Introduction Delayed onset of muscle soreness (DOMS) has been described as damaged muscle tissue membranes combined with a secondary inﬂammatory condition (Gleeson et al., 1995; Wilmore and Costill, 2004; Connolly et al., 2003) resulting from unaccustomed eccentric contractions (Taleg, 1973; Newman et al., 1983a,b; Armstrong, 1984; Denegar and Perrin, 1992) and maximal isometric contractions (Clarkson et al., 1986). Although many variables are reported in the quantiﬁcation of muscle damage, the typical symptoms associated with DOMS are loss of strength, pain, muscle tenderness, stiffness, swelling and elevated levels of the enzyme creatine kinase (McHugh et al., 1999). Symptoms can vary from mild muscle tenderness to severe debilitating pain (Cheung et al., 2003).
DOMS is a well researched phenomenon and the morphological injury to the muscle has been well described, however the mechanism underlying the injury remains poorly understood. For many years, DOMS was attributed to an accumulation of the metabolic end products of exercise resulting in elevated muscle lactate. This assumption is now understood to be unconnected to DOMS. It is now proposed that the soreness may be the result of, amongst others, mechanical (Newman et al., 1983a,b; Armstrong, 1984; Stauber et al., 1990) or biochemical (Armstrong, 1984; McIntyre et al., 1995) factors.
Research suggests that the soreness typically appears between 8 and 24 h post-exercise, peaks at 24e48 h and can last for up to 7 days (Cleak and Eston, 1992; Howell et al., 1993).