Chronic Pain and Chronic Fatigue Research Group, Department of Human Physiology, Faculty of Physical Education & Physiotherapy, Vrije Universiteit Brussel, Brussels, Belgium.
Pain Physician. 2012 Jul;15(3 Suppl):ES205-13.
Exercise is an effective treatment for various chronic pain disorders, including fibromyalgia, chronic neck pain, osteoarthritis, rheumatoid arthritis, and chronic low back pain. Although the clinical benefits of exercise therapy in these populations are well established (i.e. evidence based), it is currently unclear whether exercise has positive effects on the processes involved in chronic pain (e.g. central pain modulation).
Reviewing the available evidence addressing the effects of exercise on central pain modulation in patients with chronic pain.
Narrative review.
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.
The reviewed studies examined acute effects of exercise rather than long-term effects of exercise therapy.
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.
运动是治疗各种慢性疼痛疾病的有效方法，包括纤维肌痛、慢性颈痛、骨关节炎、类风湿关节炎和慢性腰痛。尽管运动疗法对这些人群的临床益处已得到充分证实（即基于证据），但目前尚不清楚运动是否对慢性疼痛涉及的过程（如中枢疼痛调节）有积极影响。
综述现有证据，以了解运动对慢性疼痛患者中枢疼痛调节的影响。
叙述性综述。
运动可激活健康个体的内源性镇痛。运动后疼痛阈值增加是由于内啡肽的释放和（脊髓）上的疼痛抑制机制的激活，这是由大脑协调的。运动触发垂体（外周）和下丘脑（中枢）β-内啡肽的释放，进而分别通过激活外周和中枢μ-阿片受体来实现镇痛作用。下丘脑通过其对导水管周围灰质的投射，具有激活下行疼痛抑制机制的能力。然而，一些研究小组已经表明，在慢性疼痛患者中，内源性镇痛对运动的反应出现了功能障碍。肌肉收缩可在健康、无痛的人群以及骨关节炎或类风湿关节炎患者中激活全身性内源性镇痛，但在纤维肌痛患者中会导致全身性疼痛敏感性增加。在患有局部肌肉疼痛（如肩肌痛）的患者中，非疼痛肌肉的运动可激活全身性内源性镇痛。然而，在运动肌肉或远处部位，运动疼痛肌肉不会改变疼痛敏感性。
综述中研究的是运动的急性影响，而不是运动疗法的长期影响。
已经表明，慢性疼痛患者对运动的反应出现了功能障碍，中枢疼痛调节出现了异常，这表明运动疗法应该因人而异，重点是预防症状发作。本文讨论了这些发现如何转化为康复实践以及未来的研究方向。
