Delayed onset muscle soreness

Delayed onset muscle soreness (DOMS) is the pain and stiffness felt in muscles several hours to days after unaccustomed or strenuous exercise. Delayed onset muscle soreness (DOMS) is the pain and stiffness felt in muscles several hours to days after unaccustomed or strenuous exercise. The soreness is felt most strongly 24 to 72 hours after the exercise.:63 It is thought to be caused by eccentric (lengthening) exercise, which causes small-scale damage (microtrauma) to the muscle fibers. After such exercise, the muscle adapts rapidly to prevent muscle damage, and thereby soreness, if the exercise is repeated.:76 Delayed onset muscle soreness is one symptom of exercise-induced muscle damage. The other is acute muscle soreness, which appears during and immediately after exercise. The soreness is perceived as a dull, aching pain in the affected muscle, often combined with tenderness and stiffness. The pain is typically felt only when the muscle is stretched, contracted or put under pressure, not when it is at rest.:63 This tenderness, a characteristic symptom of DOMS, is also referred to as 'muscular mechanical hyperalgesia'. Although there is variance among exercises and individuals, the soreness usually increases in intensity in the first 24 hours after exercise. It peaks from 24 to 72 hours, then subsides and disappears up to seven days after exercise.:63 The muscle soreness is caused by eccentric exercise, that is, exercise consisting of eccentric (lengthening) contractions of the muscle. Isometric (static) exercise causes much less soreness, and concentric (shortening) exercise causes none.:63 The mechanism of delayed onset muscle soreness is not completely understood, but the pain is ultimately thought to be a result of microtrauma – mechanical damage at a very small scale – to the muscles being exercised. DOMS was first described in 1902 by Theodore Hough, who concluded that this kind of soreness is 'fundamentally the result of ruptures within the muscle'.:63 According to this 'muscle damage' theory of DOMS, these ruptures are microscopic lesions at the Z-line of the muscle sarcomere. The soreness has been attributed to the increased tension force and muscle lengthening from eccentric exercise. This may cause the actin and myosin cross-bridges to separate prior to relaxation, ultimately causing greater tension on the remaining active motor units. This increases the risk of broadening, smearing, and damage to the sarcomere. When microtrauma occurs to these structures, nociceptors (pain receptors) within the muscle's connective tissues are stimulated and cause a sensation of pain. Another explanation for the pain associated with DOMS is the 'enzyme efflux' theory. Following microtrauma, calcium that is normally stored in the sarcoplasmic reticulum accumulates in the damaged muscles. Cellular respiration is inhibited and ATP needed to actively transport calcium back into the sarcoplasmic reticulum is also slowed. This accumulation of calcium may activate proteases and phospholipases which in turn break down and degenerate muscle protein. This causes inflammation, and in turn pain due to the accumulation of histamines, prostaglandins, and potassium.