Muscle physiology and cold reactivity in the fibromyalgia syndrome

The lack of a reproducible pathophysiologic abnormality continues to be a major obstacle in the widespread acceptance of the fibromyalgia syndrome (FMS) and constitutes and 'intellectual block' to a focused research effort. There is a general perception that the pain component of this syndrome arises from muscle or muscle tendon junctions. These are the sites of the so called tender points, and most patients localize their pain as muscular in origin. However, biopsy studies have failed to demonstrate a specific muscle lesion unique to FMS. For more than 40 years there has been a poorly defined concept that the symptoms of FMS are due to a temporary reduction of muscle blood flow, possibly due to muscle spasm, or an accumulation of lactic acid and other waste products. These concepts have led to the hypothesis that muscle pain causes a positive feedback cycle of local muscle spasm, which in turn causes local ischemia, delayed elimination of metabolic waste products and hence more pain, and so on. These concepts are examined in relation to: (1) contemporary knowledge of muscle metabolism and regional blood flow; and (2) recent studies of FMS which have assessed muscle metabolism, muscle oxygenation, respiratory gas exchange, muscle blood flow, and cold reactivity.