Every now and then I do a workout that has some movements in it that I haven’t done in a while. Every time I do one of those, I’m pretty sore the next day. It got me thinking what exactly is DOMS? Yes, microscopic muscle damage and lactic acid buildup; we’ve all heard that before. Is that really what it is? Am I the only person that thinks about this stuff (you can say yes)? Today I’m going to review what exactly happens during DOMS, down to the physiology (so it will get a little scientific). I will also review strategies laid out to prevent it or decrease it and review the supporting literature.
Let’s jump right into it. There are many theories of the mechanisms of DOMS. Those theories include the lactic acid theory, the muscle spasm theory, the muscle damage theory, the inflammation theory, and the enzyme efflux theory. Since I’m probably going to bore you to death outlining the events causing DOMS, I will just summarize them all instead of reviewing each theory. All the theories have their merits, but all of them also fall short and have substantial criticisms. This has lead researchers to believe that a single theory cannot explain DOMS, rather a combination of most of them explains a sequence of events of the DOMS phenomenon. Cheung et al outlines the sequence combining models from Armstrong, Smith, and Smith and Jackson:
High tensile forces produced during eccentric muscle activity cause disruption of structural proteins in muscle fibres, particularly at the weakened z-lines. This is accompanied by excessive strain of the connective tissue at the myotendinous junction and surrounding muscle fibres (connective tissue damage theory and muscle Tissue Fluid Theory, and muscle damage theory).
Damage to the sarcolemma results in the accumulation of calcium that inhibits cellular respiration. ATP production is hindered and calcium homeostasis is disturbed. High calcium concentrations activate calcium-dependent proteolytic enzymes that degrade the z-line of sarcomeres, troponin and tropomyosin (enzyme efflux theory).
Within a few hours there is a significant elevation in circulating neutrophils (inflammation theory).
Intracellular components and markers of connective tissue damage and muscle damage (e.g. HP and CK) diffuse into the plasma and interstitium. These substances serve to attract monocytes between 6–12 hours that in turn convert to macrophages. Mast cells and histamine production are activated (inflammation theory). Within hours there is a significant elevation in circulating neutrophils at the injury site (inflammation theory).
Monocytes/macrophages peak in number at 48 hours. Upon exposure to the inflammatory environment, macrophages produce prostaglandin (PGE2) that sensitizes type III and IV nerve endings to mechanical, chemical or thermal stimulation (inflammation theory).
The accumulation of histamine, potassium and kinins from active phagocytosis and cellular necrosis in addition to elevated pressure from tissue edema and increased local temperature could et al then activate nociceptors within the muscle fibres and the muscle tendon junction (inflammation theory).
These events lead to the sensation of DOMS. Soreness may be increased with movement as the increased intramuscular pressure creates a mechanical stimulus for pain receptors already sensitized by PGE2.
Did I lose you in all that science talk? I apologize if I did. Let’s talk about the stuff you really want to know. Can you prevent it and/or get rid of it quick? There have been a lot of proposed treatment strategies and there are numerous studies on the interventions. DOMS can inhibit performance by a number of factors including reduction of joint ROM, shock attenuation, and peak torque. DOMS also causes alterations in muscle sequencing and recruitment patterns. Those could lead to unaccustomed stress and compensatory patterns which heighten the risk for injury. Know how to prevent or limit DOMS is extremely practical.
Treatments that have been proposed for DOMS include electric stimulation (TENS), ultrasound, NSAIDs, cryotherapy, compression, massage, and hyperbaric oxygen treatments. Unfortunately there are ample studies out there showing no effect on DOMS from any of the above listed interventions. I will not review the studies showing how they don’t work, but if you want them leave a comment in the box below. Rather, I will go into the treatment options that have strong evidence or promising evidence. The best treatment options for DOMS as of now are light exercise and stretching. Ironically enough there are not a lot of high quality studies demonstrating the efficacy. Exercise and stretching are thought to promote circulation and therefore oxygenation of the “injured” tissue. Proper warm-ups have also been shown to decrease DOMS which I touched on last week in my blog here. Pearcey et al examined the effects of foam rolling on DOMS and found substantially improved quad tenderness and substantial effects in sprint time, power, and dynamic strength-endurance. The subjects performed 10x10x60% back squats then performed 20 minutes of foam rolling immediately, 24hr, and 48hr after exercise. Foam rolling included the quads, hamstrings, adductors, ITB, and glutes. The study by Pearcey et al demonstrates practical use of foam rolling to improve post-exercise recovery which will help set you up for optimal performance during your next workout. Another promising treatment is curcumin supplementation. Curcumin is the active ingredient in Tumeric (a spice). Nicol et al demonstrated that Curcumin supplementation significantly reduced pain during the single leg squat, glute stretch, squat jump, and CK activity (a biomarker for tissue damage). It also increased interleukin-6 concentrations at 0hr and 48hr post exercise.
Those are the mechanisms and treatment strategies for DOMS as researchers understand them today. Hopefully you found this information useful and practical. If you have any questions please leave them below!
References
Cheung, K., Hume, P., & Maxwell, L. (2003). Delayed onset muscle soreness: Treatment strategies and performance factors. Sports Medicine, 33(2), 145-164.
Connolly, D., Sayers, S., & McHugh, M. (2003). Treatment and prevention of delayed onset muscle soreness. Journal of Strength and Conditioning Research, 17(1), 197-208.
Nicol, L., Rowlands, D., Fazakerly, R., & Kellett, J. (2015). Curcumin supplementation likely attenuates delayed onset muscle soreness (DOMS). European Journal of Applied Physiology, 115, 1769-1777.
Pearcey, G., Bradbury-Squires, D., Kawamoto, J., Drinkwater, E., Behm, D., & Button, D. (2015). Foam rolling for delayed-onset muscle soreness and recovery of dynamic performance measures . Journal of Athletic Training, 50(1), 5-13.