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Delayed-Onset Muscle Soreness Alters Mechanical Sensitivity, but Not Thermal Sensitivity or Pain Modulatory Function.
Peterson, Jessica; Chesbro, Grant; Bemben, Michael G; Larson, Rebecca D; Pereira, Hugo M; Black, Christopher D.
Affiliation
  • Peterson J; Department of Health and Exercise Science, University of Oklahoma, Norman, OK, USA.
  • Chesbro G; Department of Kinesiology, New Mexico State University, Las Cruces, NM, USA.
  • Bemben MG; North Florida Foundation of Research and Education, Malcom Randall Veterans Medical Center, Gainesville, FL, USA.
  • Larson RD; Department of Health and Exercise Science, University of Oklahoma, Norman, OK, USA.
  • Pereira HM; Department of Health and Exercise Science, University of Oklahoma, Norman, OK, USA.
  • Black CD; Department of Health and Exercise Science, University of Oklahoma, Norman, OK, USA.
J Pain Res ; 17: 571-581, 2024.
Article in En | MEDLINE | ID: mdl-38347855
ABSTRACT

Introduction:

Many clinical musculoskeletal pain conditions are characterized by chronic inflammation that sensitizes nociceptors. An unresolved issue is whether inflammation affects all nociceptors in a similar manner. Exercise-induced muscle damage (EIMD) has been proposed as a model for simulating clinical inflammatory pain in healthy samples. We sought to test the effect of EIMD on various painful stimuli (pressure and thermal), central pain processing (via the nociceptive flexion reflex) and endogenous pain modulation via conditioned pain modulation and exercise-induced hypoalgesia.

Methods:

Eighteen participants (9F, age 24.6 ± 3.3) were recruited for repeated measures testing and each completed pain sensitivity testing prior to and 48 hours after an eccentric exercise protocol. The participants performed a minimum of 6 rounds of 10 eccentric knee extension exercises to induce muscle damage and localized inflammation in the right quadriceps. Force decrements, knee range-of-motion, and delayed onset muscle soreness (DOMS) were used to quantify EIMD.

Results:

There was a significant main effect of time for pressure pain (%diff; -58.9 ± 23.1; p = 0.02, ηp2 = 0.28) but no significant main effect was observed for limb (%diff; -15.5 ± 23.9; p = 0.53, ηp2 = 0.02). In contrast, there was a significant interaction between time and limb (p < 0.001, ηp2 = 0.47) whereby participants had lower pressure pain sensitivity in the right leg only after the damage protocol (%diff; -105.9 ± 29.2; p = 0.002).

Discussion:

Individuals with chronic inflammatory pain usually have an increased sensitivity to pressure, thermal, and electrical stimuli, however, our sample, following muscle damage to induce acute inflammation only had sensitivity to mechanical pain. Exercise induced inflammation may reflect a peripheral sensitivity localized to the damaged muscle rather than a global sensitivity like those with chronic pain display.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Type of study: Diagnostic_studies / Guideline Language: En Journal: J Pain Res Year: 2024 Document type: Article Affiliation country: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Type of study: Diagnostic_studies / Guideline Language: En Journal: J Pain Res Year: 2024 Document type: Article Affiliation country: United States