Jump to content

Delayed onset muscle soreness

From Wikipedia, the free encyclopedia

Delayed onset muscle soreness
Other namesMuscle fever
SpecialtySports medicine

Delayed onset muscle soreness (DOMS) is the pain and stiffness felt in muscles after unaccustomed or strenuous exercise. The soreness is felt most strongly 24 to 72 hours after the exercise.[1][2]: 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.[1][2]: 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.

Signs and symptoms[edit]

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.[2]: 63  This tenderness, a characteristic symptom of DOMS, is also referred to as "muscular mechanical hyperalgesia".[3]

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.[2]: 63 


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.[2]: 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,[4] who concluded that this kind of soreness is "fundamentally the result of ruptures within the muscle".[2]: 63  According to this "muscle damage" theory of DOMS, these ruptures are microscopic lesions at the Z-line of the muscle sarcomere.[5] The soreness has been attributed to the increased tension force and muscle lengthening from eccentric exercise.[6] This may cause the actin and myosin cross-bridges to separate prior to relaxation, ultimately causing greater tension on the remaining active motor units.[6] 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.[7]

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.[8] This causes inflammation, and in turn pain due to the accumulation of histamines, prostaglandins, and potassium.[7][9]

An earlier theory posited that DOMS is connected to the build-up of lactic acid in the blood, which was thought to continue being produced following exercise. This build-up of lactic acid was thought to be a toxic metabolic waste product that caused the perception of pain at a delayed stage. This theory has been largely rejected, as concentric contractions which also produce lactic acid have been unable to cause DOMS.[5] Additionally, lactic acid is known from multiple studies to return to normal levels within one hour of exercise, and therefore cannot cause the pain that occurs much later.[7]

Mizumura et al. argue, in contrast to the conventional view, that muscle damage is a sufficient but not necessary condition for DOMS, and that a crucial role is played by the activation of the B2 bradykinin receptornerve growth factor (NGF) and the COX-2-glial cell line-derived neurotrophic factor (GDNF) pathways.[10] A recent theory of Sonkodi et al., that incorporates the findings of Mizumura et al., proposes that the microdamage to the muscles is only the secondary phase of DOMS injury mechanism and suggests that the primary damage is the microinjury of the proprioceptive type Ia sensory fiber terminals within the muscle spindle.[11]

Relation to other effects[edit]

Although delayed onset muscle soreness is a symptom associated with muscle damage, its magnitude does not necessarily reflect the magnitude of muscle damage.[2]: 66–67 

Soreness is one of the temporary changes caused in muscles by unaccustomed eccentric exercise. Other such changes include decreased muscle strength, reduced range of motion, and muscle swelling.[2]: 66  It has been shown, however, that these changes develop independently in time from one another and that the soreness is therefore not the cause of the reduction in muscle function.[2]: 66 

Possible function as a warning sign[edit]

Soreness might conceivably serve as a warning to reduce muscle activity to prevent injury or further injury. With delayed onset muscle soreness (DOMS) caused by eccentric exercise (muscle lengthening), it was observed that light concentric exercise (muscle shortening) during DOMS can cause initially more pain but was followed by a temporary alleviation of soreness with no adverse effects on muscle function or recovery being observed.[2]: 68  Furthermore, eccentric exercise during DOMS was found to not exacerbate muscle damage, nor did it have an adverse effect on recovery, indicating that soreness is not necessarily a warning sign to reduce the usage of the affected muscle.[2]: 68  However, it was also observed that a second bout of eccentric exercise within one week of the initial exercise did lead to decreased muscle function immediately afterward.[2]: 70 

Repeated-bout effect[edit]

After performing an unaccustomed eccentric exercise and exhibiting severe soreness, the muscle rapidly adapts to reduce further damage from the same exercise. This is called the "repeated-bout effect".[12]

As a result of this effect, not only is the soreness reduced the next time the exercise is performed, but other indicators of muscle damage, such as swelling, reduced strength, and reduced range of motion, are also more quickly recovered from. The effect is mostly, but not wholly, specific to the exercised muscle; experiments have shown that some of the protective effects is also conferred on other muscles.[2]: 69 

