William C Hedderson1, Paul A Borsa2, Roger B Fillingim3, Stephen A Coombes2, Chris J Hass2, Steven Z George4. 1. Department of Exercise and Sport Science, University of Central Arkansas, Conway, AR. 2. Departments of Applied Physiology and Kinesiology. 3. Community Dentistry and Behavioral Science, University of Florida, Gainesville, FL. 4. Department of Orthopaedic Surgery and Duke Clinical Research Institute, Duke University, Durham, NC.
Abstract
OBJECTIVES: The relationship between elevated inflammatory cytokine levels and peak pain intensity following acute musculoskeletal injury has not been fully elucidated in high risk subgroups. Identifying the role that these cytokines have on pain responses may help with developing tailored therapeutic approaches. METHODS: Data were collected from 54 participants who were vulnerable to a robust pain response and delayed recovery following musculoskeletal injury. Participants completed baseline active and resting pain measurements and a blood draw before an exercised induced shoulder muscle injury. Participants returned at 24 and 48 hours postinjury for follow-up pain measurements and blood draws. Blood plasma was analyzed for interleukin (IL)-1β, IL-6, IL-8, IL-10, and tumor necrosis factor α. Pearson bivariate correlations were performed between cytokines and pain measurements to identify candidate variables for stepwise multiple linear regression predicting pain intensity reports. RESULTS: Pearson bivariate correlation identified 13/45 correlations between inflammatory cytokines and resting pain intensity and 9/45 between inflammatory cytokines and active pain (P<0.05, r≥0.3 or r≤-0.3). This led to 5 stepwise multiple linear regression models, of which 4 met the statistical criterion (P<0.0167); including IL-10 baseline plasma concentrations predicting active pain (r=0.19) and resting pain (r=0.15) intensity 48 hours postinjury. IL-6 and IL-10 plasma concentrations at 48 hours were respectively associated with active and resting pain at 48 hours. DISCUSSION: These findings suggest that elevated concentrations of inflammatory cytokines, specifically IL-10 (at baseline and 48 h) and IL-6 (at 48 h), may play a role in heightened pain responses following exercise-induced muscle injury.
OBJECTIVES: The relationship between elevated inflammatory cytokine levels and peak pain intensity following acute musculoskeletal injury has not been fully elucidated in high risk subgroups. Identifying the role that these cytokines have on pain responses may help with developing tailored therapeutic approaches. METHODS: Data were collected from 54 participants who were vulnerable to a robust pain response and delayed recovery following musculoskeletal injury. Participants completed baseline active and resting pain measurements and a blood draw before an exercised induced shoulder muscle injury. Participants returned at 24 and 48 hours postinjury for follow-up pain measurements and blood draws. Blood plasma was analyzed for interleukin (IL)-1β, IL-6, IL-8, IL-10, and tumor necrosis factor α. Pearson bivariate correlations were performed between cytokines and pain measurements to identify candidate variables for stepwise multiple linear regression predicting pain intensity reports. RESULTS: Pearson bivariate correlation identified 13/45 correlations between inflammatory cytokines and resting pain intensity and 9/45 between inflammatory cytokines and active pain (P<0.05, r≥0.3 or r≤-0.3). This led to 5 stepwise multiple linear regression models, of which 4 met the statistical criterion (P<0.0167); including IL-10 baseline plasma concentrations predicting active pain (r=0.19) and resting pain (r=0.15) intensity 48 hours postinjury. IL-6 and IL-10 plasma concentrations at 48 hours were respectively associated with active and resting pain at 48 hours. DISCUSSION: These findings suggest that elevated concentrations of inflammatory cytokines, specifically IL-10 (at baseline and 48 h) and IL-6 (at 48 h), may play a role in heightened pain responses following exercise-induced muscle injury.
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