Low back pain is responsible for 60.1 million years lived with disability amongst working-age adults (1). The economic burden and drug programs for CLBP are similar to other high-cost conditions (2), such as cardiovascular diseases, cancer, mental health and autoimmune diseases, and 80%–90% of these cost are due to production losses (1). Chronic low-back pain (CLBP) is defined as pain lasting >3 months (with or without associated leg pain), located between the lower rib margins and the gluteal folds (1, 3). CLBP is classified as non-specific when no causative nociceptor factors can be identified. It can emerge intrinsically from the spine, intervertebral discs, or surrounding soft tissue (4). A recent study reported that the “Mo-fi-disc” scoring system, which considers the combined effect of paraspinal muscles, end-plates, and discs, is a significant predictor of the intensity of LBP (OR = 1.193, 95% CI 1.05–1.349, p = 0.005) (5).

In the lumbar spine, the erector spinae (ES) muscle is responsible for global stability and torque generation (6). At upper lumbar levels, the thoracic fibers of the lumbar erector spinae contribute between 70% and 86% of the total extensor moment (7). The ES controls spinal orientation and balances the external forces applied to the trunk (6) by producing a compressive and posterior shearing force at L1–L4 in the upright posture (7–9).

Lumbar ES muscle degeneration has been associated with non-specific CLBP. This degeneration is characterized by macroscopic or microscopic changes (10). Macroscopic changes can be observed via changes in muscle cross-sectional area (CSA) and intramuscular fatty infiltration (FI). Microscopic changes present as changes in muscle fiber type and as microtears in the tissue (10). Although the link between CLBP and morphological muscle changes of the lumbar multifidus (LM) muscle has been thoroughly examined in the literature (11), there is inconclusive evidence regarding a similar association for the ES. One study reported that elderly patients with CLBP had a smaller ES CSA compared to aged matched controls without CLBP (12). Another study showed increased paraspinal muscle FI in patients with continuous vs. recurrent CLBP, but no difference was observed in ES CSA (13). A third study found that patients with severe intervertebral disc degeneration (IDD) were more likely to have increased FI in the ES, and that female participants with symptomatic IDD had greater FI infiltration in the ES at L5–S1 than matched male participants (14). Indeed, a model to predict in vivo intervertebral disc function was recently developed, allowing for a better evaluation of the etiology of CLBP as it pertains to intervertebral disc function (15). Facet joint tropism at the upper lumbar levels has also been associated with higher levels of paraspinal muscles FI (both ES and LM) at lower lumbar levels (16). Overall, while atrophy of the paraspinal muscles may be more present in lower levels of the lumbar spine compared to the upper levels, evidence for ES-specific atrophy is lacking (10). Other factors such as age, sex, body mass index (BMI) and disuse have also been associated with paraspinal muscle FI. Microscopically, CLBP patients show a similar fiber type distribution to healthy controls with about 64% of type I fibers in paraspinal muscles (17).

The current recommendations for the treatment of CLBP suggest that first-line care should be non-pharmacological (18). Indeed, a large clinical trial found that cognitive functional therapy was more effective in the treatment of CLBP and more cost effective than usual care (19). Another treatment option is neuromuscular electrical stimulation (NMES), which uses surface electrodes to transmit electrical current and depolarize nerves, leading to muscle contraction. There is limited evidence that NMES therapy is effective in treating the muscular and functional deficits seen with CLBP. NMES paired with trunk muscle training increased function (20, 21), and decreased pain and low-back pain-related disability in patients with CLBP (22). NMES therapy of the lumbar ES improved trunk balance (e.g., static and dynamic), postural control, recovery of ambulation, and health-related quality of life in stroke patients (21). NMES therapy also increased LM CSA in patients ≥65 years old (23). On the other hand, a 4-week NMES intervention showed no change in function and no pain reduction in patients with CLBP (24).

To our knowledge, no studies have investigated the impact of NMES on ES CSA and FI in CLBP patients. Therefore, the aim of this study was to examine the effect of a 10-week NMES intervention on ES CSA and FI, from L1–L2 to L5–S1, in a cohort of CLBP patients. We hypothesized that NMES therapy would increase CSA and reduce FI of the ES from pre- to post-intervention.

