Pro Natural Bodybuilder, Dr. Andrew Chappell PhD, MSc, BSc (Hons), RNutr (Sport/Exercise)
- Delayed Onset Muscle Soreness (DOMS) is caused by eccentric or unaccustomed exercise
- DOMS usually peaks 1 to 3 days post exercise, but can persit up to 10 days
- Removing the eccentric portion of resistance training reduces the likelihood of DOMS
- DOMS is not caused just by muscle damage but rather a combination of muscle damage, oxidative damage, swelling, over stretched muscle fibres, damaged components of muscle fibres interacting with pain receptors.
- Force production or athletic performance can be reduced for up to 9 days post exercise where a large amount of DOMS is induced.
- DOMS is not necessarily a good indicator of progress and your body becomes accustomed to exercise.
- Photographs, measurements, and recording of poundage’s make for better metrics to track progress
- Nutritional supplements seem to be largely ineffective at treating DOMS, however a healthy balanced diet should always be advocated.
- Ice, and massage can offer temporary relief from DOMS, but pharmacological intervention is the most sure-fire way to reduced DOMS.
No Pain, No Gain! Or so the mantra goes. I decided to write this article to help clear up some of the common misconception that surround delayed onset muscle soreness (DOMS). For those interested I’ve published in this topic so be sure to check out the link to the paper below:
Gray, P., Chappell, A., Jenkinson, A.M., Thies, F. and Gray, S.R., 2014. Fish oil supplementation reduces markers of oxidative stress but not muscle soreness after eccentric exercise. International journal of sport nutrition and exercise metabolism, 24(2), pp.206-214.
With that in mind, I hope you will consider the following article an accurate account of DOMS. Which will hopefully quash the myth of no pain, no gain.
What is Delayed Onset Muscle Soreness (DOMS)?
Delayed onset muscle soreness is described as a dull aching feeling that peaks between 1 – 3 days after exercise and may last up to 7 -10 days (Nosaka et al 2011). DOMS is primarily caused by eccentric, or unaccustomed exercise (Byrnes et al. 1985). So that’s exercise like downhill running, the negative part of a rep when you resistance train or generally doing exercise you’re not used to performing. Exercises performed with an eccentric component results in significant muscle soreness (measured by the visual analogue scale (VAS)) compared with concentric exercise or isometric exercise. It has long since been established that eccentric exercise is the primary cause of DOMS (Gleeson et al. 2003). So if you don’t want muscle soreness don’t do eccentric portions of the movement. Think Olympic weight lifting and how those athletes can do multiple training sessions per day.
It is important however to point out that although eccentric exercise causes DOMS, the relationship with muscle damage -determined by measuring cytoplasmic enzymes-is poor. E.g. DOMS doesn’t equate to muscle damage. So just because your particularly sore doesn’t mean you’ve caused a large amount of muscle damage. Further evidence to support this fact is that muscle stem cells, known as satellite cells are recruited in response to muscle damage. These satellite cells which help facilitate muscle growth and are also poorly associated with DOMS. For reviews on this subject see Komii et al 2000 and Nosaka 2011. The methodologies used in muscle soreness studies are worth noting, they often involve doing 10 to 20 sets, of 10 reps, of purely eccentric exercise. Similar methods were used for our study featured above and all subjects reported intense DOMS and used considerable effort, during the trial.
Let’s recap: DOMS peaks 1 to 3 days post exercise, it’s caused by eccentric exercise, and lots of DOMS doesn’t necessarily mean muscle damage
For any personal trainers reading this, if you want to make your clients feel like they’ve worked extra hard or like they’ve got their money’s worth, negatives are a great way to cause that little extra bit of muscle soreness. The more savy trainers out there should have realised that performing eccentric-less reps will allows for more volume and frequency.
