Slacklining as therapy to address non-specific low back pain in the presence of multifidus arthrogenic muscle inhibition

Low back pain (LBP) represents the most prevalent, problematic and painful of musculoskeletal conditions that affects both the individual and society with health and economic concerns. LBP is a heterogeneous condition with multiple diagnoses and causes. In the absence of consensus definitions, partly because of terminology inconsistency, it is further referred to as non-specific LBP (NSLBP). In NSLBP patients, the lumbar multifidus (MF), a key stabilizing muscle, has a depleted role due to recognized myocellular lipid infiltration and wasting, with the potential primary cause hypothesized as arthrogenic muscle inhibition (AMI). This link between AMI and NSLBP continues to gain increasing recognition. To date there is no ‘gold standard’ or consensus treatment to alleviate symptoms and disability due to NSLBP, though the advocated interventions are numerous, with marked variations in costs and levels of supportive evidence. However, there is consensus that NSLBP management be cost-effective, self-administered, educational, exercise-based, and use multi-modal and multi-disciplinary approaches. An adjuvant therapy fulfilling these consensus criteria is ‘slacklining’, within an overall rehabilitation program. Slacklining, the neuromechanical action of balance retention on a tightened band, induces strategic indirect-involuntary therapeutic muscle activation exercise incorporating spinal motor control. Though several models have been proposed, understanding slacklining’s neuro-motor mechanism of action remains incomplete. Slacklining has demonstrated clinical effects to overcome AMI in peripheral joints, particularly the knee, and is reported in clinical case-studies as showing promising results in reducing NSLBP related to MF deficiency induced through AMI (MF-AMI). Therefore, this paper aims to: rationalize why and how adjuvant, slacklining therapeutic exercise may positively affect patients with NSLBP, due to MF-AMI induced depletion of spinal stabilization; considers current understandings and interventions for NSLBP, including the contributing role of MF-AMI; and details the reasons why slacklining could be considered as a potential adjuvant intervention for NSLBP through its indirect-involuntary action. This action is hypothesized to occur through an over-ride or inhibition of central down-regulatory induced muscle insufficiency, present due to AMI. This subsequently allows neuroplasticity, normal neuro-motor sequencing and muscle re-activation, which facilitates innate advantageous spinal stabilization. This in-turn addresses and reduces NSLBP, its concurrent symptoms and functional disability. This process is hypothesized to occur through four neuro-physiological processing pathways: finite neural delay; movement-control phenotypes; inhibition of action and the innate primordial imperative; and accentuated corticospinal drive. Further research is recommended to investigate these hypotheses and the effect of slacklining as an adjuvant therapy in cohort and control studies of NSLBP populations.