Skeletal Muscle: Understanding DOMS

Uzbekistan’s Aytjan Khalmakhanov in action during his bout against Japan’s Kyotaro Sogabe. REUTERS/Chalinee Thirasupa.

Few conditions are as familiar to athletes, and yet as poorly understood, as delayed onset muscle soreness (DOMS). For recreational athletes, it is an inconvenience; for elite competitors, it can disrupt training loads, alter biomechanics, and increase injury risk. Yet despite more than a century of research, scientists still debate exactly what causes it. 

Delayed onset muscle soreness is characterized by delayed muscle soreness, stiffness, swelling, reduced force-generating capacity, altered biomechanics, and impaired proprioceptive function following exercise⁽¹⁾. Mechanical hyperalgesia, pain on movement and palpation, is the dominant clinical feature⁽²⁾. 

It typically follows unaccustomed or high-intensity eccentric exercise such as downhill running, plyometrics, or heavy resistance training^(3,4). Unlike acute exercise-induced pain, DOMS develops after a symptom-free period of 12–24 hours, peaks between 24 and 72 hours, and usually resolves within seven days (see figure 1)^(1-3).  

The pain-free period makes DOMS somewhat mysterious. Although it is generally self-limiting and does not require medical treatment, the associated loss of strength, altered movement patterns, and reduced proprioception may increase the risk of subsequent injury, particularly in high-performance athletes⁽¹⁾. Thus, preventing and treating DOMS, especially in high-performance sports, is particularly valuable⁽³⁾. 

Early theories attributed DOMS to muscle damage, lactic acid accumulation, muscle spasm, connective tissue injury, and inflammation (see table 1). These hypotheses were gradually replaced as research showed inconsistencies between muscle damage, inflammation, and the timing of soreness⁽¹⁾.

Theodore Hough first described DOMS in 1902 in his classic study in the American Journal of Physiology, titled Ergographic Studies in Muscular Soreness. He proposed a hypothesis of rupture of the muscle fiber (or connective tissue between muscle fibers) as the cause of DOMS because soreness was observed after quick and strong contraction.

"...for elite competitors, it can disrupt training loads, alter biomechanics, and increase injury risk."

Eccentric Exercises

Danish physiologist Erling Asmussen published his foundational observations on DOMS in 1956 in an article titled Observations on Experimental Muscular Soreness in the journal Acta Rheumatologica Scandinavica. He showed that lengthening (negative/eccentric) contractions cause significant delayed soreness one to two days later, whereas shortening (positive/concentric) contractions of equal intensity rarely do. He concluded that the soreness stems from mechanical stress and micro-trauma in the intramuscular connective tissue rather than lactic acid accumulation. 

Lactic Acid

Lactic acid was once thought to be the primary cause of DOMS, but this has largely been disproven. Lactate levels return to baseline within an hour after exercise, whereas DOMS develops 12–24 hours later and peaks 24–72 hours afterward. Furthermore, concentric exercise produces far higher lactate levels than eccentric exercise but rarely causes significant DOMS. Likewise, level running generates high lactate concentrations with little soreness, whereas downhill running produces substantial DOMS despite much lower lactate levels. Together, these findings show that lactic acid cannot explain the delayed onset or severity of DOMS⁽⁴⁾.