The reason why eccentric exercise causes muscle soreness as opposed to concentric exercise is because motor fibre recruitment is lower during the eccentric phase. More tension and stress is placed on fewer fibres, so force development is actually greater across fewer fibres during this phase resulting in more damage (Ishikawa et al 2000). Now unlike a concentric contraction where actin and myosin crossbridges pass over each other via ATP splitting, eccentric exercise pulls fibres apart mechanically. This not only damages the sarcomere structure (see the diagram below) but also stretches it, causing the disruption of Z discs within the myofibril, which results in a loss of force production. This is particularly a problem for the Type 2x muscle fibres (they are responsible for large amounts of force production). This is why your lifts are significantly reduced as a result of DOMS especially when you consider Z bands are thinner in type 2 fibres. Damage typically occurs nearer the connective tissues at tendons where the myofibril is thinner. To summarise in laymen’s terms eccentric exercises causes you to do more work with less muscle fibres. This places more strain on the fibres and is what causes the DOMS.
Muscle Fibre Structure, Eccentric exercise damages Z discs and causes Actin and Myosin Fillaments to be missaligned.
What causes DOMS if it’s not just muscle damage?
Multiple variables are responsible for DOMS such as the presence of leukocytes (white blood cells) generating oxidative bursts cleaning up damage, oedema (swelling), and reactive oxygen nitrogen species (RONS), so it’s not just muscle fibre damage. When you damage a muscle fibre though you cause it to spill out all its cytosolic enzymes (caused by muscle damage) creatine kinase (CK), myoglobin, Ca+2, contractile tissues etc. this soup of muscle fibre debris aggravate nociceptors which are specialist nervous system receptors that response detect pain signals (Cheung et al. 2003). Imagine ripping open a water balloon filled with jelly or beans, the contents will go everywhere. Oxidative damage is also a culprit, Hosnuter et al. (2004) has shown the relationship between pain and RONs by inducing a super oxide dismutase (SOD) (a enzyme that mops up oxidative stress) inhibitor in rats subject to pain via a hot plate. Hosnuter et al. (2004) found rats had increased pain when SOD was inhibited. Or in other words, if you block oxidative damage in rats they don’t feel pain, effectively proving oxidative stress contributed to muscle soreness.
Loss of force production experienced via DOMS is likely to be part of the recovery processes that leads to inflammation tenderness and adaptation to exercise (Cheung et al. 2003). This is an important point here since it’s worth noting that inflammation is a highly destructive process, too much is counter-productive and leads to disease or in the case of training results in overtraining and a decline in strength. Think about it also from an evolutionary perspective, pain stops you from performing a task if your body didn’t put the break so n you now and again, sooner or later you’d break down permanently.
Gibala et al. (1995) investigated muscle force production and muscle damage following eccentric exercise and found that following eccentric exercise of the arm flexors, force production was significantly reduced for up to 96hrs post exercise, muscle biopsies revealed that up to 80% myofibre was disrupted after 48hrs. Studies by Lauritzen et al. (2009) and Kamandulis et al. (2010) found similar results with eccentric exercise reducing force production and causing a great deal of muscle damage and fibre disruption. So that’s 48hrs and your sarcomere length is still greatly disrupted an important consideration for training frequency, and for DOMS. Further studies by Rosser (2010) have also shown reduced maximum voluntary contraction (MVC) up to 9 days following eccentric exercise as well as changes in MVC at different angles, possibly attributed to sarcomere disruption and length. From these studies it’s easy to see how using DOMS as an indicator of progress could be counterproductive training until your muscles ache for days only results in large amounts of muscle damage, and could easily result in a decline in your numbers.
Highlighted below are what I would consider to be the key factors associated with DOMS:
- Unaccustomed exercise using eccentric exercise
- High muscle force damage, Sarcolemma causing release of cytosolic enzymes CK and Myoglobin
- Damage to muscle contractile myofibrils and noncontractile structures
- Ca2 and other metabolites accumulate at abnormal levels. reduced force production
- Inflammation, oedema. RONS generated via oxidative bursts and exercise aggravating nervous tissue
Can I or can’t I use DOMS as a marker of progress?
