title: 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 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.
  
  
  CONCLUSIONS
  Currently, the mechanisms responsible for EIH are unknown. This study provides support for a potential endocannabinoid mechanism of EIH following isometric exercise.
authors.affiliation: University of Wisconsin–Madison, 2000 Observatory Dr, Madison, WI 53706-1121. Koltyn@education.wisc.edu
authors.forename: Kelli F
authors.initials: KF
authors.lastname: Koltyn
authors.forename: Angelique G
authors.initials: AG
authors.lastname: Brellenthin
authors.forename: Dane B
authors.initials: DB
authors.lastname: Cook
authors.forename: Nalini
authors.initials: N
authors.lastname: Sehgal
authors.forename: Cecilia
authors.initials: C
authors.lastname: Hillard
mesh_terms: D000293:Adolescent; D000328:Adult; D000577:Amides; D001095:Arachidonic Acids / Q000097:blood; D018592:Cross-Over Studies; D004311:Double-Blind Method; D063388:Endocannabinoids / Q000097:blood; D004983:Ethanolamines / Q000097:blood; D015444:Exercise / Q000502:physiology*; D005260:Female; D005989:Glycerides / Q000097:blood; D005998:Glycine / Q000031:analogs & derivatives / Q000097:blood; D006358:Hot Temperature; D006801:Humans; D007537:Isometric Contraction / Q000502:physiology*; D008297:Male; D009829:Oleic Acids / Q000097:blood; D010146:Pain / Q000503:physiopathology*; D058748:Pain Perception / Q000502:physiology*; D017288:Pain Threshold / Q000502:physiology; D010169:Palmitic Acids / Q000097:blood; D011312:Pressure; D055815:Young Adult
chemical_list: D000577:Amides; D001095:Arachidonic Acids; D063388:Endocannabinoids; D004983:Ethanolamines; D005989:Glycerides; C465623:N-arachidonylglycine; D009829:Oleic Acids; D010169:Palmitic Acids; C488250:oleoylethanolamide; C005958:palmidrol; C094503:glyceryl 2-arachidonate; C505247:2-oleoylglycerol; D005998:Glycine