The magnitude of the effect is subject to many variations, depending for instance on the time between bouts, the number and length of eccentric contractions, and the exercise mode. It also varies between people and between indicators of muscle damage.[2]: 69  Generally, though, the protective effect lasts for at least several weeks. It seems to gradually decrease as the time between bouts increases and is undetectable after about one year.[2]: 70 

The first bout does not need to be as intense as the subsequent bouts to confer at least some protection against soreness. For instance, eccentric exercise performed at 40% of maximal strength has been shown to confer a protection of 20–60% from muscle damage incurred by a 100% strength exercise two to three weeks later.[2]: 73  Also, the repeated-bout effect appears even after a relatively small number of contractions, possibly as few as two. In one study, a first bout of 10, 20 or 50 contractions provided equal protection for a second bout of 50 contractions three weeks later.[2]: 70 

The reason for the protective effect is not yet understood. A number of possible mechanisms, which may complement one another, have been proposed. These include neural adaptations (improved use and control of the muscle by the nervous system), mechanical adaptations (increased muscle stiffness or muscle support tissue), and cellular adaptations (adaptation to inflammatory response and increased protein synthesis, among others).[2]: 74 


Delayed onset muscle soreness can be reduced or prevented by gradually increasing the intensity of a new exercise program,[13]: 112  thereby taking advantage of the repeated-bout effect.[14]

Soreness can theoretically be avoided by limiting exercise to concentric and isometric contractions,[13]: 112  but eccentric contractions in some muscles are normally unavoidable during exercise, especially when muscles are fatigued.[2]: 63  Limiting the length of eccentric muscle extensions during exercise may afford some protection against soreness, but this may also not be practical depending on the mode of exercise.

Physical activity before eccentric exercise helps to prevent delayed-onset muscle soreness.[15] Static stretching or warming up the muscles before or after exercise does not prevent soreness,[16] although there is evidence that whole body vibration therapy performed before exercise may lessen both the soreness and reduced range of motion caused by delayed onset muscle soreness.[17][18]

Other preventative measures with evidence of efficacy based on randomized controlled trials include the consumption of saffron.[19] Wearing compression garments has not been demonstrated to have a significant effect on delayed onset muscle soreness.[20]


The soreness usually disappears within about 72 hours after appearing. If treatment is desired, any measure that increases blood flow to the muscle, such as low-intensity activity, massage, nerve mobilization,[21] hot baths,[22][23] or a sauna visit may help somewhat.[13]: 112 

Immersion in cool or icy water, an occasionally recommended remedy, was found to be ineffective in alleviating DOMS in one 2011 study,[24] but effective in another.[25] There is also insufficient evidence to determine whether whole-body cryotherapy—compared with passive rest or no whole-body cryotherapy—reduces DOMS, or improves subjective recovery, after exercise.[1]

Counterintuitively, continued exercise may temporarily suppress the soreness. Exercise increases pain thresholds and pain tolerance. This effect, called exercise-induced analgesia, is known to occur in endurance training (running, cycling, swimming), but little is known about whether it also occurs in resistance training. There are claims in the literature that exercising sore muscles appears to be the best way to reduce or eliminate the soreness, but this has not yet been systematically investigated.[2]: 62–63 

Ibuprofen is not an appropriate treatment for delayed onset muscle soreness and damage.[26] It decreases soreness, but does not counteract the reduction in muscular performance caused by delayed onset muscle soreness.[27]


