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A Deep Dive into Delayed-Onset Muscle Soreness

The biology & treatment of “muscle fever,” the deep muscle soreness that surges 24-48 hours after an unfamiliar workout intensity

Paul Ingraham • 75m read

Muscle fever — such a wonderfully descriptive term — is that distinctive muscle pain that nearly everyone experiences after intense or unfamiliar exercise, often peaking as long as a day or two later. Because of the delay, it is often called D.O.M.S. for delayed-onset muscle soreness,1 as well as just post-exercise muscle soreness.

Muscle fever is a great term because DOMS makes your muscles feel sickly and gross as well as sore. Weakness is another symptom, major and measurable — but only hardened competitors are likely to test their strength while feeling so sore and oogy (though they probably should not). The nastiness starts after a bit of a delay, often after sleeping, and then continues for 24 to 72 hours. Some people don’t even notice it until the second day.2 If you do the same workout again a few days later, it’s nowhere near as bad.

The biology of DOMS remains exasperatingly unclear, and there is no “cure,” no way to actually prevent it or get through it faster. There have been many contenders over the last century, but nothing has ever been proven. At best, we can relieve the soreness with anti-inflammatory medications.

This article explores every DOMS sub-topic in substantial detail, with many references. There’s a lot of dorky, interesting science of muscle soreness ahead.

How bad can post-exercise muscle soreness get?

Sometimes DOMS is so severe that it is mistaken for a muscle strain. It can also be so serious that it’s an injury in its own right (but that’s uncommon).

For most people, most of the time, DOMS is mostly just annoying and style-cramping, particularly if you’re starting or restarting an exercise regimen, especially strength training — which is much more worthwhile than most people realize, and DOMS is one of the main things that discourages people.

The average bad case of DOMS

A few days of significant discomfort and disconcerting weakness is roughly the worst-case scenario (excluding the rare extremes, discussed next). For instance, climbing stairs might be unpleasant, but still manageable. The severity is roughly analogous to a bad sunburn or headache: unpleasant, but not excruciating or disabling.

More severe DOMS than that is unlikely without obvious overexertion. As with a sunburn, it is possible to overdo it without realizing it. But, if the overexertion wasn’t obvious, the DOMS should be mild. If you overdid it enough to know that you overdid it, but not to a ridiculous degree, DOMS should be moderate at worst.

In general, DOMS will only be extreme if the overexertion is extremely obvious. But that can happen…

Extreme DOMS and “rhabdo”

At the extremes of muscle soreness, DOMS can cause major loss of muscle function for several days and tenderness like a severe bruise. In such cases, the muscle is truly damaged. When more widespread, this is an unhealthy state known as rhabdomyolysis, or “protein poisoning” from myoglobin spilling out of damaged muscle cells. While historically associated with severe crushing injuries, overexertion can also do it,3 usually manual labor, extreme endurance exercise, or lifting weights,4 and it can be dangerous.5

If you feel sick and your urine is brown, it’s a medical emergency, and you should take yourself to a hospital. (More on rhabdo below.)

If DOMS didn’t cause this horrible soreness, then what did?

Don’t try to chalk up severe soreness to just moderately overdoing it — that is not a thing, and there is probably something else going on. Such as? Two categories:

  1. More direct injury. There are several common injuries that can mimic DOMS, such a mild muscle strains.
  2. Biological vulnerability. Vulnerability can spike from transient causes like an infection or sleep loss, or it can be more long term and serious. For instance, Ehlers–Danlos Syndrome, a connective tissue disorder, makes people get sore too easily. An old friend of mine understood his lifelong excessive DOMS when he was finally diagnosed with a common, mild form of muscular dystrophy. I will tell that story later on.


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Rub it out? Muscle “knots” are the most common problem that mimics DOMS

When I was a Registered Massage Therapist, my patients routinely hoped for DOMS relief, or some advice on how to avoid it.7

Alas, there was nothing8 I could do for them. It’s mostly a myth that DOMS can be effectively treated by massage … or anything else.9 Believe me, I’ve tried, and at a professional level! Massage therapists certainly often claim to be able to treat DOMS, but without evidence or justification. Like many health care myths, it’s not too loudly touted, just carelessly repeated and perpetuated (often in major publications, *cough*10). But medical science can barely even explain DOMS, let alone treat it — it seems to be nature’s little tax on exercise, which everyone must pay. There are no shortcuts through it. DOMS is mostly untreatable, even with massage.

Unless the problem is actually trigger points, in which case rubbing might help. Much more about the role of massage below.

DOMS timing: just how delayed is delayed-onset muscle soreness?

Although a delay of a day is typical, there seems to be a large natural range for just how delayed DOMS can be. It may start as quickly as “right away” for particularly intense and/or long workouts and as late as a full day. (The speed of onset and the severity are often related, but not necessarily.) The peak of pain is the more obviously “delayed” part of DOMS, because it almost exclusively occurs the next day, and sometimes even as far out as the middle of the second day after the workout. Personally, I’ve even had the odd third day that seemed at least as bad as the second.

This variability is probably due to both the complex biology of DOMS itself and/or the complications caused by other kinds of pain problems. For instance, if one is generally inflamed or sensitized — two common broad explanations for widespread body pain — it stands to reason that it would either accelerate the timing, or at least obscure it.

Woman playing tennis, getting ready to serve.

