• Giovane Galdino de Souza, Igor Dimitri Duarte, and Andrea de Castro Perez.
• Department of Pharmacology, Institution Federal University of Minas Gerais (UFMG), Av Antonio Carlos, UFMG, Belo Horizonte, MG, Brazil.
• Anesth. Analg.. 2013 Mar 1;116(3):703-11.

BackgroundSeveral studies have demonstrated antinociception induced by exercise; however, the specific mechanisms for this effect are not well understood. Thus, we investigated the involvement of α2-adrenergic receptors (α2-ARs) in the antinociceptive effect produced by exercise in rats and mice.MethodsMale Wistar rats performed acute aerobic (AA) and acute resistance exercise protocols, and male α2A/α2C-ARs knockout mice and their wild-type mice were also submitted to AA.ResultsAfter the exercise protocols, the nociceptive threshold of rats and wild type was increased, (except in knockout mice). This effect was reversed by yohimbine, a nonselective α2-ARs antagonist (4 mg/kg, subcutaneously [s.c.]); rauwolscine, a selective α2C-ARs antagonist (4 mg/kg, s.c.); BRL 44408, a selective α2A-ARs antagonist (4 mg/kg, s.c.) and guanethidine, a selective inhibitor of transmission in adrenergic nerves (30 mg/kg, intraperitoneal). Furthermore, when given intrathecally or intracerebroventricularly, yohimbine did not alter antinociception induced by exercise protocols. In addition, α2-ARs expression in rat brains did not change after AA and acute resistance exercise.ConclusionThese results suggest a peripheral involvement of α2-ARs in the antinociception induced by aerobic and resistance exercise.

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