Bing He Zhou

Neuromuscular neutral zones response to cyclic lumbar flexion

The in vivo lumbar spine of the anaesthetized feline was subjected to passive cyclic anterior flexion-extension at 0.25 Hz and 40 N peak load for cumulative 60 min duration. Displacement (or displacement neuromuscular neutral zones-DNNZ) and tension (or tension neuromuscular neutral zones-TNNZ) at which reflexive EMG activity from the multifidi muscles was initiated and terminated were recorded, for single-test cycles, before and for 7h after cyclic loading. Displacement and tension NNZs increased significantly after loading. The displacement NNZs decreased exponentially to near baseline by the 7th hour of rest. The tension NNZs, however, decreased to below the baseline by the 2nd to 3rd hour after loading and continued decreasing into the 7th hour. Peak EMG significantly decreased (49-57%) to below the baseline immediately after loading and then exponentially increased, exceeding the baseline by the 2nd to 3rd hour and reaching 33-59% above baseline by the 7th hour. EMG median frequency decreased after loading and then exceeded the baseline after the 3rd hour, indicating initial de-recruitment, followed by recruitment of new motor units. These findings suggest that the lumbar spine was exposed to instability for 2-3h after cyclic loading, due to concurrent laxity of the viscoelastic tissues and deficient muscular activity. A delayed neuromuscular compensation mechanism was found to exist, triggering the musculature significantly earlier and at higher magnitude than baseline, while the viscoelastic tissues were still lax. Thus, it is suggested that prolonged cyclic loading may compromise lumbar stability during the immediate 2-3h post-loading, increasing the risk of injury.

Neuromuscular neutral zones response to static lumbar flexion: Muscular stability compensator

BACKGROUND The impact of six sequential static loading and rest of the lumbar spine on the changes in the neuromuscular neutral zones and thereby on spine stability was assessed. METHODS Six 10 min sessions of static load of a moderate level each spaced by 10 min rest were applied to the in vivo feline model. Test cycles of 0.25 Hz and at the same moderate peak load were applied before and every hour after the static loading sequence up to 7h. Load, displacement and electromyographic activity of the lumbar multifidi muscles were recorded throughout. FINDINGS Displacement and tension neuromuscular neutral zones were defined as the displacement or tension, in the increase and decrease phases of each cycle, when the electromyogram initiated and ceased activity, respectively. Displacement neuromuscular neutral zones demonstrated significant (P<0.001) increase immediately post-static loading, followed by an exponential decrease to pre-loading baseline by the 7th hour. Tension neuromuscular neutral zones, however, demonstrated significant (P<0.001) increase in the 2h immediately after the static loading and a significant decrease (P<0.001) thereafter. Peak electromyogram decreased in the first 3h post-loading, but significantly (P<0.001) increased thereafter to the 7th hour. INTERPRETATION It was concluded that the first 2-3h post-static loading finds the spine with significant laxity in the viscoelastic tissues concurrently with deficient muscular activation and therefore exposed to the risk of instability. It is also evident that a neural control compensation mechanism exists where it enhances the activation of the musculature to earlier and at higher activation magnitude, 2-3h post-loading, increasing lumbar stability while the viscoelastic tissues are still lax.

High magnitude cyclic load triggers inflammatory response in lumbar ligaments

BACKGROUND Cumulative trauma disorder is commonly reported by workers engaged in prolonged repetitive/cyclic occupational activities. Recent experimental evidence confirms that relatively short periods of cyclic lumbar flexion at high loads result in substantial creep of viscoelastic tissues, prolonged periods of its recovery to baseline together with a neuromuscular disorder and exposure to instability. The biochemical process associated with the creep and neuromuscular disorder are not well explored. The purpose of the study is to identify the ligaments as one of the organs of failure and an acute inflammation as the result of failure as a preliminary step in the development of chronic inflammation that might lead to cumulative trauma disorder elicited by high magnitude cyclic loads. METHODS The lumbar spine of anaesthetized cats was subjected to cyclic flexion loading at high magnitudes for six periods of 10 min each with 10 min rest in between followed by 7h rest. Lumbar displacement was monitored throughout. Supraspinous ligaments from L-3/4, L-4/5, L-5/6 and unloaded T-10/11 were removed at the end of testing and assessed using mRNA expression for cytokine (IL-1beta, IL-6, IL-8, TNFalpha, TGFbeta). Cytokines expression in the lumbar ligaments were statistically compared to their self control in the unloaded thoracic ligament. The creep developed during the loading and its recovery during the 7h rest was calculated. FINDINGS The mean creep developed during the loading period reached 57.3% recovering to a residual value of 25.5% at the end of the 7h rest. Increase in cytokine expression was seen in all lumbar ligaments with statistical significance in the L-4/5 and L-5/6 levels. INTERPRETATION The results confirm that prolonged high magnitude cyclic loading of the lumbar spine in flexion-extension elicits substantial residual creep together with significant increases in cytokines expression, consistent with an acute inflammation, several hours post loading. Further exposure to cyclic loading over time may result in conversion to chronic inflammation.