Nothing causes DOMS more reliably in me than racquet sports. My forearm extensor muscles get viciously sore for days, every time. Partly because I rarely play more than a couple times per summer.

What triggers delayed-onset muscle soreness?

Exercise or other physical stresses outside your normal range of intensity — anything you aren’t used to. Even extremely well-conditioned athletes can get DOMS, if they train harder than usual. But as muscles get familiar with a specific stress, they quickly adapt and react much less strongly: repeated bout effect (RBE). Any theory of DOMS is going to have to account for RBE (which is very interesting, see Deyhle, also discussed below in the inflammation section).

But how far outside your exercise comfort zone can you wander before DOMS strikes? That seems to depend on many unknown factors. Exactly what it takes to make people how sore is one of the main mysteries of DOMS. But some things are fairly certain:

An amusing drawing explaining “how to head bang.” Step 1 shows a sketchily drawn heavy metal fan flinging his head and hair all the way back, and step 2 shows his head and hair all the way down. This is, of course, a really good way to get DOMS in your neck muscles.

Dancing fool

Maybe the worst DOMS I ever had was after a night of dancing and, yes, a little “head banging.” (I grew up in a Canadian logging town; AC/DC & Metallica were like gods to us.) Even a little head banging can be hard on neck muscles. I could barely lift my head off my pillow for 3 days.

The biology of delayed-onset muscle soreness

The exact cause of DOMS is unknown. Like most relatively minor aches and pains, understanding DOMS is an extremely low priority in medical science. That’s surprising when you consider the impact DOMS has on elite athletes — a group of people whose performance is collectively worth trillions of dollars, and obsessively optimized, seemingly sparing no expense. You’d think this topic, at least, would get more scientific attention. And yet we don’t really know why DOMS happens.

It is usually described as the consequence of mechanical and/or metabolic stress13 … which isn’t saying much. What else would cause DOMS? Financial stress?

DOMS is probably a slower, longer-lasting chemical cousin of the simpler, briefer “burn” of intense effort — and the chemistry of the burn is surprisingly fresh science. What exactly causes it? Which molecules? According to Pollak et al., it’s protons, lactate, and ATP — and only in concert.14 “There was essentially no response whatsoever to the individual metabolites,” explains Alex Hutchinson for Runners’ World, “so the receptors apparently respond only to the synergistic combination of all three.” It’s complicated, in other words.

Just as the burn only happens when certain molecules get mixed up, burn alone does not doom one to DOMS. But that burn is probably a pre-requisite for DOMS. For the full DOMS effect, you probably need more chemistry (more than you want).

Rhabdomyolysis and microdamage

Garden variety DOMS could essentially be a mild form of metabolic poisoning called “rhabdomyolysis” — or just “rhabdo” for short (and for the rest of this article). True rhabdo is a medical emergency in which the kidneys are poisoned by myoglobin from muscle crush injuries.15 But many physical and metabolic stresses cause milder rhabdo-like states — including intense exercise, and probably even deep tissue massages.16

There are many well-documented cases of exertional or “white collar” rhabdo.17 That term was coined by Knochel in 1990 because rhabdo was striking recreationally extreme athletes — people with white-collar jobs who voluntarily work themselves into a sorry state.18 You could also call it (for fun) recreational rhabdo. Another well-known source of rhabdo cases is military boot camp: “large numbers of [recruits] may have myoglobinemia … .”19 (After a exploring the literature, I have the impression that you could be rhabdo-ized by an especially hard sneeze.)

The mildest rhabdo — a comparatively benign cocktail of waste metabolites and by-products of tissue damage — is probably one of the reasons why we feel generally cruddy after intense physical stresses. But although “rhabdo” is a fun word, it doesn’t really say much. We know remarkably little about the biology of that state.20 Does it overlap with DOMS? If major rhabdomyolysis is muscle "macro" trauma, is mild rhabdomyolysis "microtrauma" that is synonymous with DOMS?

While it does seem plausible that intense exercise could cause microtrauma specifically — and the idea is prevalent, and it is probably involved to some extent — the research does not support this idea nearly as well as you might assume, and some even contradicts it.2122 However, it is slowly coming into focus, and a 2021 discovery sure helped to make the reality of damage clearer: muscle cell nuclei actually moving to injury sites, and getting to work patching them.23 Cool!

What about metabolic stress?

“Metabolic stress” is a more sophisticated way of looking at the cause of DOMS. Muscle cells are like little chemical factories, and they produce some unpleasant by-products — and probably more of them when working at intensities they haven’t had a chance to adapt to. It seems plausible enough in general terms, but it’s a tricky concept to pin down.

What constitutes metabolic stress, exactly? Researchers have spent decades identifying various obscure molecules produced by cells during exercise, but are any of these molecules necessarily a sign of painful metabolic wear and tear? Just because a cell produces a substance during exercise does not mean it is metabolically frazzled, or that you are going to hurt. In any event, no one has been able to find a link between DOMS and any specific biological markers.2425

For demonstration purposes, we’ll dip deeper into this subject on just one molecule. “Free radicals” or “reactive oxygen species” are unstable, highly reactive molecules that are an unavoidable by-product of cellular metabolism. “There is growing evidence that reactive oxygen species (ROS) are involved in [DOMS].”26 Unfortunately, although free radicals have an even better name than “rhabdo,” which sounds just nasty enough to cause DOMS, they don’t have the decency to actually be present in great numbers when DOMS is at its worst. Instead, “the increase [of free radicals] occurred after the peak decline in muscle function and DOMS.”27 In other words, ROS may be involved — they probably are involved — but the relationship is indirect and unclear at best. They could even simply be a by-product of some other, hidden culprit.

