Delayed Onset Muscle Soreness - Mechanism

Mechanism

Delayed onset muscle soreness was first described in 1902 by Theodore Hough, who concluded that this kind of soreness is "fundamentally the result of ruptures within the muscle". This is still considered broadly valid, although the soreness does not appear to involve the rupture of whole muscle fibers. What has been observed to accompany soreness are ultrastructural disruptions of myofilaments, especially at the Z-disc, as well as damage to the muscle's connective tissue. That tissue damage may relate most directly to soreness, as it may increase the mechanical sensitivity of the muscle nociceptors, or pain receptors, and cause pain with stretching and palpation. The delayed onset of the soreness may occur because the inflammatory response process that sensitizes the nociceptors takes some time. However, the relationship between damage, inflammation and soreness is not yet completely understood.

Two other hypotheses that have been advanced to explain the soreness, muscle spasms and the presence of lactic acid in the muscle, are now considered unlikely to be correct, since there is evidence to refute them. In particular, lactic acid is removed from the muscle within an hour of intense exercise, and therefore cannot cause the soreness which normally begins about a day later.