  1. ^ a b c Costello, Joseph T.; Baker, Philip Ra; Minett, Geoffrey M.; Bieuzen, Francois; Stewart, Ian B.; Bleakley, Chris (18 September 2015). "Whole-body cryotherapy (extreme cold air exposure) for preventing and treating muscle soreness after exercise in adults" (PDF). The Cochrane Database of Systematic Reviews. 2015 (9): CD010789. doi:10.1002/14651858.CD010789.pub2. ISSN 1469-493X. PMC 9579836. PMID 26383887.
  2. ^ a b c d e f g h i j k l m n o p q r s t Nosaka, Ken (2008). "Muscle Soreness and Damage and the Repeated-Bout Effect". In Tiidus, Peter M (ed.). Skeletal muscle damage and repair. Human Kinetics. pp. 59–76. ISBN 978-0-7360-5867-4.
  3. ^ Taguchi, T.; Matsuda, T.; Tamura, R.; Sato, J.; Mizumura, K. (2005). "Muscular mechanical hyperalgesia revealed by behavioural pain test and c-Fos expression in the spinal dorsal horn after eccentric contraction in rats". The Journal of Physiology. 564 (Pt 1): 259–268. doi:10.1113/jphysiol.2004.079483. PMC 1456042. PMID 15677691.
  4. ^ Hough, Theodore (1902). "Ergographic studies in muscular soreness". American Journal of Physiology. 1902 (7): 76–92. doi:10.1080/23267224.1902.10649879.; Hough T (1900). "Ergographic Studies in Muscular Fatigue and Soreness". J Boston Soc Med Sci. 5 (3): 81–92. PMC 2048417. PMID 19971340.
  5. ^ a b Armstrong, RB (December 1984). "Mechanisms of exercise-induced delayed onset muscular soreness: a brief review". Medicine & Science in Sports & Exercise. 16 (6): 529–38. doi:10.1249/00005768-198412000-00002. PMID 6392811.
  6. ^ a b Gulick, DT; Kimura, IF; Sitler, M; Paolone, A; Kelly, JD (April 1996). "Various treatment techniques on signs and symptoms of delayed onset muscle soreness". Journal of Athletic Training. 31 (2): 145–52. PMC 1318445. PMID 16558388.
  7. ^ a b c Cheung, K; Hume, P; Maxwell, L (2003). "Delayed onset muscle soreness: treatment strategies and performance factors". Sports Medicine. 33 (2): 145–64. doi:10.2165/00007256-200333020-00005. PMID 12617692. S2CID 26525519.
  8. ^ Stauber, WT (1989). "Eccentric action of muscles: physiology, injury, and adaptation". Exercise and Sport Sciences Reviews. 17: 157–85. doi:10.1249/00003677-198900170-00008. PMID 2676546. S2CID 73169107.
  9. ^ Armstrong, RB (August 1990). "Initial events in exercise-induced muscular injury". Medicine & Science in Sports & Exercise. 22 (4): 429–35. doi:10.1249/00005768-199008000-00002. PMID 2205778.
  10. ^ Mizumura, Kazue; Taguchi, Toru (2016). "Delayed onset muscle soreness: Involvement of neurotrophic factors". The Journal of Physiological Sciences. 66 (1): 43–52. doi:10.1007/s12576-015-0397-0. ISSN 1880-6562. PMC 10716961. PMID 26467448.
  11. ^ Sonkodi, B at al (2020). "Have We Looked in the Wrong Direction for More Than 100 Years? Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle Damage". Antioxidants. 3 (9): 212. doi:10.3390/antiox9030212. PMC 7139782. PMID 32150878.
  12. ^ Nosaka, 68–69
  13. ^ a b c Kokkinos, Peter (2009). Physical Activity and Cardiovascular Disease Prevention. Jones & Bartlett Learning. pp. 111–112. ISBN 978-0-7637-5612-3.
  14. ^ Margaritelis, Nikos V.; Theodorou, Anastasios A.; Baltzopoulos, Vasilios; Maganaris, Constantinos N.; Paschalis, Vassilis; Kyparos, Antonios; Nikolaidis, Michalis G. (10 December 2015). "Muscle damage and inflammation after eccentric exercise: can the repeated bout effect be removed?". Physiological Reports. 3 (12): e12648. doi:10.14814/phy2.12648. PMC 4760450. PMID 26660557.