What about lactic acid? Surely lactic acid is to blame?

Lactic acid is not a garbage molecule, not a “waste product” that “builds up” and cause soreness. It’s not even an acid! It’s just lactate in muscle metabolism.28 But calling it an “acid” harmonizes nicely with its reputation for being a troublemaker, especially the idea that it causes “the burn” in exhausted muscles. It is involved in that, but only partially, and not because it’s an acid!29

These pernicious, unkillable myths have been with us for many decades. They originated with “one of the classic mistakes in the history of science,” according to George Brooks, a Berkeley physiologist.30 A simplistic misinterpretation of a simple experiment on frog muscles produced the theory that lactic acid causes fatigue… and coaches and athletes and popular health articles and infographics have been repeating it ever since.

Lactate actually fuels muscles when the standard cellular engines hit their limits — which they often do. This backup system is “an essential feature of repeated intense muscle contractions, and without lactate production such repeated contractions could not occur.”31 Lactate does indeed accumulate in exhausted muscles, but only because we churn it out faster than muscles can use it, and only briefly! It’s gone within an hour; it doesn’t linger for days causing DOMS. Fatigue is complex (understatement!32) but it is not caused by muscles drowning in lactate. One reason elite athletes can do more than the rest of us is that their intense training teaches their muscles to use more lactate.

An interesting technical point: lactate production may even reduce acidosis, a view defended vigorously by Dr. Robert Robergs.33 But this is complex physiology, so not everyone agrees.34 If correct, however — and Robergs certainly makes a strong case — it would mean that blaming lactic acid for acidosis is actually the opposite of the truth.

Conventional wisdom is often a Russian doll of errors within errors within errors. Almost anything that lots of people believe is probably wrong. Or at least egregiously oversimplified.

There’s plenty more reading on this topic available if you’re interested.35

Are you on fire? Inflammation in DOMS

Evidence indicates that there is little or no inflammation present in DOMS in the first place.3637 Or (counter-intuitively) that there’s inflammation all right, but it’s not the cause of the pain: a 2015 study showed the bizarre result that inflammation holds steady or even increases after subsequent workouts.38 This suggests that exercise soreness is not caused by inflammation, but by something else that inflammation actually prevents.

That’s so weird/important, let’s repeat and rephrase: the evidence suggests that some minor inflammation present in DOMS is a reaction to whatever’s actually causing the pain. This is potentially an explanation for the repeated bout effect. Here’s the sequence of hypothetical events:

  1. unfamiliar exercise stirs up “something” (and this is uncomfortable)
  2. the immune system reacts to that (inflammation), and suppresses it over 2-4 days
  3. a few days later you do the same exercise … but this time your immune system is ready for it, so when “something” gets stirred up, it is much more effectively dealt with

And then there’s neurology!

Neurology never comes up when professionals talk DOMS. It’s really not on anyone’s radar, but it should be.

We’ve established that DOMS isn’t likely a direct result of microtrauma or metabolic stress, and inflammation is either absent or “it’s complicated.” Nothing demonstrates that more clearly than an 2011 study, which showed that it can actually spread — probably via a neurological mechanism — to adjacent muscles groups that were not exercised at all.39 I have wondered if non-local soreness could be related to a similar phenomenon, non-local muscle fatigue (NLMF) — that is, fatigue in the muscles you did not exercise.40 It’s not clear that such a thing actually happens,41 but it’s possible. (I have my eye on you, NLMF, you weirdo.)

That’s really strange. Very strange indeed. Thus DOMS may well often feel much worse and more extensive to some patients than it “should” feel … and with an explanation that isn’t really on anyone’s radar.

The biology of pain is never really straightforward, even when it appears to be.

“Reconceptualising pain according to modern pain science”, Lorimer Moseley

We should especially be thinking more about neurology because of a series of Japanese studies since 2010 showing that the pain is related to neurotrophic factors: substances secreted by muscles cells that goose nerve growth.42434445 A simpler way to say this would just be nerve growing pains. Exercise develops our nerves, and apparently that’s uncomfortable.

Not only does this account for the repeated bout effect, it might also explain the curious findings of Ayles et al.

All of this was shown in rats, not humans, and all by the same group of researchers, so it’s not time to uncork the champagne and declare victory quite yet. But it’s extremely interesting and promising, and it gets better: based on this theory, the Japanese researchers did demonstrate that the development of DOMS was “completely suppressed” by a drug that stifles neurotrophic factors. Yahtzee! And what was that drug? I’ll return to it below in the discussion of medications.

Vulnerability to DOMS from disease

We know that some diseases cause excessive post-exercise soreness, often for many years before diagnosis, and without any other symptoms.

Facioscapulohumeral Muscular Dystrophy (FSHD) is one of the most fascinating examples. It’s a common, mild form of muscular dystrophy that primarily affects the muscles of the shoulder and face. I have an old friend with FSHD; his symptoms were so subtle that he wasn’t even trying to figure it out when he was a younger man. Until his upper trapezius wasting away, in his late thirties — a classic symptom, but he was initially misdiagnosed with frozen shoulder among other things.

