Elsevier

The Journal of Pain

Volume 15, Issue 12, December 2014, Pages 1294-1304
The Journal of Pain

Original Report
Mechanisms of Exercise-Induced Hypoalgesia

https://doi.org/10.1016/j.jpain.2014.09.006Get rights and content
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Highlights

  • EIH occurred following short-duration isometric exercise.

  • Endocannabinoid levels were found to be elevated following exercise.

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.

Key words

Pain
analgesia
opioids
endocannabinoids

Cited by (0)

Research was conducted at the University of Wisconsin Hospital and Clinics: Clinical Research Unit.

This research was supported by National Institutes of Health grants R21AR057159 and 1UL1RR025011 and by the Research and Education Component of the Advancing a Healthier Wisconsin Endowment at the Medical College of Wisconsin.

The authors have no conflicts of interest to disclose.