Mechanisms of Exercise-Induced Hypoalgesia

Abstract The purpose of this study was to examine opioid and endocannabinoid mechanisms of exercise-induced hypoalgesia (EIH). Fifty-eight men and women (mean age = 21 years) completed 3 sessions. During the first session, participants were familiarized with the temporal summation of heat pain and p...

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Bibliographic Details
Published inThe journal of pain Vol. 15; no. 12; pp. 1294 - 1304
Main Authors Koltyn, Kelli F, Brellenthin, Angelique G, Cook, Dane B, Sehgal, Nalini, Hillard, Cecilia
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.12.2014
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Summary:Abstract The purpose of this study was to examine opioid and endocannabinoid mechanisms of exercise-induced hypoalgesia (EIH). Fifty-eight men and women (mean age = 21 years) completed 3 sessions. During the first session, participants were familiarized with the temporal summation of heat pain and pressure pain protocols. In the exercise sessions, following double-blind administration of either an opioid antagonist (50 mg naltrexone) or placebo, participants rated the intensity of heat pulses and indicated their pressure pain thresholds and pressure pain ratings before and after 3 minutes of submaximal isometric exercise. Blood was drawn before and after exercise. Results indicated that circulating concentrations of 2 endocannabinoids, N -arachidonylethanolamine and 2-arachidonoylglycerol, as well as related lipids oleoylethanolamide, palmitoylethanolamide, N -docosahexaenoylethanolamine, and 2-oleoylglycerol, increased significantly ( P  < .05) following exercise. Pressure pain thresholds increased significantly ( P  < .05), whereas pressure pain ratings decreased significantly ( P  < .05) following exercise. Also, temporal summation ratings were significantly lower ( P  < .05) following exercise. These changes in pain responses did not differ between the placebo and naltrexone conditions ( P  > .05). A significant association was found between EIH and docosahexaenoylethanolamine. These results suggest involvement of a nonopioid mechanism in EIH following isometric exercise. Perspective Currently, the mechanisms responsible for EIH are unknown. This study provides support for a potential endocannabinoid mechanism of EIH following isometric exercise.
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ISSN:1526-5900
1528-8447
DOI:10.1016/j.jpain.2014.09.006