When he finally got the correct diagnosis, he started to see how the disease explained an awful lot about his life, many experiences and personal “quirks”… like his lifelong tendency to excessive soreness after exercise! Even his father’s life made more sense: the disease is genetic, and he obviously struggled with it, stoically, undiagnosed from cradle to grave. Biology is destiny, and this condition is a really good example of it. How many people out there are in that multi-decade period of wondering why they get so sore so easily, before finally being diagnosed with FSHD?

FSHD is a well-described genetic pathology. There is nothing squishy or uncertain about the diagnosis. And yet the mechanism by which FSHD causes soreness in the absence of any other symptoms is simply unknown, even though it seems ike a valuable clue. And if a disease like FSHD can do it without anyone knowing how, there are almost certainly several other pathological ways soreness can happen that have no explanation.

Exercise intolerance as a symptom

Myalgic encephalomyelitis, also often know as chronic fatigue syndrome, is almost defined by a poor reaction to exercise. It’s most significant symptom s “exercise intolerance”: severe exacerbation of symptoms following exertion, which includes soreness, but is definitely not just soreness. Indeed, “fatigue” doesn’t begin to express the seriousness of what these patient feel. They are are not just tired and out of shape, and exercise therapy not only won’t help, but can do significant harm.46

Although ME is disturbingly non-rare, it’s probably much less common that all the other illnesses that also cause exercise intolerance. Virtually any form of illness will make people feel more fragile and fatigued. This state is driven by the mechanism of neuroinflammation, a very basic biology alarm system that suppresses activity in all sick and injured animals.47 It’s probably not the specific mechanism of DOMS, but there could be overlap. It’s possible that many undiagnosed conditions are causing low-grade neuroinflammation, making people feel just slightly off… and more likely to be sore after a workout. Mild exercise intolerance.


What can you do about DOMS? Treating post-exercise muscle soreness

People have been trying to treat exercise-induced muscle soreness since forever — mostly unsuccessfully, I’m afraid. The products keep coming, and the marketing gets updated, but not much has really changed since the Anti-Stiff days. Since we still don’t (yet) know what causes DOMS, it’s unsurprising that anything like a cure has yet to be discovered. Even if we understood it, we still might not be able to do anything about it.

Almost nothing tried to date seems to be even remotely impressive. For instance, a 2003 review of the subject concluded, “Cryotherapy, stretching, homeopathy,48 ultrasound and electrical current modalities have demonstrated no effect on the alleviation of muscle soreness or other DOMS symptoms.”49 Other reviews have similarly dismissive conclusions.50

Low quality old illustration of a shirtless gentleman with an old-timey mustache, rubbing an ointment on his forearm, with the caption “strengthes the muscles.”

Anti-Stiff! From an ad in Cycling: An Illustrated Weekly, 1891. Anti-Stiff was “a muscle rub intended to ward off aches & fatigue during a variety of sporting endeavours” (hat tip to “Its promoter claimed, ‘Some athletes are so fond of it that they rub it all over them.’” The more the merrier!

Every popular treatment for DOMS

First, these are the options that are underwhelming and cannot really be taken seriously:

And then there are some marginally more promising treatment options that still fall well short of actually being “proven” and/or practical. They are only somewhat promising at best — but better than nothing. Each of these is covered in more detail below:

There is a broad consensus that nothing really decisively helps DOMS,69 and the best way to prevent it is … just get it over with. In other words, only DOMS prevents DOMS!

Except maybe Indian food. And heat. And maybe sunshine and fish. Or Vitamin I. The next few sections are devoted to a few of the slightly more promising options.

Vitamin I: the effects of ibuprofen on pain, prevention, function, and healing

Ibuprofen (and other anti-inflammatory drugs, the NSAIDS) have been shown to modestly reduce the pain of DOMS.7071 (Note that popular topical NSAIDs, like Voltaren, may be mostly ineffective,72 especially on big muscles, probably because the drug can’t be absorbed into deep enough tissue).

But there’s more to this than just treating pain. Are anti-inflammatories just a Band-Aid? Is there any meaningful benefit other than pain relief? Can they make the muscles work better? Could they prevent DOMS from happening in the first place, or accelerate recovery? In summary …

Anti-inflammatories for function

NSAIDs do not reduce the muscle weakness that goes along with the pain. For instance, if you had severe DOMS in your quadriceps, taking ibuprofen would probably reduce your pain, but you would still not be able to jump as high as usual.

Update: A small 2021 study presented evidence that contradicts the conventional wisdom that NSAIDs only treat the pain. It showed increased strength and reduced fatigue in powerlifters. It is possible that this was a minor effect, a spin-off benefit of pain control. Notably — and this was the focus of the study — ibuprofen did not reduce oxidative stress, which is what you’d expect if it was effective at preventing soreness and other unpleasant biological consequences of intense exercise.73 It likely remains broadly true that ibuprofen doesn’t really meaningfully enhance recovery, but this data is an interesting wrinkle.

Anti-inflammatories for prevention

They don’t prevent DOMS either, not even a little bit. The science is quite clear on this point: a 2006 experiment tested the effect of ibuprofen on hard core marathoners.74 The results were so strongly at odds with beliefs that Aschwanden used the research as a main example in an article about how hard it is to get people to accept new evidence:75

Among runners of ultra-long-distance races, ibuprofen use is so common that when scientist David Nieman tried to study the drug’s use at the Western States Endurance Run in California’s Sierra Nevada mountains he could hardly find participants willing to run the grueling 100-mile race without it.

