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The science of DOMS

Delayed onset muscle soreness (DOMS) is a phenomenon that just about anyone who has ever taken part in exercise will be familiar with, but what is it and what causes it? This is something that is often misunderstood and linked to out-dated theories. But first lets take a look at what actually defines DOMS.



Symptoms

The onset of DOMS usually begins around 24 hours following exercise and can last anywhere up to five or even seven days (Byrnes & Clarkson, 1986), although this is exceptionally long. Symptoms generally peak around the 72 hour point, and are characterised by localised soreness, reduced range of movement and reduced muscle function (Cheung, Hume, & Maxwell, 2003). These symptoms are generally worse with novices and reduce in magnitude the more trained an individual becomes.


What causes DOMS?

It is well established that DOMS occurs mostly after unfamiliar exercise (such as running or conducting weight training for the first time), eccentric exercise or long bouts of exercise. This is due to an increase in exercise-induced muscle damage (EIMD), although contrary to popular belief, the level of soreness experienced is not directly linked to the amount of muscle damage resulting from exercise (Nosaka, Newton, & Sacco, 2002).

Several theories exist for the mechanisms of DOMS:

· Damage to connective tissue

· Damage to muscle fibres

· Disrupted calcium homeostasis due to damage to the sarcolemma

· The inflammatory response to exercise

· Lactic acid build up

· Muscle spasm


Cheung et al., (2003)proposed that the latter two theories are unlikely and that the true cause of DOMS is most likely a combination of the remaining theories, which essentially tells us that the initial mechanical damage during exercise and the secondary metabolic damage afterwards are what cause these symptoms.



Dealing with DOMS

Due to the uncomfortable nature of DOMS, many strategies have emerged to help alleviate these, including compression garments, cryotherapy, massage and Non-steroidal anti-inflammatory drugs (NSAIDs). It is important to remember that these can only help to limit the secondary metabolic damage, and we cannot significantly reduce the initial mechanical damage without changing the exercise conducted in the first place. The effectiveness of each strategy above has been researched at length and each would warrant an entire article in itself. However, the most effective and impressive method is simply adaptation. The repeated bout effect (RBE) describes the protective mechanism applied by the body, in which following tissue damage an adaptive process takes place, leaving the muscle more resistant to damage during future exercise bouts (Morgan & Allen, 1999). This response is most effective in the first two weeks of occurring but can last for up to six months between bouts (Connolly, Reed, & McHugh, 2002).



Summary

Delayed onset muscle soreness is a sometimes unavoidable issue, however avoiding sudden increases in unfamiliar, eccentric or long duration exercise will help prevent excessive soreness, particularly in individuals with little training experience. Recovery strategies do exist to help alleviate symptoms, however rest and adaptation appears to be the most effective method for reducing DOMS in subsequent training sessions.




References

Byrnes, W. C., & Clarkson, P. M. (1986). Delayed onset muscle soreness and training. Clinics in Sports Medicine, 5(3), 605–614.

Cheung, K., Hume, P., & Maxwell, L. (2003). Delayed Onset Muscle Soreness. Sports Medicine, 33(2), 145–164.

Connolly, D. a J., Reed, B. V., & McHugh, M. P. (2002). The repeated bout effect: Does evidence for a crossover effect exist? Journal of Sports Science and Medicine, 1(3), 80–86.

Morgan, D. L., & Allen, D. G. (1999). Early events in stretch-induced muscle damage. Journal of Applied Physiology, 87(6), 2007–2015.

Nosaka, K., Newton, M., & Sacco, P. (2002). Delayed-onset muscle soreness does not reflect the magnitude of eccentric exercise-induced muscle damage. Scandinavian Journal of Medicine & Science in Sports,12(6), 337–346.





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