Frequency of cyclic lumbar loading is a risk factor for cumulative trauma disorder

Epidemiologic studies indicate that repetitive (cyclic) occupational activities lead to a cumulative trauma disorder (CTD), and the frequency or velocity of the movement is one of the risk factors. Experimental neurophysiological evidence to confirm the epidemiology is not available. The response of the multifidus muscles to cyclic loading in anterior lumbar flexion–extension was assessed to test the hypothesis that high‐frequency loading may induce an acute neuromuscular disorder leading to CTD. Two groups of feline preparations were subjected to cyclic loading with a peak of 20 N: one at 0.25 HZ and the second at 0.5 HZ, with an equal number of cycles. Electromyogram (EMG), lumbar displacement and load were recorded throughout the loading periods and during single‐cycle tests over a 7‐hour rest period following the load–rest sessions. A model was developed to quantify the creep and neuromuscular responses, and analysis of variance (ANOVA) was applied to assess significance of the results. The group exposed to 0.5 HZ exhibited spontaneous spasms followed by sustained spasms during the loading periods. During the 7‐hour recovery period, a significant (P < 0.001) delayed hyperexcitability as well as sustained spasms of the multifidi were present in the last 5 hours, confirming a significant (P < 0.024 to P < 0.042) acute neuromuscular disorder. High‐frequency cyclic loading of the lumbar spine may trigger a severe acute neuromuscular disorder, as evidenced by the sustained spasms and delayed hyperexcitability, and should be considered as a risk factor. We suggest that workers avoid high‐frequency exposure to cyclic activity in order to prevent the development of cumulative trauma disorder. Muscle Nerve, 2008

High-frequency loading of lumbar ligaments increases proinflammatory cytokines expression in a feline model of repetitive musculoskeletal disorder

BACKGROUND CONTEXT Cumulative (repetitive) lumbar disorder is common in the workforce, and the associated epidemiology points out high risk for lifting heavy loads, performing many repetitions, and performing movements at high velocity. Experimental verification of viscoelastic tissue degradation and a neuromuscular disorder exist for cyclic work under heavy loads. Experimental validation for a disorder because of cyclic loads under high-velocity movement is missing. PURPOSE Obtain experimental verification that high-velocity lumbar flexion-extension results in significant increase of proinflammatory cytokines in the viscoelastic tissues. STUDY DESIGN Laboratory experiments using two in vivo feline model groups subjected to cyclic flexion-extension at low and high velocity. METHODS Seven hours after cumulative 60 minutes of cyclic flexion-extension at moderate load of 40 N and 0.25 Hz for first group and 0.5 Hz for the second group, the supraspinous ligaments of L3-L4 to L5-L6 were harvested and subjected to cytokines (interleukin [IL]-1β, IL-6, IL-8, tumor necrosis factor-α, and transforming growth factor-β1) analysis. Two-way mixed model analysis of variance with a post hoc analysis were used to assess any significant differences (p<.05) in cytokines expression level between the two groups as well as main effect and interaction with lumbar levels. RESULTS Expression levels of the five cytokines were significantly increased in the group subjected to the high-frequency loading. CONCLUSIONS Exposure of the lumbar spine to high-velocity flexion-extension triggers a significant increase in proinflammatory cytokines, indicating pronounced changes consistent with an acute inflammation. Further exposure to activity over prolonged periods may trigger chronic inflammation and tissue degeneration as the source of cumulative lumbar disorder.

Acute repetitive lumbar syndrome: A multi-component insight into the disorder

PURPOSE Repetitive Lumbar Injury (RLI) is common in individuals engaged in long term performance of repetitive occupational/sports activities with the spine. The triggering source of the disorder, tissues involved in the failure and biomechanical, neuromuscular, and biological processes active in the initiation and development of the disorder, are not known. The purpose is, therefore, to test, using in-vivo feline model and healthy human subjects, the hypothesis that RLI due to prolonged exposure to repetitive lumbar flexion-extension is triggered by an acute inflammation in the viscoelastic tissues and is characterized by lingering residual creep, pronounced changes in neuromuscular control and transient changes in lumbar stability. This report, therefore, is a summary of a lengthy research program consisting of multiple projects. METHODS A series of experimental data was obtained from in-vivo feline groups and normal humans subjected to prolonged cyclic lumbar flexion-extension at high and low loads, high and low velocities, few and many repetitions, as well as short and long in-between rest periods, while recording lumbar displacement and multifidi EMG. Neutrophil and cytokines expression analysis were performed on the dissected feline supraspinous ligaments before loading (control) and 7 h post-loading. A comprehensive, time based model was designed to represent the creep, motor control, tissue biology and stability derived from the experimental data. RESULTS Prolonged cyclic loading induced creep in the spine, reduced muscular activity, triggered spasms and reduced stability followed, several hours later, by acute inflammation/tissue degradation, muscular hyperexcitability and hyperstability. Fast movement, high loads, many repetitions and short rest periods, triggered the full disorder, whereas low velocities, low loads, long rest and few repetitions, triggered only minor but statistically significant pro-inflammatory tissue degradation and significantly reduced stability. CONCLUSION Viscoelastic tissue failure via inflammation is the source of RLI and is also the process which governs the mechanical and neuromuscular characteristic symptoms of the disorder. The experimental data validates the hypothesis and provides insights into the development of potential treatments and prevention.