Nieman, director of the Human Performance Lab at Appalachian State University, eventually did recruit the subjects he needed for the study, comparing pain and inflammation in runners who took ibuprofen during the race with those who didn’t, and the results were unequivocal. Ibuprofen failed to reduce muscle pain or soreness, and blood tests revealed that ibuprofen takers actually experienced greater levels of inflammation than those who eschewed the drug. “There is absolutely no reason for runners to be using ibuprofen,” Nieman says.

The following year, Nieman returned to the Western States race and presented his findings to runners. Afterward, he asked whether his study results would change their habits. The answer was a resounding no. “They really, really think it’s helping,” Nieman says. “Even in the face of data showing that it doesn’t help, they still use it.”


Anti-inflammatories and healing

“We can put a man on the moon,” but we still don’t really know what non-steroidal anti-inflammatories do for injured/sore muscles other than relieve pain. It’s nice to think they might facilitate healing, but the opposite is just as possible: they might impair healing by suppressing aspects of inflammation that are necessary for healing.

The role of inflammation in DOMS is extremely unclear (understatement). As discussed above, Deyhle et al. showed that inflammation actually increases as the pain fades away — an extremely odd finding. So it’s complicated! No wonder the evidence on the effects of NSAIDs is so mixed.

A 2017 review of 41 relevant scientific papers, the first of its kind, concluded that NSAIDs may cause a “small to medium” drop in various signs of injury in the short term, compared to recovery without NSAIDs.76 Curiously, the effect is more pronounced in the lower body.

Also odd: recovery impairment was detected, but only in animals. So don’t feed your dog NSAIDs after a hard evening of fetch.

Most of the studies reviewed by Morelli et al. had a low risk of bias (which is a bit unusual in musculoskeletal medicine), and yet the eight studies that did have a higher risk of bias account for a substantial amount of the benefit detected. Take them out and the positive result starts to look downright unimpressive: a minor effect, on the margin of statistical significance. Arguably those studies should not have been included at all. So the question still does not seem to be clearly answered, and the healing benefits are unpredictable and/or modest at best.

COX-2 inhibitors: an anti-inflammatory used for something else

Earlier I introduced a series of Japanese rat studies that suggest DOMS is basically “neurological growing pains” (summarized by Mizumura et al.). This was substantiated by preventing DOMS using COX-2 inhibitors, which specifically inhibit neurotrophic growth factors. This is not their primary purpose: COX-2 inhibitors are anti-inflammatory meds by nature, a much-maligned type of NSAID with major safety issues, and the only remaining drug of this type for sale in the US is Celebrex (celecoxib). If Celebrex can be clearly shown to prevent DOMS in humans, that’s a huge deal, not because it’s a viable treatment — preventing DOMS almost certainly isn’t valuable enough to be worth the side effects of COX-2 inhibitors — but because it would prove the mechanism of DOMS … a profound knowledge upgrade.

Waiting it out or working through it: the role of rest vs. more exercise in DOMS treatment

“Rest” is the only thing that is guaranteed to “work” for DOMS — if you wait, you will feel better. But you can’t rest harder or better to get it over with quicker. It takes as long as it takes.

But we are impatient animals, and “working through it” is a popular way to try to get to the far side of DOMS quicker. Going back to the scene of the crime, fighting fire with fire, hair of the dog that bit you. This is sometimes called “active recovery.”77

Depending on how sore you are and how hard you try, exercise may help or harm. Harm is absolutely possible: usually just more soreness, but it can be disturbingly severe in rare cases. As for whether it can help? It is possible, but it’s mostly a speculative long-shot.

Should you exercise while sore? Will it do any harm?

We usually start asking ourselves these questions in exactly the situation where they of greatest concern: when we are really quite sore and considering about doing the same workout again. That specific scenario is rarely a good idea.

But it depends, of course. The risk is a function of both the severity of the soreness and the intensity of the exercise. Here’s a rule of thumb: your caution should increase with your soreness. But only a chart will do here:

Exercise versus Soreness
SAFE safe safe safe?
safe risky risky risky
safe risky dangerous dangerous
safe? risky dangerous Darwin Award
This table shows the risk that any given exercise intensity will aggravate soreness of a given severity and/or undermine the benefits of the exercise, assuming repetition of the same type of exercise that made you sore in the first place.?In this chart, I was focusing on the risk of making soreness worse (more intense and/or longer prolongued). The effect on the physiological benefits of exercising is probably not quite the same, but it’s a good bet that they correlate roughly. That is, moderate exercise with strong soreness does not just risk making the soreness worse, but also undermining the physiological benefits of doing the workout. My hunch is that you can undermine your benefits before aggravating soreness — but that’s the kind of hypothesis that really needs to be tested, and no one has. Exercise intensity is relative to your fitness level: a 10k run is “extreme” for a couch potato, not a marathoner.

You can overdose on literally anything, including exercise. The more sore you are, the easier it is to overdose. Our tolerance for exercise drops while we are in recovery from the last dose.