  15. ^ Rahnama, N; Rahmani-Nia, F; Ebrahim, K (1 January 2005). "The isolated and combined effects of selected physical activity and ibuprofen on delayed-onset muscle soreness". Journal of Sports Sciences. 23 (8): 843–850. doi:10.1080/02640410400021989. PMID 16195036. S2CID 27071063. Retrieved 31 January 2023.
  16. ^ Herbert, Robert D.; de Noronha, Marcos; Kamper, Steven J. (6 July 2011). "Stretching to prevent or reduce muscle soreness after exercise". The Cochrane Database of Systematic Reviews (7): CD004577. doi:10.1002/14651858.CD004577.pub3. ISSN 1469-493X. PMID 21735398.
  17. ^ Aminian-Far, A; Hadian, MR; Olyaei, G; Talebian, S; Bakhtiary, AH (2011). "Whole-body vibration and the prevention and treatment of delayed-onset muscle soreness". J Athl Train. 46 (1): 43–9. doi:10.4085/1062-6050-46.1.43. PMC 3017487. PMID 21214349.
  18. ^ Veqar, Z; Imtiyaz, S (2014). "Vibration Therapy in Management of Delayed Onset Muscle Soreness (DOMS)". J Clin Diagn Res. 8 (6): LE01-4. doi:10.7860/JCDR/2014/7323.4434. PMC 4127040. PMID 25121012.
  19. ^ Meamarbashi, A; Rajabi, A (2015). "Preventive effects of 10-day supplementation with saffron and indomethacin on the delayed-onset muscle soreness". Clin J Sport Med. 25 (2): 105–12. doi:10.1097/JSM.0000000000000113. PMID 24915175. S2CID 3257497.
  20. ^ Heiss, R; Hotfiel, T; Kellermannfirst3=M; May, MS; Wuest, W; Janka, R; et al. (2018). "Effect of Compression Garments on the Development of Edema and Soreness in Delayed-Onset Muscle Soreness". J Sports Sci Med. 17 (3): 392–401. PMC 6090402. PMID 30116112.{{cite journal}}: CS1 maint: numeric names: authors list (link)
  21. ^ " Romero-moraleda B, Touche R La, Lerma-lara S, Ferrer-Peña R, Paredes V, Peinado A, Muñoz-García D. 2017. Neurodynamic mobilization and foam rolling improved delayed-onset muscle soreness in a healthy adult population: a randomized controlled clinical trial". 1–19.
  22. ^ Heeren, Kris (30 April 2014). "Effects of therapeutic massage on gait and pain after delayed onset muscle soreness". Journal of Exercise Rehabilitation. 10 (2): 136–140. doi:10.12965/jer.140106. PMC 4025548. PMID 24877051.
  23. ^ Heeren, Kris (3 February 2023). "5 Scientifically Proven Reasons to Use a Hot Tub for Muscle Soreness". gymposts. Retrieved 3 February 2023.
  24. ^ Sellwood, K. L.; Brukner, P.; Williams, D.; Nicol, A.; Hinman, R. (2007). "Ice-water immersion and delayed-onset muscle soreness: A randomised controlled trial". British Journal of Sports Medicine. 41 (6): 392–397. doi:10.1136/bjsm.2006.033985. PMC 2465319. PMID 17261562.
  25. ^ Snyder, J. G.; Ambegaonkar, J. P.; Winchester, J. B.; McBride, J. M.; Andre, M. J.; Nelson, A. G. (2011). "Efficacy of Cold-Water Immersion in Treating Delayed Onset Muscle Soreness in Male Distance Runners". Medicine & Science in Sports & Exercise. 43 (5): 766. doi:10.1249/01.MSS.0000402128.66983.f7.
  26. ^ Donnelly, A E; Maughan, R J; Whiting, P H (1 September 1990). "Effects of ibuprofen on exercise-induced muscle soreness and indices of muscle damage". British Journal of Sports Medicine. 24 (3): 191–195. doi:10.1136/bjsm.24.3.191. PMC 1478782. PMID 2078806. Retrieved 31 January 2023.
  27. ^ Tokmakidis, SP; Kokkinidis, EA; Smilios, I; Douda, H (February 2003). "The effects of ibuprofen on delayed muscle soreness and muscular performance after eccentric exercise". Journal of Strength and Conditioning Research. 17 (1): 53–9. doi:10.1519/1533-4287(2003)017<0053:teoiod>2.0.co;2. PMID 12580656. S2CID 30385225. Retrieved 31 January 2023.