Our findings suggest that a 10-week StimaWELL 120MTRS NMES therapy led to minimal changes in ES CSA and FI in patients with CLBP. Only a significant decrease in CSA at the right L2–L3 ES was observed, which highlights the lack of consistency of the effect of NMES between levels and sides. These results are inconsistent with previous reports stating that NMES increases CSA in healthy and diseased populations (33). These discrepancies could be due to various methodological factors described below. In terms of muscle composition, a significant decrease in FI was only observable at the left ES at L5–S1. The latter findings may be due to the higher levels of FI pre-intervention on this side as compared to the right side. Higher paraspinal muscle FI values on the left side in CLBP was also reported in a recent study (34) Our findings regarding the reversibility of FI is aligned with a recent systematic review which investigated the effect of exercise therapy on FI in CLBP patients (35). This systematic review, however, was based on a small number of available studies, and highlighted several methodological concerns (e.g., study design) and clinical heterogeneity (e.g., imaging acquisition methods) (35). To our knowledge, no other study has measured the effect of NMES therapy on FI in any muscle.

Our results did not show major differences in CSA or FI changes between the phasic and combined stimulation of the StimaWELL 120MTRS device to participants with CLBP. A greater decrease in FI was observed in the combined group at the right L3–L4 and L4–L5 ES. The minimal detectable change at 95% confidence for LM CSA post-treatment is 100 mm² in patients with CLBP (36). This relatively large amount of perceivable change could explain why no significant difference in ES CSA was observed. There is no known value for ES FI minimal detectable change, however the presence of FI in paraspinal muscle has been associated with inflammatory dysregulation (37). While some animal models have studied the anti-inflammatory properties of omega-3 fatty acids in reducing inflammation and promoting neurodegeneration in spinal cord injury (38), the therapeutic effect of such intervention in patients remains to be investigated.

Both the phasic and the combined group included a frequency of 50 Hz, which could explain the similarities in the outcome between the groups. A frequency between 25 and 75 Hz is considered optimal for increasing muscle force—thus promoting hypertrophy—as it creates full tetanic contraction of the muscle (33). Lower non-tetanic frequencies between 2 and 10 Hz lead to low-force muscle twitches but high metabolic demand, which can in turn lead to an increase in oxidative capacity and a shift from type IIx fibers to type IIa fibers (33). In our study, the protocols were differentiated by the presence of a low-frequency signal in the combined group, but no difference in CSA or FI change scores was observed between the protocols.

To the best of our knowledge, only one study assessed the effect of NMES on paraspinal CSA. Jandova et al. (2020) used ultrasound to assess paraspinal muscle morphology and reported a 5.6% (left) and 7.1% (right) increase in LM CSA following 8-weeks of NMES muscle training in healthy individuals aged ≥65 years-old (23). Two other ultrasound studies with similar protocols measured the LM muscle thickness of women (aged 18–30) with CLBP (39, 40). They both noted an increase in the L4 and L5 LM muscle segments after 12 sessions of NMES therapy over 4 weeks (39, 40). Batistella et al. (2020) reported a lower baseline CS thickness in their NMES group compared to their control group at baseline (p = 0.031). But the difference resolved in the subsequent evaluations (week 4: p = 0.229; week 8: p = 0.195), suggesting that NMES increased LM thickness (39). Additionally, Pelegrini et al. (2019) reported no difference in LM thickness between their NMES and control groups at baseline (p = 0.110) but significant differences in the subsequent evaluations (week 4: p = 0.005; week 8: p = 0.016), also suggesting an increase in thickness following NMES therapy (40). Thickness correlates with CSA in the LM at L4 and L5 in males and females with CLBP (41). In comparison to our study, Pelegrini et al. (2019) used a frequency of 1 kHz, modulated at 50 Hz, with a burst duration of 4 milliseconds whereas Batistella et al. (2020) used a frequency of 2,500 Hz, modulated at 50 Hz, 50% cycle, at rise/one-decay/off times—respectively 2, 8, 2, 12 s (40). Both used an Ibramed® device (Amparo, Sao Paulo, Brazil). This difference in NMES parameters could have impacted the outcome. The difference in imaging modalities (e.g., ultrasound vs. MRI) may have also contributed to the inconsistent findings. Our study used MRI, considered the gold standard to assess skeletal muscle morphology (11).

Compared to our intervention which involved 2 NMES sessions per week, prior protocols have consisted of 3 or more NMES sessions per week (39, 40). Greater improvement in quadriceps femoris strength was reported with 3 NMES sessions / week compared to 2 NMES sessions / week (42), and some NMES protocols recommend up to 2 sessions per day with portable units (33). Which is not feasible with the StimaWELL 120MTRS device. Although improvements in muscle size have been found after only 6, and 8 weeks of NMES therapy (33), these protocols included 3–5 treatments per week (43–48).