Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise? Full Text
Pain Physician, 07/17/2012
Nijs J et al. – A dysfunctional response of patients with chronic pain and aberrations in central pain modulation to exercise has been shown, indicating that exercise therapy should be individually tailored with emphasis on prevention of symptom flares. The paper discusses the translation of these findings to rehabilitation practice together with future research avenues.
- Exercise activates endogenous analgesia in healthy individuals.
- The increased pain threshold following exercise is due to the release of endogenous opioids and activation of (supra)spinal nociceptive inhibitory mechanisms orchestrated by the brain.
- Exercise triggers the release of beta–endorphins from the pituitary (peripherally) and the hypothalamus (centrally), which in turn enables analgesic effects by activating μ–opioid receptors peripherally and centrally, respectively.
- The hypothalamus, through its projections on the periaqueductal grey, has the capacity to activate descending nociceptive inhibitory mechanisms.
- However, several groups have shown dysfunctioning of endogenous analgesia in response to exercise in patients with chronic pain.
- Muscle contractions activate generalized endogenous analgesia in healthy, pain–free humans and patients with either osteoarthritis or rheumatoid arthritis, but result in increased generalised pain sensitivity in fibromyalgia patients.
- In patients having local muscular pain (e.g. shoulder myalgia), exercising non–painful muscles activates generalized endogenous analgesia.
- However, exercising painful muscles does not change pain sensitivity either in the exercising muscle or at distant locations.
