Update September 2014: This is one of the oldest articles on this site, from a time when I was much more convinced that throwing lots of words at people was a good way to teach and to engage with people interested in improving their bodies. While I don’t discount any of the information or conclusions here as such, be warned that this piece is written in a way that I wouldn’t endorse today. Your mileage may vary!
If you’ve ever done any kind of hard activity, you’ve had sore muscles. It’s inevitable, even to couch potatoes. If you exercise on any regular basis, it’s guaranteed you’ve gotten sore from it.
Muscle pain is just expected with exercise. What I’m going to talk about here is known more specifically as Delayed Onset Muscle Soreness, or just DOMS for short.
This is to separate it from any muscle pain or discomfort that might happen during your workouts, like the burning sensation that can occur when you do high reps or any kind of endurance training.
In contrast, DOMS is residual pain and stiffness in the muscles that occurs the day or two following exercise.
Sometimes people will mix the two up. But the burning that comes from exercise is a different process, and it doesn’t have anything to do with getting sore a day or two later.
The main goal of this article is to look at the physical causes of muscle soreness, how it relates to exercise, and what (if anything) you can do about it.
A lot of people assume that muscle soreness is a sign of an effective workout, that you’ve damaged the muscle tissue, and that soreness means the muscle is growing.
These beliefs are all incorrect to some degree or another, and along with explaining the causes of DOMS, I want to touch on what’s wrong with those statements.
What Causes Muscle Soreness
It’s been a long-held belief in bodybuilding and gym-rat fitness circles that muscle soreness is caused when tiny tears that happen in the muscle in response to weight training.
This is an example of sound-bite science. There’s a kernel of truth there, but some hasty assumptions and logical leaps that make it incorrect.
It is true that stretching of the muscle while it’s under tension (called the eccentric or lowering phase of a movement) is known to cause a type of damage to the muscle. This damage affects both the individual muscle fibers and connective tissues that surround the muscle fibers.
We call this cellular microtrauma, and in a way it is similar to tiny tears in the cell’s membrane.
Why this happens is still unclear; there are theories, but nothing conclusive. There’s speculation that when you lower a heavy weight, you change the way that motor units are involved in the lift. Since less motor units are activated and able to help in lowering the weight, more stress is put on fewer fibers.
Some groups have observed that there’s a difference in the way that the muscle proteins connect and detach during contraction, which physically damages those structures. Still others have noticed that calcium ions, normally responsible for contraction of the muscle, can build up and exaggerate damage.
It’s possible that all of these, and potentially other things, contribute to cellular microtrauma. All that’s important to know is that it happens; when your muscles are exposed to any sufficient amount of eccentric exercise, the tissue shows several signs of being damaged.
This can result from anything that involves eccentric muscle action, not just weight training. Even running or something as seemingly innocent as Yoga can be a culprit. As a consequence, just about any activity you can think of can cause soreness.
The muscles will adjust to soreness with time. If you’re unaccustomed to doing a particular exercise or activity, you can bank on being sore the next day or two. But if you keep up the activity, you’ll soon stop getting sore.
In research, this has been labeled the repeated bout effect. What we see is that after exposure to eccentric exercise, any follow-up exercise session won’t tend to make the damage any worse.
Your muscle and connective tissues adapt to the stress. This, again, is a poorly-understood process that could be the result of several avenues.
The big candidates for this adaptation are changes in motor unit activation (so that more fibers handle the weight), thickening of the connective tissues around the muscle, and of course bigger and stronger muscles. Regardless of the cause, the muscles adapt so that future exposures to the same conditions won’t cause any further damage. So we know there’s some kind of adaptive force in play here.
The question is whether or not muscle soreness has anything to do with muscle growth, though. Repeated bout is well and good, but it doesn’t answer that question.
From the looks of things, DOMS and actual muscle growth don’t have much to do with each other.
The process of inflammation is how the body handles damages to it’s tissues. Any time you get injured, inflammation is the response. It’s why an injury will swell, turn red, get hot, and so on. The body is reacting to the injury by breaking down the damaged tissues and bringing in specialized cells that assist in repair.
Traditionally it’s been thought that this inflammation process applied to muscle injury and repair, and this has extended to the damage caused by exercise. And there is research showing that tissue breakdown and inflammation do occur in human muscles.
