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==Mechanism==
==Mechanism==
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.
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. Hi it's emma


DOMS was first described in 1902 by [[Theodore Hough]],<ref>{{cite journal|last=Hough|first=Theodore|year=1902|title=Ergographic studies in muscular soreness|journal=[[American Journal of Physiology]]|volume=1902|issue=7|pages=76–92|doi=10.1080/23267224.1902.10649879}}; {{cite journal|pmc=2048417|pmid=19971340 | volume=5 | title=ERGOGRAPHIC STUDIES IN MUSCULAR FATIGUE AND SORENESS|year=1900|journal=J Boston Soc Med Sci|pages=81–92|author=Hough T}}</ref> who concluded that this kind of soreness is "fundamentally the result of ruptures within the muscle".<ref name = "Nosaka_2008"/>{{rp|63}} According to this "muscle damage" theory of DOMS, these ruptures are microscopic [[lesion]]s at the Z-line of the muscle [[sarcomere]].<ref name="Armstrong 529–38">{{cite journal|last=Armstrong|first=RB|title=Mechanisms of exercise-induced delayed onset muscular soreness: a brief review|journal=Medicine and science in sports and exercise|date=December 1984|volume=16|issue=6|pages=529–38|pmid=6392811|doi=10.1249/00005768-198412000-00002}}</ref> The soreness has been attributed to the increased tension force and muscle lengthening from eccentric exercise.<ref name="Gulick 145–52">{{cite journal|last=Gulick|first=DT|author2=Kimura, IF |author3=Sitler, M |author4=Paolone, A |author5= Kelly, JD |title=Various treatment techniques on signs and symptoms of delayed onset muscle soreness|journal=Journal of athletic training|date=April 1996|volume=31|issue=2|pages=145–52|pmid=16558388}}</ref> This may cause the [[actin]] and [[myosin]] cross-bridges to separate prior to relaxation, ultimately causing greater tension on the remaining active [[motor units]].<ref name="Gulick 145–52"/> This increases the risk of broadening, smearing, and damage to the sarcomere. When microtrauma occurs to these structures, [[nociceptor]]s (pain receptors) within muscle connective tissues are stimulated and cause the sensation of pain.<ref name="Cheung 2003 145–64">{{cite journal|last=Cheung|first=K|author2=Hume, P |author3=Maxwell, L |title=Delayed onset muscle soreness: treatment strategies and performance factors|journal=Sports medicine (Auckland, N.Z.)|year=2003|volume=33|issue=2|pages=145–64|pmid=12617692|doi=10.2165/00007256-200333020-00005}}</ref>
DOMS was first described in 1902 by [[Theodore Hough]],<ref>{{cite journal|last=Hough|first=Theodore|year=1902|title=Ergographic studies in muscular soreness|journal=[[American Journal of Physiology]]|volume=1902|issue=7|pages=76–92|doi=10.1080/23267224.1902.10649879}}; {{cite journal|pmc=2048417|pmid=19971340 | volume=5 | title=ERGOGRAPHIC STUDIES IN MUSCULAR FATIGUE AND SORENESS|year=1900|journal=J Boston Soc Med Sci|pages=81–92|author=Hough T}}</ref> who concluded that this kind of soreness is "fundamentally the result of ruptures within the muscle".<ref name = "Nosaka_2008"/>{{rp|63}} According to this "muscle damage" theory of DOMS, these ruptures are microscopic [[lesion]]s at the Z-line of the muscle [[sarcomere]].<ref name="Armstrong 529–38">{{cite journal|last=Armstrong|first=RB|title=Mechanisms of exercise-induced delayed onset muscular soreness: a brief review|journal=Medicine and science in sports and exercise|date=December 1984|volume=16|issue=6|pages=529–38|pmid=6392811|doi=10.1249/00005768-198412000-00002}}</ref> The soreness has been attributed to the increased tension force and muscle lengthening from eccentric exercise.<ref name="Gulick 145–52">{{cite journal|last=Gulick|first=DT|author2=Kimura, IF |author3=Sitler, M |author4=Paolone, A |author5= Kelly, JD |title=Various treatment techniques on signs and symptoms of delayed onset muscle soreness|journal=Journal of athletic training|date=April 1996|volume=31|issue=2|pages=145–52|pmid=16558388}}</ref> This may cause the [[actin]] and [[myosin]] cross-bridges to separate prior to relaxation, ultimately causing greater tension on the remaining active [[motor units]].<ref name="Gulick 145–52"/> This increases the risk of broadening, smearing, and damage to the sarcomere. When microtrauma occurs to these structures, [[nociceptor]]s (pain receptors) within muscle connective tissues are stimulated and cause the sensation of pain.<ref name="Cheung 2003 145–64">{{cite journal|last=Cheung|first=K|author2=Hume, P |author3=Maxwell, L |title=Delayed onset muscle soreness: treatment strategies and performance factors|journal=Sports medicine (Auckland, N.Z.)|year=2003|volume=33|issue=2|pages=145–64|pmid=12617692|doi=10.2165/00007256-200333020-00005}}</ref>

Revision as of 14:19, 30 November 2016

Delayed onset muscle soreness (DOMS), also called muscle fever, 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.[1][2]: 63  It is thought to be caused by eccentric (lengthening) exercise, which causes 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.

