Prins and colleagues (2017) [18] concluded in their systematic review that there is no conclusive evidence to support spinal splinting in individuals with LBP.

Despite the conflicting findings of the systematic review by Prins and colleagues (2017) [18], there are some studies reporting increased intrinsic trunk stiffness in individuals with recurrent [17] or experimentally-induced LBP [19]. Even so, measurement of intrinsic trunk stiffness does not indicate, whether potential alterations are related to muscle or connective tissue. Changes of connective tissues have been frequently associated with LBP [20, 21]. While these changes may have an impact on intrinsic trunk stiffness, their contribution has yet to be determined. Importantly, the assessment of back muscle stiffness may represent a window of opportunity to offer additional insights into changes of trunk mechanical properties in association with LBP.

Ultrasound-based measurements and myotonometry are novel approaches that enable the assessment of tissue stiffness by measuring mechanical tissue deformation. Ultrasound-based measurements include shear wave elastography (SWE) and strain elastography (STE). The former measures the velocity of propagation of an ultrasound-induced shear wave within the tissue [22], while the latter measures tissue deformation following mechanical pressure, which is applied manually from the examiner by compressing the skin and underlying tissue [23]. In contrast, myotonometry is performed using myotonometer, a device that applies small compressive forces to the skin and measures deformation of superficial tissues. Both SWE and myotonometry appear to correlate well with exerted muscle force (r = 0.82 – 0.98) [24, 25] and muscle activity (r = 0.70-0.98) [26, 27]. Additionally, both methods were proven to be reliable for measuring back muscle stiffness (SWE: ICC = 0.53 – 0.79, myotonometry: ICC = 0.81 – 0.96) [28, 29].

Current evidence from single studies suggests that people with LBP display higher back muscle stiffness compared to asymptomatic individuals [30‐33]. However, due to inconsistent findings and different methodologies used to assess stiffness, a synthesis of the evidence is warranted. Therefore, the aim of our study was to conduct a systematic review and meta-analysis on the changes of resting and active back muscle stiffness in relation to LBP. Our findings could offer additional insights into the relationship between trunk mechanical properties and LBP. We hypothesized that individuals with LBP have higher back muscle stiffness compared to asymptomatic individuals.

The aim of this systematic review with meta-analysis was to evaluate changes in muscle stiffness in individuals with LBP. Our meta-analyses revealed that resting MF and ES stiffness is significantly higher in individuals with LBP. However, the certainty of evidence was low to moderate at best, therefore our findings should be interpreted with extreme caution. In contrast, the results of studies, that measured muscle stiffness during submaximal contractions appear, to be somewhat conflicting.

Our findings indicate that in general LBP may be associated with increased resting trunk muscle stiffness. This is in some contrast with an extensive systematic review conducted by Prins et al. (2017) [18], which found no differences in trunk stiffness between individuals with and without LBP. The authors included studies that measured trunk stiffness and muscle activity following unexpected perturbations. Intrinsic trunk stiffness depends on both muscle and connective tissue stiffness. That being said, it is possible that the observed increased trunk extensor stiffness represents a compensation for altered connective tissue stiffness and therefore does not result in increased intrinsic trunk stiffness. However, since LBP is associated with increased rather than decreased connective tissue stiffness [21, 48], this should manifest as higher intrinsic trunk stiffness. Several studies included in the aforementioned review applied perturbations to the upper or lower extremities, thus including another potential source of compensatory strategies that could influence trunk kinematics (e.g. elbow or hip movements). Also, the majority of studies measured EMG activity as the primary outcome, which does not per se reflect trunk mechanical properties.

Muscle stiffness appears to correlate well with muscle force [24] and EMG activity [27]. The observed higher levels of trunk muscle stiffness in individuals with LBP could be associated with increased EMG muscle activity. Indeed, individuals with LBP often show increased trunk muscle activity during standing [15], walking [16] or forward flexion [49]. Nevertheless, in a recent review, Van Dieën et al. (2019) [50] concluded that changes in muscle activity and motor control in individuals with LBP display high intra- and interindividual variability. In fact, while some studies reported increased trunk muscle activity during standing [51], others found either no differences [52] or even lower activity levels [53]. The authors added that the heterogeneous nature of LBP should be taken into account when studying associations between motor control and LBP. In addition to muscle activity, the stiffness of a muscle is also determined by its structural and morphological characteristics. Changes in MF structure and morphology, such as atrophy and fat infiltration, have been previously described in individuals with LBP [54]. However, these changes are in odds with our results, as both atrophy [55, 56] and fat infiltration [57] are associated with decreased muscle stiffness. Our findings could be explained by other morphological changes. For instance, experimentally induced intervertebral disc degeneration in animal specimens seems to lead to a more pronounced increase in muscle bundle compared to muscle fibre stiffness, which is most likely associated with proliferation of connective tissue [58]. In terms of fibre distribution, LBP can lead to a transition from type I to type II muscle fibres of the MF [59]. Type II fibres have been shown to be less stiff compared to type I [60], hence a reduction in muscle stiffness would be expected. However, since type II fibres are less fatigue-resistant, it is possible that muscles may exhibit higher levels of fatigue throughout daily activities. Kumamoto and colleagues (2021) [61] found that a 60-s bout of sustained trunk extension resulted in increased MF stiffness. Accordingly, fatiguing of type II fibres in individuals with LBP might lead to increased muscle stiffness. Conversely, study findings from other muscle groups suggest that resting muscle stiffness either remains unchanged [62] or decreases [63] following fatiguing protocols, hence definitive conclusions cannot be drawn. In summary, although the exact underlying mechanism of increased trunk muscle stiffness in LBP is yet to be proven, it is clear that several factors may play an important role.