Recent research has looked at markers of inflammation and muscle damage along with indicators of the growth response in human muscle. The results of this new research are interesting, and some of these older assumptions have been called into question.
Sarcomeres, which are the protein structures in your muscle fibers that actually contract, are known to become damaged after eccentric exercise. This disruption of sarcomeres was thought to be a sign of damage, and associated with inflammation.
In animal research, where most of this was done, this is probably what happens. A similar process does happen in humans, but there’s some exceptions.
The research of Yu et al (2002a, 2002b, 2003, 2004) has shown that sarcomere disruption is actually the beginnings of tissue remodeling in human muscle. Tissue remodeling is a process of changes in the tissue that will end up with it being larger; this is how the body creates a bigger muscle, in other words.
Further, we see that growth can occur with no markers of muscle damage (LaStayo et al, 2007). While human muscles can be damaged and inflamed by exercise, they don’t have to be in order to grow.
In humans, actual muscle damage and inflammation seem to happen only in cases of very high volumes of work – usually after marathon runs and similar extreme endurance activities.
Strength training, by contrast, seems to have a much lesser effect. While higher volumes of eccentric strength training can create muscle damage and inflammation, the severity seems to be much lighter as compared to high-intensity endurance exercise.
A study by Crameri et al (2007) indicates that muscle damage doesn’t really correlate to soreness. This experiment compared electrical muscle stimulation (ES) with voluntary contractions, and found that the ES protocol created far more muscle fiber ‘damage’.
However, the DOMS experienced by the two groups wasn’t any different. The pain of DOMS was actually attributed to the inflammation of the extracellular matrix – which is connective tissue that binds the muscle fibers together.
All of this would strongly indicate that connective tissues are the source of the actual pain and soreness, not the muscle fibers themselves. The damaging effects of exercise on actual muscle fibers don’t correlate with pain.
This is of interest because it means that inflammation and pain don’t indicate damaged muscle fibers per se. There’s tissue damage, and muscle fibers can be damaged along with that, but there’s no actual relation between muscle fiber damage and the pain you feel.
Taken together, there’s a very good chance that the processes behind DOMS and those responsible for muscle growth are only loosely related.
The damage and inflammation created in muscle seems to be dose-dependent. The more eccentric work done, the greater the damage and resulting inflammation. But we also see that damage and inflammation can happen without any growth signal, as in the case of marathon runs. Likewise, muscle growth can happen without inflammation, as seen in the studies showing growth responses without any significant tissue damage.
Inflammation and Muscle Growth
Because of this information and the conclusions we can draw, it might seem that tissue damage and muscle growth aren’t linked. But it’s a bit more complex than that.
Increased muscle protein synthesis, or building up of new proteins, is what’s required for muscle growth to happen. This is balanced out by muscle protein breakdown. To grow, we have to increase MPS more than MPB (Tipton and Ferrando, 2008).
In practice, we see that both processes of building up and breaking down are strongly linked. When you increase MPS, MPB will tend to increase as well. This increases the overall protein turnover, or the total amount of protein coming in and out of the muscle.
Increased protein turnover with a net increase in MPS rates will result in more proteins building up in the muscle – growth, in other words.
In muscle, this process is linked to physical changes in the sarcomeres. It was once thought that these changes were a result of damage, but it’s been shown that this is actually the beginnings of the growth process. We see that both elevated protein synthesis and tissue remodeling can occur with no markers of inflammation.
Yet, inflammation of the muscle still seems to be integral to the growth process. Even though there’s no direct link as yet between inflammation and increased protein synthesis, there’s a strong correlation.
There are certain proteins in the outer membrane and connective tissues of the muscle fibers that are responsible for transmitting signals deeper into the cell. When the fiber becomes more resistant to damage, it’s thought that it also becomes more resistant to this signaling. When a muscle is “protected” from eccentric damage, it also seems less sensitive to mechanical signals that stimulate growth.
This could be one reason that it’s progressively harder to trigger growth with weight training. The more conditioned a muscle is, the harder it is to make it grow.
That’s one possible link, although it’s still just a correlation. It just happens that resistance to eccentric damage and growth signaling are linked by that one process. It doesn’t mean that the two things are directly connected.
