Does exercise increase or decrease pain? Central mechanisms underlying these two phenomena
original abstract†Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.
Exercise is an integral part of the rehabilitation of patients suffering a variety of chronic musculoskeletal conditions, such as fibromyalgia, chronic low back pain and myofascial pain. Regular physical activity is recommended for treatment of chronic pain and its effectiveness has been established in clinical trials for people with a variety of pain conditions. However, exercise can also increase pain making participation in rehabilitation challenging for the person with pain. Animal models of exercise-induced pain have been developed and point to central mechanisms underlying this phenomena, such as increased activation of NMDA receptors in pain-modulating areas. Meanwhile, a variety of basic science studies testing different exercise protocols, show exercise-induced analgesia involves activation of central inhibitory pathways. Opioid, serotonin and NMDA mechanisms acting in rostral ventromedial medulla (RVM) promote analgesia associated with exercise. This review explores and discusses current evidence on central mechanisms underlying exercised-induced pain and analgesia.
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These two articles on PainScience.com cite Lima 2017 as a source:
- PS Trigger Points & Myofascial Pain Syndrome — A guide to the unfinished science of muscle pain, with reviews of every theory and self-treatment and therapy option
- PS A Rational Guide to Fibromyalgia — The science of the mysterious disease of pain, exhaustion, and mental fog
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