Although our meta-analysis revealed a significant difference in resting MF stiffness between participants with and without LBP, two studies found no differences between groups [43, 45]. Chan and colleagues (2012) [43] assessed stiffness using the STE, which seems to be more examiner-dependent compared to SWE [64]. Pinto et al. (2022) [45] on the other hand utilized SWE and obtained substantially higher (43.3 kPa) values of resting MF stiffness compared to the other included studies (4.8 – 6.8 kPa). Conversely, with the exception of Wu et al. (2019) [33], all studies that measured trunk extensor stiffness using myotonometry found no differences between participants with and without LBP. Among these, two included only participants with acute [46] and subacute LBP [47]. Thus, it is plausible that changes in muscle stiffness could be specific to chronic LBP. Yet, Ilahi et al. (2020) [30] included participants with chronic LBP and found no differences when analyzing both genders, although a significant difference was observed when only female subjects were compared. Importantly, we must consider the limitations of myotonometry, when interpreting the findings of the aforementioned studies. Myotonometry measures the mechanical deformation of superficial tissues following the application of a compressive force. Therefore, tissues other than muscle, such as superficial connective tissue and subcutaneous fat may also affect the results. Not surprisingly, Bravo-Sanchez et al. (2021) [30] reported a positive correlation between thigh superficial connective tissue thickness, determined by magnetic resonance imaging, and muscle stiffness, measured with myotonometry. Individuals with LBP were shown to have a higher cross-sectional area of the superficial thoracolumbar fascia [21], thus it is plausible that increased stiffness might be partially related to changes of the connective tissue and not by the changes in the muscle itself.

The evidence regarding changes in MF stiffness during submaximal contraction in people with LBP is somewhat conflicting. Two of the included studies found no differences in active MF stiffness [31, 44]. Murillo et al. [44] measured muscle stiffness during an isometric trunk extension test, whereas Koppenhaver et al., 2020 [31] used the prone contralateral arm lift test. Although this test has been shown to elicit contraction and increased activity of the MF [65], one must be cautious when interpreting their results. Indeed, during this task intermuscular coordination and muscle activity could vary considerably between individuals. This is partially supported by a relatively high standard deviation compared to the mean (22.6 ± 9.8) reported by the authors. In contrast to the previously mentioned studies, Chan et al. 2012 [43] observed increased MF stiffness in individuals with LBP during static forward stooping (25 and 45° spinal flexion). Although we cannot conclusively determine the origin of this finding, we offer some possible explanations. During forward stooping the spine assumes a forward flexed position. In this position the forces acting on the spine differ from loading close to a neutral position in standing. More specifically, the spine is subjected to shear forces, leading to an increased need for stability [66]. Consequently, the central nervous system increases trunk muscle coactivation to meet stability demands, resulting in increased muscle stiffness. In individuals with LBP this increase in trunk bracing could be more pronounced due to impaired motor control [50], which would explain higher levels of muscle stiffness. Furthermore, individuals with LBP often adopt the belief that their spine needs to be protected during bending [67]. Increased muscle activity and stiffness might represent a strategy to deal with this belief. To the best of our knowledge, there are currently no studies using myotonometry for assessment of muscle stiffness during submaximal contraction in people with LBP.

A higher degree of muscle stiffness might be an important factor in the occurrence or persistence of LBP symptoms and disability. In an acute episode of LBP elevated trunk muscle stiffness could limit excessive spinal movement, thus likely protecting the spine from harmful loads and further injury [17]. Conversely, long-term increases in muscle stiffness could result in increased compressive forces on the spine [68], possibly leading to facet joint or intervertebral disc impairments. Also, increased muscle stiffness could lead to decreased movement efficiency and an associated higher energy expenditure. All things considered, reduction of muscle stiffness could be one of the goals when treating LBP patients. Interestingly, research has shown that some of the frequently applied physiotherapeutic interventions in LBP treatment such as dry needling [69], sustained natural apophyseal glides [70], electrotherapy and myofascial release [71] lead to a reduction of muscle stiffness. While it is not clear whether this reduction in stiffness is mediated by improvement in pain or vice versa, it does indicate a potential role of addressing muscle stiffness in LBP management. In terms of examination, muscle stiffness assessment might be useful to evaluate progress of patients with LBP in clinical settings. In this context, myotonometry might be a more suitable option due to its practical applicability.

The aim of this systematic review with meta-analysis was to investigate changes in trunk muscle stiffness in relation to LBP. Our findings suggest that there is low to moderate certainty of evidence of higher resting MF and ES stiffness in individuals with LBP compared with asymptomatic controls. On the other hand, evidence for altered MF stiffness during submaximal contraction is somewhat conflicting. All things considered, we advise extreme caution when interpreting our study results, due to a limited certainty of evidence, small number of included studies and differences in methodology of tissue stiffness assessment.