When certain anti-inflammatory drugs are taken, what we see is that protein synthesis rates are very low as compared to groups that didn’t take the drugs (Trappe et al, 2002).
Specifically we see this in a type of drug called non-steroidal anti-inflammatory drugs, or NSAIDS. This includes things like ibuprofen, naproxen, and acetaminophen.
Researchers have traced this to the COX-2 enzyme, which is involved in some steps of the inflammation process. It seems that when COX-2 is blocked by drugs, protein synthesis and resulting growth is impaired.
Taking drugs that block COX-2 seems to compromise muscle. However, there’s some recent research that calls this into question, at least with lower doses. Krentz et al (2008) showed that 400mg of ibuprofen per day had no negative effects during the six weeks of the study.
The research by Trappe et al used maximum over the counter doses, so this could be a dose-response matter.
Obviously we’ve got a little conflict here. Some of this research is telling us that we don’t need muscle damage and inflammation for growth to occur; but we also observe that blocking some steps in the inflammation process can affect protein synthesis.
What are the possible explanations for this?
The time course of the changes is one possible avenue. Inflammation takes awhile to kick in, and is probably responsible for the longer-term changes in MPS rates. This is different from the processes that govern the immediate post-exercise changes.
Since protein synthesis rates in the muscle increase for upwards of 24 to 48 hours after an exercise session, it’s possible that inhibiting the inflammation effects would become more relevant over time even if there’s no problems immediately after the workout.
The process of long-term muscle growth requires satellite cells, which are immature muscle fibers found around muscle tissue. Under certain conditions, satellite cells are triggered to increase in number and become more like full-grown muscle fibers.
When an existing muscle fiber is damaged, these developing satellite cells will contribute their nuclei to those damaged fibers. The more nuclei that a muscle fiber has, the more protein synthesis it can support, and the bigger it gets.
Inflammation is strongly linked to the processes that activate satellite cells, and this is where COX-2 most likely contributes.
One of the biggest activators of satellite cells is a group of growth factors called prostaglandins. Specifically prostaglandin E2 (PGE2) has shown that it not only triggers satellite cell activity, but contributes to protein synthesis in existing fibers. Obviously, PGE2 is something you want around after a workout.
It just happens that COX-2 is what regulates the synthesis of prostaglandins, and thus it’s linked to this long-term growth process. When you block the actions of COX-2, you wind up blocking that long-term process (Trappe et al, 2001).
Now, I’m not so worried about the effects of painkillers blocking growth; that’s not the point. The point is to show that inflammation does play a role of some sort – it’s just that the role isn’t what most people assume it is.
This is backed up somewhat by the fact that eccentric exercise doesn’t seem to impact protein synthesis rates any more than other kinds of weight training (Phillips et al, 1997; Moore et al, 2005; Cuthbertson et al, 2006), but it does seem to correlate with greater muscle growth and protein turnover in some cases (Nedergaard et al, 2007).
Increases in muscle size without any noticeable increases in post-exercise MPS rates is hard to explain, unless you account for the contribution of satellite cells.
However, I have to stress again – DOMS itself is not a by-product of muscle fiber inflammation. Being sore does not mean that your muscles are undergoing growth. They might be undergoing repair, but these are not the same things.
I’m going tag-heavy here because emphasis is important.
Inflammation and Overtraining
The other issue that comes up is the protocols used in the research. Many of them, well, they don’t resemble any kind of realistic workout. This is a needed compromise, since sometimes you have to exaggerate an effect in order to get data, but nobody’s going to be doing something crazy like 8 sets of 10 maximum eccentric contractions.
Nobody’s doing that in the gym, not if they’re getting results.
Other methods use very high volumes of downhill running, which creates an eccentric movement every time you absorb the impact of landing. Downhill running can rack up a lot of volume in a hurry when compared even to some of the more outrageous strength protocols.
The extreme cases like that are connected with fiber necrosis, which is the actual death and breakdown of muscle tissue. This isn’t really expected in moderate exercise, which most people are doing. In fact, that degree of tissue damage isn’t likely to be helping you out if a bigger/stronger muscle is your goal.
Quite the opposite, actually.
