Neuromuscular manifestations of viscoelastic tissue degradation following high and low risk repetitive lumbar flexion.

Cumulative lumbar disorder is common in individuals engaged in long term performance of repetitive and static occupational/sports activities with the spine. The triggering source and of the disorder, the tissues involved in the failure and the biomechanical, neuromuscular, and biological processes active in the initiation and development of the disorder are not known. The hypothesis is forwarded that static and repetitive (cyclic) lumbar flexion-extension and the associated repeated stretch of the various viscoelastic tissues (ligaments, fascia, facet capsule, discs, etc.) causes micro-damage in their collagen fibers followed by an acute inflammation, triggering pain and reflexive muscle spasms/hyper-excitability. Continued exposure to activities, over time, converts the acute inflammation into a chronic one, viscoelastic tissues remodeling/degeneration, modified motor control strategy and permanent disability. Changes in lumbar stability are expected during the development of the disorder. A series of experimental data from in-vivo feline is reviewed and integrated with supporting evidence from the literature to gain a valuable insight into the multi-factorial development of the disorder. Prolonged cyclic lumbar flexion-extension at high loads, high velocities, many repetitions and short in between rest periods induced transient creep/laxity in the spine, muscle spasms and reduced stability followed, several hours later, by an acute inflammation/tissue degradation, muscular hyper-excitability and increased stability. The major findings assert that viscoelastic tissues sub-failure damage is the source and inflammation is the process which governs the mechanical and neuromuscular characteristic symptoms of the disorder. A comprehensive model of the disorder is presented. The experimental data validates the hypothesis as well as provide insights into the development of potential treatment and prevention of the disorder. Copyright Â