At best, pushing through the pain is just probably harmless at lower intensities and severities. More likely, you risk no harm, but you do waste your time by sabotaging the body’s adaptive response to exercise. At worst? Serious injury is possible, and the greatest risk is rhabdomyolysis (see above, paywalled). (There is an even greater risk beyond that, but it’s quite speculative.78)

Exactly “how much is too much” is impossible to know: it’s a moving target, dancing to the tune of many complex variables. This is the rabbit hole of what constitutes safe/optimal “recovery time,” the Holy Grail of elite athletics. Trying to do a deep dive into the science of load management this is like diving into a 3-foot deep pool: you’re going to hit bottom. There are just too many unknowns.79

Can exercising while sore actually help?

Moderate active recovery may be safe … but can it actually help? Is it a fitness optimization? Can light exercise make DOMS tamer and briefer, enhancing your recovery? Can it reduce the risk of other injuries?

Probably not. But no one really knows, because active recovery is much less studied than hangover cures! It’s one those widely held beliefs that exists in a near perfect scientific vacuum. There are a few trials in the context of recovery from elite team sports like football (soccer) that are fairly relevant, but they aren’t anywhere near enough to truly answer the question … and they are are discouraging. Querido et al. in 2022:80

…the effects of exercise in the recovery of physical, physiological, and perceptive outcomes have been reported as not significant, which is in agreement with the findings of the present study.

(And it’s not like Querido et al. had unreasonably high standards: they endorsed two other recovery methods despite mediocre evidence of efficacy.81)

I know of just one relevant study outside the context of professional sports: a 2003 experiment that showed that a session of yoga modestly reduced soreness up to a day later compared to no yoga. But it’s such a small signal from a tiny study, just 24 people, that it really isn’t worth anything on its own.82

The research clearly shows that exercise relieves soreness while you are doing it, but there is very little data on how it changes the next day or two of soreness. Many experts assert that the pain-killing effect of exercise is temporary, but I cannot find any data that actually supports that belief one way or the other.

What is the effect of chronic pain and illness on active recovery?

The effect of exercise on people with chronic pain is complicated.83 DOMS is often exaggerated in this population — more easily triggered, worse, with slower recovery — and that makes recovery trickier and riskier. But it’s still the same challenge in principle.

But many people may struggle with a truly different, dysfunctional responses to exercise: “exercise intolerance” involves physiologically wonky consequences, probably in addition to exaggerated DOMS. Famously, just advancing more carefully does not solve this problem.84 For these patients, all bets are off, all rules of thumb are on probation, and considerable caution is advisable. It is still possible that load management basically works the same way with some cases exercise intolerance (albeit with a much lower threshold and worse consequences for training errors). But it’s also possible that it is doomed to failure — as you’d expect from trying to exercise while sick!

The heat hope

Everyone will be pleased to know that one study (predictably European) showed some benefits to hot tubbing, specifically “warm underwater jet massage”85 — aaaah. However, it was a small and flawed piece of research — and most people know from personal experience that a soak in a hot tub may “take the edge off it,” but this hardly constitutes a miracle cure for DOMS. This evidence is too weak to take to the bank.

In 2006, we got some better science news: surprisingly good results in treating DOMS in the low back with a “heat wrap,” a wearable device that applies heat for hours at a time.86 It’s another small study, just 17 test subjects, but more persuasive.

Eureka? Proof needs more data, but this makes it well worth trying heat on your sore muscles after exercise. Happy heating! See the thermotherapy guide.

The fish hope

Fish oil has shown some potential to aid with recovery from exercise.87 The evidence is not compelling, but it’s noteworthy, especially the apparent effect on strength and ROM recovery.

But I’d say the take-home message is to eat more fish, rather than fish oil in capsules — because there’s plenty of evidence that fish are better for you than fish oil pills.

The curcumin hope

Illustration of ground turmeric root, source of curcumin, that might just actually help delayed-onset muscle soreness.

Curcumin is the interesting molecule in the bright orange South Indian spice, turmeric. It “exerts potent anti-inflammatory effects.” Although we’ve just discussed evidence that inflammation may not be a factor in DOMS, here’s some new evidence that it is: in a 2015 study, “curcumin caused moderate to large reductions in pain” in 17 men with very sore leg muscles.88 It also helped some aspects of strength loss. The effect size here passes the “impress me” test. These results constitute the only really good science news about any kind of treatment for DOMS. Now it just needs to be replicated! Which is why I won’t give it any more attention at this time: this is good, promising news, but it absolutely needs to be verified.

Note that curcumin is poorly absorbed without other agents such as black pepper extract (piperine). There are several completely unproven products that promise better absorption by various means, so caveat emptor.

Massage, DOMS, and a lot of irony

What of massage therapy? We’ve got to deal with massage in more detail, because it’s the king of treatments presumed effective. And its reputation got a big boost in early 2018 from a low-quality meta-analysis (more on Dupuy et al. below).

Photo of a woman receiving a massage. The scene is peaceful, but biological toxic waste hazard symbol is superimposed on her back.

Oh, irony

Massage can cause some soreness & malaise, rather than relieving it.

Massage therapists and enthusiasts often claim DOMS prevention and cure as a benefit of massage. Unfortunately, what evidence there is to support this damns it with faint praise — it doesn’t work well enough to be impressive89 — and plenty of evidence goes the other way,90 including my own careful personal testing. At best, massage has mild therapeutic effects on DOMS that are largely mitigated or cancelled out by mild side effects.