Seeing muscle damage from some of the crazy research protocols is hardly a surprise, but it also doesn’t mean that it will apply to your workouts. This just illustrates one of the potential problems of chasing DOMS.
The other problem is systemic inflammation that comes up from this. When you damage your tissues like this with extreme exercise, they release inflammatory signals called cytokines.
Cytokine levels are strongly correlated with muscle damage, especially in cases like downhill running, and large volumes of strength training are shown to elevate cytokine levels as well.
If you’re one of those with the goal of getting sore every workout, and you do a metric ass-ton of training to make that happen, chances are you’re causing a good degree of inflammation.
This isn’t an issue if you only do it occasionally, but if you do this several times a week, you’re going to feel it sooner or later – cytokines and inflammation are strongly linked to the overtraining phenomenon.
The more muscle damage you cause, and the more often you do it, the more likely you are to seriously compromise your gains.
It’s a necessary thing if you’re training to be an endurance athlete, but if strength/power or muscle mass are your goals, you need to avoid excessive work loads.
Suggestions and Conclusion
Just to reiterate, one more time:
There’s no link between muscle soreness and protein synthesis; no link between muscle soreness and long-term growth; and no link between muscle soreness and muscle fiber damage.
Muscle soreness happens when you create enough total damage to aggravate the connective tissues. This will sometimes correlate with a muscle-stimulating, growth-inducing workout. But just as often, it has nothing to do with muscle stimulation.
Just because you’re not sore doesn’t mean your muscles aren’t inflamed and growing. Likewise, sore muscles don’t mean you had a good workout.
DOMS itself will be caused by any eccentric exercise that you do for enough total reps. The less accustomed you are to that type of exercise, the worse the soreness will be after the fact.
The actual tissue damage you do in a workout is a result of both high intensity and large volume. The more of either, or both, the more ‘damage’ will result. Some ‘damage’ is good, as it seems to link to satellite cell activity, but too much is bad.
Since we can’t use DOMS as a reliable indicator of muscle fiber ‘damage’ or growth remodeling, it’s pointless to use DOMS as a sign that you’ve effectively worked your muscles.
Sometimes people hear “eccentric” and think of the old bodybuilder technique of negatives. Negatives are where you load up a very heavy weight, then just lower it slowly. Usually the recommendation is given for 120% to 130% of your 1RM.
This is an example of an accentuated eccentric, where you intentionally emphasize the lowering phase. You can do accentuated eccentrics with lighter weights, too. But this particular kind of strength training isn’t the only place you encounter eccentric overload.
Downhill running is one method tested in the research, and it creates far more muscle ‘damage’ than most observed weight-training protocols. Working the legs to paste with downhill running has a much greater impact than eccentric work for the elbow flexors (bicep curls), as one example.
This is probably due to the large amount of muscle involved, as the legs are a big muscle group compared to the arms, and the total volume of work done. Even a moderate distance run will involve more “reps” than almost any strength workout you’d ever do.
The fact that a damaging distance run creates less growth than strength training, which creates mild damage by comparison, is telling.
It’s my thinking that there’s an optimal amount of damage that should occur in a strength workout. Obviously you need some kind of disruption to go on so you can get those satellite cells working.
But doing too much work, and causing too much damage, just breaks down tissue and increases recovery time without giving you any real benefits.
Hence my emphasis on varying the difficulty of your workouts, instead of just mindlessly blasting your muscles into pulp at every chance. But that’s a different rant.
When you’re toying with your workouts, you have to be careful. Heavy eccentric movements can slip in from unexpected places. It doesn’t just happen from intentionally loading up the bar and doing negatives.
If you’re taking a lot of your sets to failure, you’re probably kicking off this process. When you near the point of failure, you’re actually putting a large eccentric stress on the fibers that are tiring out.
Same idea when you do a lot of volume and exhaust yourself by doing a lot of sets.
Even grinding through a 1RM is going to involve a lot of eccentric work on squatting and pressing exercises. You can drop a deadlift or a row without too much trouble, but a squat or press requires you to lower the bar first. On a heavy weight, that’s an automatic eccentric overload.