The answer to this question is not really, so the old saying “No pain, No gain” isn’t a sure fire sign your improving. Although DOMS is caused in part by muscle damage the links aren’t that strong. DOMS maybe simply caused by one of the other factors highlighted above, you can’t be sure that it’s not the result of over expressed RONS because of your lack of antioxidants in your diet or damaged connective tissue rather than muscle damage. Maybe the great pump you got has caused extra swelling and you followed a high sodium diet for a few days and your holding extra water. In short it’s not a great marker of progress especially when you consider as you adapt to the stresses of your workout/exercise/training so too will your muscles/connective tissue/immune system and antioxidant capacity if anything you may find your tolerance to DOMS increases and your incidence of DOMS decreases.
The best markers of training are simple measurements, photographs and a diary. If you want to gauge your progress in the gym take photo’s ever couple of months, measure your arms, legs, chest etc. with a tape and write it down and check your poundage’s are going up, rather than how sore you feel.
So what can you do about DOMS?
Few studies have proved to be effective in the treatment of DOMS with the exception of pharmacological intervention. Pain killers seem to be the best option in treating muscle soreness, however the catch 22 maybe that your limiting the potential adaptations from exercise. Stretching regimes, effective warming up and cooling down, ice, heat packs, and massage have all been proven to offer short term relief but are rarely effective in the long term. Luckily nutritional interventions hold plenty of potential and anecdotal evidence points towards the use of products like glutamine a semi-essential amino acid and whey protein for reduced muscle soreness. Combine this with an effective recovery routine and you’re likely to find muscle soreness is reduced while providing your body with essential nutrients in your bid to achieve those training goals.
When you consider how detrimental causing large amounts of muscle damage can be to your body and your progress. If programming and nutrition is osmething your interested in to help you reach your goals then why not sign up to ProPrepCoaching by following the link below. I feel it’s appropriate to finish this article by including my favourite bodybuilding quote by the great Lee Haney “stimulate, don’t annihilate”.
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Byrnes, W.C., Clarkson, P.M., White, J.S., Hsieh, S.S., Frykman, P.N. and Maughan, R.J., 1985. Delayed onset muscle soreness following repeated bouts of downhill running. Journal of applied physiology, 59(3), pp.710-715.
Cheung, K., Hume, P.A. and Maxwell, L., 2003. Delayed onset muscle soreness. Sports medicine, 33(2), pp.145-164.
Gibala, M.J., MacDougall, J.D., Tarnopolsky, M.A., Stauber, W.T. and Elorriaga, A., 1995. Changes in human skeletal muscle ultrastructure and force production after acute resistance exercise. Journal of Applied Physiology, 78(2), pp.702-708.
Gleeson, N., Eston, R., Marginson, V. and McHugh, M., 2003. Effects of prior concentric training on eccentric exercise induced muscle damage. British journal of sports medicine, 37(2), pp.119-125.
Hoşnuter, M., Gürel, A., Babucçu, O., Armutcu, F., Kargi, E. and Işikdemir, A., 2004. The effect of CAPE on lipid peroxidation and nitric oxide levels in the plasma of rats following thermal injury. Burns, 30(2), pp.121-125.
Ishikawa, M., Dousset, E., Avela, J., Kyröläinen, H., Kallio, J., Linnamo, V., Kuitunen, S., Nicol, C. and Komi, P.V., 2006. Changes in the soleus muscle architecture after exhausting stretch-shortening cycle exercise in humans. European journal of applied physiology, 97(3), p.298.
Kamandulis, S., Skurvydas, A., Masiulis, N., Mamkus, G. and Westerblad, H., 2010. The decrease in electrically evoked force production is delayed by a previous bout of stretch–shortening cycle exercise. Acta physiologica, 198(1), pp.91-98.
Lauritzen, F., Paulsen, G., Raastad, T., Bergersen, L.H. and Owe, S.G., 2009. Gross ultrastructural changes and necrotic fiber segments in elbow flexor muscles after maximal voluntary eccentric action in humans. Journal of Applied Physiology, 107(6), pp.1923-1934.
Nosaka, K., 2011. Exercise-induced muscle damage and delayed onset muscle soreness (DOMS).
Rosser, N.A., 2010. The non-invasive mechanomyographic assessment of skeletal muscle and recovery from injury.