It’s more likely that massage actually causes some soreness and malaise itself — just like exercise does. The sensations are incredibly similar.

A 2007 survey of 100 massage patients91 found that 10% of 100 patients receiving massage therapy reported “some minor discomfort” in the day following treatment. This would mainly be the familiar slight soreness that is common after a massage, known as “post-massage soreness and malaise” (PMSM) — and although 10% is plenty, it is almost certainly too small a number.92

But the irony deepens! Massage as a DOMS treatment is also often “explained” with a myth — that massage detoxifies. This is an unsavory association. Detox language in health care is usually bollocks. In the case of massage, the detoxification claim never made much sense, there’s no evidence for it, and if anything there’s evidence that massage is somewhat toxifying — probably by causing a little rhabdo. I make that case in a lot of detail in another article:

Is there any hope? Some other way that massage could help DOMS? Even while possibly causing some at the same time? No explanation other than detoxification has ever been suggested … until just recently.

Can massage reduce DOMS by reducing inflammation?

No. (You can go to the next section now, if you like.) As of early 2012, there’s a candidate for a new explanation of how massage works … or a new myth. It’s a lot more likely that it’s a new myth.

According to the headlines and the researchers themselves, massage supposedly “reduces inflammation,” based on a gene profiling experiment that got a lot of press. (A lot.) It’s bollocks. Unfortunately, the researchers tried to explain a therapeutic effect that is either an illusion or a minor outcome, and they generally over-interpreted the significance of a handful of proteins. The upshot is that it’s much ado about nothing and doesn’t really change our understanding of massaging DOMS.93

Although this fact was distinctly under-emphasized, the study identified literally hundreds of changes in gene expression caused by exercise — compared to just five changes caused by massage. The take-home message from that is simple: exercise changes cellular behaviour, massage does not. That is not really any kind of a surprise.

Enough theory! Does massage help DOMS or not?

We don’t have to know how something works to test to see if it works. And massage for DOMS has been tested. The upshot is that the results are mixed and underwhelming. Damned with faint praise.

In 1998 — around the time I was starting my training as a massage therapist, actually — E. Ernst published a review of papers on this subject in the British Journal of Sports Medicine.94 Ernst concluded that, “Massage therapy may be a promising treatment for DOMS. Definitive studies are warranted.”95 That sounded like good news for massage therapy! However, actually reading the paper discouraged me.

Digging into the details always seems to have that effect.

Ernst found only seven studies worth considering, and most of these had “serious methodological flaws” and “very small sample sizes.” Of the seven, three are inconclusive or show no effect on massage therapy on DOMS, and four “imply a positive symptomatic effect” or a “positive trend.” I was not particularly impressed by any of those positive effects or trends — they all seemed ambiguous to me, even if you ignore the “serious methodological flaws.” I could not come to the same optimistic-sounding conclusion that Mr. Ernst did.

Since that time, I have not seen any new studies or evidence to alter my opinion. Another review in 2003 judged massage to be “less promising” than anti-inflammatories, which are themselves so unremarkable.96 A 2008 review found “moderate data supporting its use” — wow — continuing the pattern of damning DOMS-massage with faint praise, and pulling a barely-positive conclusion out of weak data.97 Readers have been telling me for years now that they believe there is new evidence that “massage works” for DOMS, but when I go looking, I can’t find any data that seems the least bit impressive. For example, one the best studies I could find, a 2006 paper by Zainuddin et al., found barely statistically significant evidence of modest pain relief only, possibly quite brief, with no effect on the weakness whatsoever (no study has ever found that).98 And that’s roughly as good as it gets. When people tell me that there is “good evidence” that massage is effective for DOMS, this is what they’re talking about. I acknowledge that some of the evidence is indeed “positive” — that is undeniable — but it fails to impress.

Another (bad) reason people believe that massage might help DOMS is because of a misleading science story from 2012. Supposedly researchers discovered that massage reduces inflammation. Even if this was clearly relevant to the biology of DOMS (and it’s not), the conclusion was hype: there’s no way that reseach demonstrated any such thing.

Since we don’t know much about what causes DOMS, and we don’t know much about how massage therapy works (and probably never will), it’s difficult to even guess about how massage therapy is supposed to help. While it does seem likely that massage therapy probably has some positive effect on DOMS, those effects are likely to be limited, and to vary widely depending on the therapist, the individual, and the circumstances. And so I remain skeptical that massage therapy can be claimed to generally prevent or reduce the intensity of DOMS, let alone actually “cure” it. Massage therapy should not be promoted or purchased for this reason. Fortunately, there are plenty of other reasons to have massage therapy: see Why Massage Therapy?

And there are also plenty of other myths! There’s a full list of them in the related reading section below.

That troublesome 2018 study that declared victory for massage therapy

In early 2018, many massage therapists jumped to cite a new scientific paper, Dupuy et al.99 because it seemed to confirm their bias100 that massage helps post-exercise muscle soreness. And no wonder! The conclusion reads:

Massage seems to be the most effective method for reducing DOMS and perceived fatigue.

So massage therapists were tripping over themselves sharing it on Facebook, retweeting it, and posting it on their clinic blogs. Such conclusions are literally good for business. “From the Department of the Obvious,” one MT quipped. Another triumphantly declared of this article, “ gets it wrong again!” As if one new publication beats all the analysis of the evidence I’ve published here over the years.

