Neurophysiological Mechanisms of Exercise-Induced Hypoalgesia

Physical exercise is an important component in the treatment and rehabilitation of many patients with chronic pain, and is vital to the overall health and wellbeing of any individual. Laboratory studies report that acute exercise reduces sensitivity to painful stimuli, indicative of a hypoalgesic response. This phenomenon has been termed exercise-induced analgesia or exercise-induced hypoalgesia (EIH). Exercise activates different endogenous analgesia mechanisms in several ways. The stress that accompanies exercise causes a release of endogenous opioids and the activation of supra-spinal nociceptive inhibitory mechanisms modulated by the brain. Furthermore, the increase of stress hormones during exercise triggers the release of β-endorphins from the pituitary and the hypothalamus, which in turn induces analgesic effects by activating μ-opioid receptors peripherally and centrally, respectively. Also, exercise may be accompanied by muscle pain that could inhibit pain in remote areas via another EIH mechanism, the diffuse noxious inhibitory control. However, it is important to bear in mind that some chronic pain patients show a dysfunction of the endogenous analgesia mechanisms, and therefore may experience increased pain sensitivity and symptom flares during and/or following physical exercise. A comprehensive understanding of how exercise influences pain perception is thus necessary to optimize the clinical utility of exercise as a method of pain management.