Reduced tolerance of exercise in fibromyalgia may be a consequence of impaired microcirculation initiated by deficient action of nitric oxide

Med Hypotheses. 2006;66(5):950-2. doi: 10.1016/j.mehy.2005.11.028. Epub 2006 Jan 10.


Although the underlying mechanism responsible for muscular fatigue and exercise intolerance remains to be elucidated, it is reported two major mechanisms, central and peripheral hypothesis. As a peripheral mechanism, there are few reports on abnormalities of the microcirculation in patients with fibromyalgia. The key point to note is that ischemia associated with a modest decline in tissue oxygen causes muscle fatigue. It has been shown that have been found low muscle levels of phosphates and abnormalities in microcirculation in fibromyalgia. Based on several novel data, production abnormalities of nitric oxide level might lead to symptoms of fatigue as a long term effect. There a vicious cycle concerning impairment of microcirculation in FM. The cycle is firstly initiated decrease of production of nitric oxide in the endothelial level by some trigger factors. Changed level of nitric oxide may cause microcirculation abnormalities in the tissue levels, muscular region. At the end of these phases, muscular fatigue and exercise intolerance may progressively develop in the FM. It is possible that this theory appears to provide a physiopathological explanation for decreased exercise capacity in patients with fibromyalgia. This paper describes a plausible mechanism for the development of exercise intolerance on microcirculation abnormalities.

MeSH terms

  • Exercise Tolerance*
  • Fatigue / etiology
  • Fatigue / physiopathology*
  • Fibromyalgia / complications
  • Fibromyalgia / physiopathology*
  • Humans
  • Microcirculation / physiopathology*
  • Models, Biological
  • Muscle, Skeletal / blood supply*
  • Muscle, Skeletal / physiopathology*
  • Nitric Oxide / metabolism*


  • Nitric Oxide