Almost all hypotheses of muscle pain maintain that the pain results from muscle cell activation. The mechanisms so far proposed for the generation of pain are related to hypoxia, effects of energy deficit, or intracellular calcium accumulation, leading to muscle cell damage. However, it has not been possible to find reliable causal associations between pain and muscle activation as measured by electromyography (EMG). Explanations of the pathogenesis of pain have to account for the activation of sensory nerves that mediate information of potential tissue injury to the nerve system, the nociceptors. The finding that sustained activation of low-threshold motor units occur in computer work (the 'Cinderella hypothesis') does not explain the genesis of muscle pain. There is a paucity of reliable evidence of associations between muscle cell damage and work-related muscle pain. Some of the available data indicate that muscle fibre activity may be a consequence of pain rather than a cause. A hypothesis pertaining to work situations with cognitive tasks and low-level muscle activity is presented. This hypothesis proposes that muscle pain originates from the blood vessel-nociceptor interactions of the connective tissue of the muscle. Possible candidate mediators are discussed.
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