Summary and Keywords
Exercise is known to exert an influence on pain. Specifically, sensitivity to pain decreases both during and following a single bout of exercise—a phenomenon that has been termed exercise-induced hypoalgesia (EIH). EIH has been shown to occur following a variety of types of exercise including aerobic, dynamic resistance, as well as intermittent and continuous isometric exercise, and with a variety of types of pain stimuli including pressure, thermal, and electrical, among others. Depending upon the type of exercise, the intensity and duration of the exercise bout may affect the magnitude of EIH observed. EIH also may be influenced by presence of chronic pain. In individuals with chronic pain conditions, exercise can have both hypo- and hyperalgesic effects, again depending on the specifics of the exercise stimulus itself.
The mechanisms underlying EIH have not been definitively established. However, a number of potentially viable mechanisms have been examined including: release of stress mediators such as adrenocorticotrophic hormone and growth hormone (GH), stimulation of the endogenous opioid system, interactions between the pain modulatory system and the cardiovascular system resulting from shared neurological pathways, activation of the endocannabinoid (eCB) system, and engagement of supraspinal pain inhibitory mechanisms via conditioned pain modulation (CPM). There is also some evidence that psychosocial factors, including pain-related beliefs like catastrophizing and expectation, may influence EIH.
Research in EIH has several important implications for research and practice. In healthy adults, reduced sensitivity to pain is a salient benefit of exercise and EIH responses may play a role in exercise adherence. For chronic pain patients, research on EIH has the potential to uncover mechanisms related to maintenance of chronic pain. Improving our understanding of how and why hyperalgesia occurs following exercise in these patients can aid in understanding central nervous system mechanisms of disease maintenance and ultimately may help to avoid symptom exacerbation with exercise. However, there remain practical and mechanistic questions to be examined. Translating reductions in pain sensitivity that occur with exercise under controlled laboratory conditions to situations that are more naturalistic will be an important next step for promoting physical activity as a treatment for pain.
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