Delayed trunk muscle reflex responses increase the risk of low back injuries.

STUDY DESIGN: Prospective observational study with a 2- to 3-year follow-up. OBJECTIVES: To determine whether delayed muscle reflex response to sudden trunk loading is a result of or a risk factor for sustaining a low back injury (LBI). SUMMARY OF BACKGROUND DATA: Differences in motor control have been identified in individuals with chronic low back pain and in athletes with a history of LBI when compared with controls. However, it is not known whether these changes are a risk for or a result of LBI. METHODS: Muscle reflex latencies in response to a quick force release in trunk flexion, extension, and lateral bending were measured in 303 college athletes. Information was also obtained regarding their personal data, athletic experience, and history of LBI. The data were entered into a binary logistic regression model to identify the predictors of future LBI. RESULTS.: A total of 292 athletes were used for the final analysis (148 females and 144 males). During the follow-up period, 31 (11%) athletes sustained an LBI. The regression model, consisting of history of LBI, body weight, and the latency of muscles shutting off during flexion and lateral bending load releases, predicted correctly 74% of LBI outcomes. The odds of sustaining LBI increased 2.8-fold when a history of LBI was present and increased by 3% with each millisecond of abdominal muscle shut-off latency. On average, this latency was 14 milliseconds longer for athletes who sustained LBI in comparison to athletes who did not sustain LBI (77 [36] vs. 63 [31]). There were no significant changes in any of the muscle response latencies on retest following the injury. CONCLUSIONS: The delayed muscle reflex response significantly increases the odds of sustaining an LBI. These delayed latencies appear to be a preexisting risk factor and not the effect of an LBI.

Sustained orbital shear stress stimulates smooth muscle cell proliferation via the extracellular signal-regulated protein kinase 1/2 pathway.

OBJECTIVE: Nonlaminar shear stress stimulates smooth muscle cell (SMC) proliferation and migration in vivo, especially after an endothelial-denuding injury. To determine whether sustained shear stress directly stimulates SMC proliferation in vitro, the effect of orbital shear stress on SMC proliferation, phenotype, and extracellular signal-regulated protein kinase 1/2 (ERK1/2) phosphorylation was examined. METHODS: Bovine SMCs were exposed to orbital shear stress (210 rpm) for up to 10 days, with and without the ERK1/2 upstream pathway inhibitor PD98059 (10 microM) or the p38 pathway inhibitor SB203580 (10 microM). Proliferation was directly counted and assessed with proliferation cell nuclear antigen. Western blotting was used to assess activation of SMC ERK1/2 and SMC phenotype markers. RESULTS: SMCs exposed to sustained orbital shear stress (10 days) had 75% increased proliferation after 10 days compared with static conditions. Expression of markers of the contractile phenotype (alpha-actin, calponin) was decreased, and markers of the synthetic phenotype (vimentin, beta-actin) were increased. ERK1/2 was phosphorylated in the presence of orbital shear stress, and orbital shear-stress-stimulated SMC proliferation was inhibited in the presence of PD98059 but sustained in the presence of SB203580. Orbital shear-stress-induced changes in SMC phenotype were also inhibited in the presence of PD98059. CONCLUSION: Orbital shear stress directly stimulates SMC proliferation in long-term culture in vitro and is mediated, at least partially, by the ERK1/2 pathway. The ERK1/2 pathway may also mediate the orbital shear-stress-stimulated switch from SMC contractile to synthetic phenotype. These results suggest that shear-stress-stimulated SMC proliferation after vascular injury is mediated by a pathway amenable to pharmacologic manipulation.

Comparison of motion restriction and trunk stiffness provided by three thoracolumbosacral orthoses (TLSOs).

The amounts of thoracic and lumbar spine motion restriction and passive trunk stiffness provided by three thoracolumbosacral orthoses (TLSOs) (Aspen TLSO, Boston Body Jacket, and CAMP TLSO) were compared. Ten subjects executed maximum trunk flexion, extension, and lateral bending motions. The spine motion was measured noninvasively with a thin strain gauge device (Flexducer), and passive trunk stiffness around the neutral posture was estimated from an electromyography-assisted biomechanical model. No significant differences in either the restriction of motion or the amount of added passive trunk stiffness were found between the three orthoses. The subjects also did not perceive any difference in the restriction of motion but rated the Aspen TLSO significantly more comfortable than the other two orthoses. The rigid custom orthosis design may not be important for restricting the spine motion and providing passive trunk stiffness, or there may be other measures that reflect better the function of orthoses.