Characteristics

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 

Cause

The 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 

Mechanism

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. Hi it's emma

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 muscle connective tissues are stimulated and cause the 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]

Relation to other effects

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

Soreness might conceivably serve as a warning to reduce muscle activity so as to prevent further injury. However, further activity temporarily alleviates the soreness, even though it causes more pain initially. Continued use of the sore muscle also has no adverse effect on recovery from soreness and does not exacerbate muscle damage.[2]: 68  It is therefore unlikely that soreness is in fact a warning sign not to use the affected muscle.[2]: 68 

Repeated-bout effect

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".[10]

As a result of this effect, not only is the soreness reduced, 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 effect 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 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 in order 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 to 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 

Prevention

Delayed onset muscle soreness can be reduced or prevented by gradually increasing the intensity of a new exercise program,[11]: 112  thereby taking advantage of the repeated-bout effect.

Soreness can theoretically be avoided by limiting exercise to concentric and isometric contractions.[11]: 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. A study comparing arm muscle training at different starting lengths found that training at the short length reduced muscle damage indicators by about 50% compared to the long length, but this effect was not found in leg muscles.[2]: 71 

Static stretching or warming up the muscles does not prevent soreness.[12][13][needs update] Overstretching can by itself cause soreness.

The use of correctly fitted, medical-grade, graduated compression garments such as socks and calf sleeves during the workout can reduce muscle oscillation and thus some of the micro-tears that contribute to DOMS.[14] Proper nutrition to manage electrolytes and glycogen before and after exertion has also been proposed as a way to ease soreness.[15][16] Consuming more vitamin C may not prevent soreness,[17] but oral curcumin (2.5 gram, twice daily) likely reduces it.[18]

Treatment

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, hot baths, or a sauna visit may help somewhat.[11]: 112 

Immersion in cool or icy water, an occasionally recommended remedy, was found to be ineffective in alleviating DOMS in one 2011 study,[19] but effective in another.[20] 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 

References

Template:Research help

  1. ^ a b c Costello, Joseph T.; Baker, Philip Ra; Minett, Geoffrey M.; Bieuzen, Francois; Stewart, Ian B.; Bleakley, Chris (2015-09-18). "Whole-body cryotherapy (extreme cold air exposure) for preventing and treating muscle soreness after exercise in adults". The Cochrane Database of Systematic Reviews. 9: CD010789. doi:10.1002/14651858.CD010789.pub2. ISSN 1469-493X. 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: 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 and science in sports and 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. PMID 16558388.
  7. ^ a b c Cheung, K; Hume, P; Maxwell, L (2003). "Delayed onset muscle soreness: treatment strategies and performance factors". Sports medicine (Auckland, N.Z.). 33 (2): 145–64. doi:10.2165/00007256-200333020-00005. PMID 12617692.
  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.
  9. ^ Armstrong, RB (August 1990). "Initial events in exercise-induced muscular injury". Medicine and science in sports and exercise. 22 (4): 429–35. doi:10.1249/00005768-199008000-00002. PMID 2205778.
  10. ^ Nosaka, 68–69
  11. ^ a b c Kokkinos, Peter (2009). Physical Activity and Cardiovascular Disease Prevention. Jones & Bartlett Learning. pp. 111–112. ISBN 978-0-7637-5612-3.
  12. ^ High, DM; Howley ET; Franks BD (December 1989). "The effects of static stretching and warm-up on prevention of delayed-onset muscle soreness". Res Q Exerc Sport. 60 (4): 357–61. doi:10.1080/02701367.1989.10607463. PMID 2489863.
  13. ^ Herbert, R. D.; De Noronha, M. (2007). Herbert, Robert D (ed.). "Stretching to prevent or reduce muscle soreness after exercise". Cochrane Database of Systematic Reviews: CD004577. doi:10.1002/14651858.CD004577.pub2. PMID 17943822.
  14. ^ Kraemer, William; Jill A. Bush; Robbin B. Wickham; Craig R. Denegar; Ana L. Gómez; Lincoln A. Gotshalk; Noel D. Duncan; Jeff S. Volek; Margot Putukian; Wayne J. Sebastianelli (2001). "Influence of Compression Therapy on Symptoms Following Soft Tissue Injury from Maximal Eccentric Exercise". J Orthop Sports Phys Ther. 31 (6): 282–90. doi:10.2519/jospt.2001.31.6.282. PMID 11411623.
  15. ^ Connolly, Declan. "Treatment and Prevention of Delayed Onset Muscle Soreness" (PDF). National Strength & Conditioning Association. Retrieved 8 October 2012.
  16. ^ Kraemer, William (March 2006). "The effects of amino acid supplementation on hormonal responses to resistance training overreaching". Metabolism. 55 (3): 282–91. doi:10.1016/j.metabol.2005.08.023.
  17. ^ Connolly, D A J; Lauzon, C; Agnew, J; Dunn, M; Reed, B (2006). "The effects of vitamin C supplementation on symptoms of delayed onset muscle soreness". Journal of Sports Medicine and Physical Fitness. 46 (3): 462–7. doi:10.1249/00005768-200505001-01641. PMID 16998453.
  18. ^ Nicol, L M; Rowlands, D S; Fazarkerly, R; Kellet, J (2015). "Curcumin supplementation likely attenuates delayed onset muscle soreness (DOMS)". Eur J App Physiol. 115 (8): 1769–77. doi:10.1007/s00421-015-3152-6. PMID 25795285.
  19. ^ 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.
  20. ^ 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: 766. doi:10.1249/01.MSS.0000402128.66983.f7.
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