The grinding seems to be the common point. When you have to fight through fatigue, you’re creating a lot of eccentric damage in those muscle fibers that get tired. It doesn’t particularly matter where the fatigue comes from, but tired muscle fibers that are forced to move are going to be worked over pretty good.
Sometimes this is a good thing. But sometimes it isn’t. You want some hard workouts, but you don’t have to destroy your muscles every time you step in the gym.
Make sure to reserve the harder types of training for workouts that intentionally overload your muscles. In lighter sessions, try to avoid these methods.
While I’m not convinced that NSAIDS or other anti-inflammatories in moderate doses are going to just crush your gains, it’d probably be a good idea to keep it moderate. Large doses taken on a regular basis could well add up to some long-term effects on muscle growth. Along those lines, there’s some data to indicate that painkillers don’t affect DOMS pain that much anyway (Barlas et al, 2000; Stone et al, 2002; Rahnama et al, 2005).
People get addicted to the idea of muscle soreness because it’s quick feedback. It’s not really a bad or stupid assumption; if you didn’t know any different, I can see why you’d connect the two processes. You exercise, you get sore muscles. Exercise harder, and get even more sore. It’s reasonable enough if you don’t have any information to tell you otherwise.
From there, people just assume that hard workouts = sore muscles = effective. But that’s not the case. It’s a case where correlation is mistaken for causation.
We know that workouts can still be effective even if you’re not sore, because exercise is still effective after you stop getting sore from it. Being sore, stiff, and exhausted might feel good, but it’s not a replacement for training intelligently.
- Barlas P, Craig JA, Robinson J, Walsh DM, Baxter GD, Allen JM. Managing delayed-onset muscle soreness: lack of effect of selected oral systemic analgesics. Arch Phys Med Rehabil. 2000 Jul;81(7):966-72.
- Clarkson PM, Hubal MJ. Exercise-induced muscle damage in humans. Am J Phys Med Rehabil. 2002 Nov;81(11 Suppl):S52-69.
- Cuthbertson DJ, Babraj J, Smith K, Wilkes E, Fedele MJ, Esser K, Rennie M. Anabolic signaling and protein synthesis in human skeletal muscle after dynamic shortening or lengthening exercise. Am J Physiol Endocrinol Metab 290: E731–E738, 2006.
- Hirose L, Nosaka K, Newton M, Laveder A, Kano M, Peake J, Suzuki K. Changes in inflammatory mediators following eccentric exercise of the elbow flexors. Exerc Immunol Rev. 2004;10:75-90.
- Krentz JR, Quest B, Farthing JP, Quest DW, Chilibeck PD. The effects of ibuprofen on muscle hypertrophy, strength, and soreness during resistance training. Appl Physiol Nutr Metab. 2008 Jun;33(3):470-5.
- LaStayo P, McDonagh P, Lipovic D, Napoles P, Bartholomew A, Esser K, Lindstedt S. Elderly patients and high force resistance exercise – a descriptive report: can an anabolic, muscle growth response occur without muscle damage or inflammation? J Geriatr Phys Ther. 2007;30(3):128-34.
- MacIntyre DL, Reid WD, McKenzie DC. Delayed muscle soreness. The inflammatory response to muscle injury and its clinical implications. Sports Med. 1995 Jul;20(1):24-40.
- McHugh MP, Connolly DA, Eston RG, Gleim GW. Exercise-induced muscle damage and potential mechanisms for the repeated bout effect. Sports Med. 1999 Mar;27(3):157-70.
- McHugh MP. Recent advances in the understanding of the repeated bout effect: the protective effect against muscle damage from a single bout of eccentric exercise. Scand J Med Sci Sports. 2003 Apr;13(2):88-97.
- Moore DR, Phillips SM, Babraj JA, Smith K, Rennie MJ. Myofibrillar and collagen protein synthesis in human skeletal muscle in young men after maximal shortening and lengthening contractions. Am J Physiol Endocrinol Metab 288: E1153–E1159, 2005.
- Nedergaard A, Vissing K, Overgaard K, Kjaer M, Schjerling P. Expression patterns of atrogenic and ubiquitin proteasome component genes with exercise: effect of different loading patterns and repeated exercise bouts. J Appl Physiol. 2007 Nov;103(5):1513-22.
