Clinical symptoms of chronic muscle conditions like fibromyalgia (FM), include pain, stiffness, subjective weakness, and muscle fatigue. Pain in FM is usually described as fluctuating and always associated with local or generalized tenderness (hyperalgesia and/or allodynia). This tenderness related to FM pain depends on increased peripheral and/or central nervous system responsiveness to peripheral stimuli which can be either noxious (hyperalgesia) or nonnoxious (allodynia). For example, patients with muscle hyperalgesia will rate painful muscle stimuli higher than normal controls, whereas patients with allodynia may perceive light touch as painful, something that a “normal” individual will never describe as painful. The pathogenesis of such peripheral and/or central nervous system changes in FM is unclear, but peripheral tissue changes, specifically in muscles have been implicated. Indirect evidence from interventions that attenuate tonic peripheral impulse input in patients with FM suggest that overall FM pain is dependent on signals from deep tissues. More importantly, allodynia and hyperalgesia can be improved or abolished by removal of peripheral impulse input. Another potential mechanism for FM pain is central disinhibition. However, this pain mechanism also depends on tonic impulse input even if only inadequately inhibited. Thus a promising approach to understanding FM pain is to determine whether abnormal activity of receptors in deep tissues is fundamental to the development and maintenance of this chronic pain disorder.