Physical exercise is increasingly recognized as an effective treatment to reduce pain and improve function in a variety of pain conditions. Studies in humans and non-human animals have shown that a single session of physical exercise can reduce pain perception to experimental stimuli. The mechanisms underlying this exercise-induced hypoalgesia (EIH) remain elusive. Central and peripheral processes have been proposed, but their relative contributions remain unknown. Among others, the sympatho-adrenergic system could be involved in another well-known phenomenon, stress-induced analgesia (SIA). This project aims (1) to shed light on the processes underlying EIH in humans, (2) to explore whether EIH and SIA may share some similar processes, and (3) to test the possible involvement of peripheral α2-adrenergic receptors (α2-AR) in EIH and SIA, and kynurenic acid (KynA, a circulating myokine that transiently increases following exercise) in EIH. First, we will characterize the effects of a single session of aerobic exercise on the sensitivity to stimuli activating skin versus muscle nociceptors, within or outside exercising body parts. We will also evaluate whether exercise modulates secondary hyperalgesia due to central sensitization. Then, we will test whether α2-AR activation contributes to EIH and/or SIA by evaluating the effects of an α2-AR antagonist (single oral dose of yohimbine) compared to placebo. Finally, we will evaluate the contribution of KynA to EIH by relating, across participants and over time, the post-exercise reduction in experimentally induced pain with the post-exercise plasmatic increase of KynA.