- Nosaka K, Sakamoto K, Newton M, Sacco P. The repeated bout effect of reduced-load eccentric exercise on elbow flexor muscle damage. Eur J Appl Physiol. 2001 Jul;85(1-2):34-40.
- Peake JM, Nosaka K, Muthalib M, Suzuki K. Systemic inflammatory responses to maximal versus submaximal lengthening contractions of the elbow flexors. Exerc Immunol Rev. 2006;12:72-85.
- Peake J, Nosaka K, Suzuki K. Characterization of inflammatory responses to eccentric exercise in humans. Exerc Immunol Rev. 2005;11:64-85.
- Peake JM, Suzuki K, Hordern M, Wilson G, Nosaka K, Coombes JS. Plasma cytokine changes in relation to exercise intensity and muscle damage. Eur J Appl Physiol. 2005 Dec;95(5-6):514-21.
- Peake JM, Suzuki K, Wilson G, Hordern M, Nosaka K, Mackinnon L, Coombes JS. Exercise-induced muscle damage, plasma cytokines, and markers of neutrophil activation. Med Sci Sports Exerc. 2005 May;37(5):737-45.
- Phillips SM, Tipton KD, Aarsland A, Wolf SE, Wolfe RR. Mixed muscle protein synthesis and breakdown after resistance exercise in humans. Am J Physiol Endocrinol Metab 273: E99–E107, 1997.
- Rahnama N, Rahmani-Nia F, Ebrahim K. The isolated and combined effects of selected physical activity and ibuprofen on delayed-onset muscle soreness. J Sports Sci. 2005 Aug;23(8):843-50.
- Stone MB, Merrick MA, Ingersoll CD, Edwards JE. Preliminary comparison of bromelain and Ibuprofen for delayed onset muscle soreness management. Clin J Sport Med. 2002 Nov;12(6):373-8.
- Suzuki K, Peake J, Nosaka K, Okutsu M, Abbiss CR, Surriano R, Bishop D, Quod MJ, Lee H, Martin DT, Laursen PB. Changes in markers of muscle damage, inflammation and HSP70 after an Ironman Triathlon race. Eur J Appl Physiol. 2006 Dec;98(6):525-34.
- Tipton KD, Ferrando AA. Improving muscle mass: response of muscle metabolism to exercise, nutrition and anabolic agents. Essays Biochem. 2008;44:85-98.
- Trappe TA, Fluckey JD, White F, Lambert CP, Evans WJ. Skeletal muscle PGF(2)(alpha) and PGE(2) in response to eccentric resistance exercise: influence of ibuprofen acetaminophen. J Clin Endocrinol Metab. 2001 Oct;86(10):5067-70.
- Trappe TA, White F, Lambert CP, Cesar D, Hellerstein M, Evans WJ. Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis. Am J Physiol Endocrinol Metab. 2002 Mar;282(3):E551-6.
- Woolstenhulme MT, Conlee RK, Drummond MJ, Stites AW, Parcell AC. Temporal response of desmin and dystrophin proteins to progressive resistance exercise in human skeletal muscle. J Appl Physiol. 2006 Jun;100(6):1876-82.
- Yu JG, Malm C, Thornell LE. Eccentric contractions leading to DOMS do not cause loss of desmin nor fibre necrosis in human muscle. Histochem Cell Biol. 2002 Jul;118(1):29-34.
- Yu JG, Thornell LE. Desmin and actin alterations in human muscles affected by delayed onset muscle soreness: a high resolution immunocytochemical study. Histochem Cell Biol. 2002 Aug;118(2):171-9.
- Yu JG, Fürst DO, Thornell LE. The mode of myofibril remodelling in human skeletal muscle affected by DOMS induced by eccentric contractions. Histochem Cell Biol. 2003 May;119(5):383-93.
- Yu JG, Carlsson L, Thornell LE. Evidence for myofibril remodeling as opposed to myofibril damage in human muscles with DOMS: an ultrastructural and immunoelectron microscopic study. Histochem Cell Biol. 2004 Mar;121(3):219-27.
3 thoughts on “Why Your Muscles Get Sore: Delayed Onset Muscle Soreness (DOMS) and Exercise”
is doms equally occurring in both fast and slow twitch muscle fibres?
Comments are closed.