Dupuy et al. is a classic “garbage in, garbage out” meta-analysis that establishes nothing … except, perhaps, the opposite of the “positive” conclusion. Just read the fine print! There’s a strong and classic pattern of publication bias in the data, with better quality studies finding nothing of interest, and the shittier ones consistently skewing towards the positive.

Alex Hutchinson wrote about this paper for Outside, and included a terrific summary of how publication bias is exposed by funnel plots (a must-read for anyone trying to make sense of research). This kind of thing is the legacy of decades of publish-or-perish pressure in academia. Recovery science is a mess, most of the studies are just junk, and so most meta-analyses are too… and there’s a lot of them. John Ioannidis:101

The production of systematic reviews and meta-analyses has reached epidemic proportions. Possibly, the large majority of produced systematic reviews and meta-analyses are unnecessary, misleading, and/or conflicted.

This one is so useless that I wouldn’t even be citing it here if it hadn’t made “headlines.” I’m bringing it up only for the sake of hype control. It’s not good for anything except being a fine example of the clutteration of medical science with low quality meta-analyses.

P.S. Everything I just wrote about Dupuy et al. applies to another meta-analysis from a year earlier, in 2017, Guo et al.102

From the Lab of Me: a massage experiment with a sample size of one

Purpose: To test massage-aided recovery from delayed onset (post-exercise) muscle soreness. Systemic steam heating — I have a lovely steam room at my disposal — was used as an adjunctive therapy.

Methods: I totally thrashed my biceps at the gym, deliberately pushing into the danger zone to generate wicked DOMS. It worked a charm: my guns were mighty sore by the end of the day. Soreness spiked with the slightest contraction, making it easy to evaluate. The next morning, sensitivity was equally savage on both sides. In a toasty steam room, I massaged the crap out of my left upper arm for several minutes, using strong deep palm stroking, which was super unpleasant. The things I do for science! Then I compared soreness at regular intervals by flexing simultaneously.

Results: Soreness in my biceps was identical at all testing points after massage: 5 and 20 minutes later, and about 1, 6, 12, 24, 36, 48 and 72 hours later. The soreness was extremely intense from 24 to 48 hours, fading quickly after that — the usual pattern of recovery. And entirely symmetrical.

Conclusion: Neither strong massage or heat produced any effect on DOMS in this little guinea pig.

Meaner, longer DOMS as a symptom of other health problems

DOMS can be made worse by some other health problems — possibly quite a few of them. Although DOMS is not caused by medical vulnerabilities per se, it’s possible that it would be a non-issue otherwise. It’s even possible that it’s a canary in the coal mine: particularly fierce DOMS might actually be one of the only symptoms of a medical vulnerability. But how can you tell? Pain is totally subjective and it’s nearly impossible to tell if your DOMS is actually excessive. Comparing notes with other people is difficult, because people love to complain and may bitterly vouch for the severity of their own DOMS — and, for all you know, maybe they really are having a problem of their own.

There’s really no way to know, except to do your best to judge the severity of your DOMS, and see if it appears to be part of a pattern of other symptoms. For instance, you might suspect vitamin D deficiency if your DOMS seems a bit nuts and your head is sweating a lot (a more distinctive symptom of vitamin D deficiency), and you live in northern British Columbia and rarely see the sun.

DOMS is just a part of a broader spectrum of challenges to “exercise recovery.” There are many possible reasons why people might struggle to recover from exercise. It might just be more acute fatigue. For instance, another deficiency, iron, would cause fatigue and a variety of other symptoms — but it probably wouldn’t make DOMS worse. But there are undoubtedly other problems, like sleep disturbance (discussed below), that will aggravate DOMS specifically.

Most health problems that will aggravate DOMS are either relatively obvious, or nearly impossible to diagnose, or untreatable. For the purposes of this article, I’m going to focus on just a couple problems (for now) that seem most worth considering: vitamin D deficiency and insomnia. Both are common, both can be helped, with a clear benefit to DOMS.

Vitamin D deficiency

Inadequate vitamin D is probably more common than once suspected — at least 1 in 20 people in the lowest estimates,103 and possibly many more.104 It can cause subtle widespread pain that may be misdiagnosed as fibromyalgia and/or chronic fatigue syndrome, including symptoms like muscle and bone aching, fatigue and weakness, lower pain threshold, and — here’s the punchline — fiercer DOMS that takes longer to resolve.

There’s no direct evidence available on this topic (surprise surprise). Despite that, the indirect evidence is actually far stronger than most of the direct evidence available on other topics. We have at least three hard facts for premises: vitamin D deficiency really is common, definitely makes DOMS worse, and (obviously) can be treated with appropriate supplementation.

If you have the impression that you’re struggling to recover from exercise, that the consequences of a workout are out of proportion, vitamin D deficiency is worth investigating. For more information, see Vitamin D for Pain.

Insomnia and sleep disturbance in DOMS

Sleep deprivation makes pain worse, muscle pain in particular, and probably DOMS as well. There is no direct scientific evidence of this that I am aware of. However, anyone who has ever been severely sleep deprived will tell you that it causes a distinctive and unpleasant feeling of “fragility” which seems quite likely to make one more vulnerable to DOMS.

Photograph of me playing ultimate frisbee, an intense sport that regularly makes me extremely sore, even though I’m quite well adapted to it.

Ultimate is an intense Frisbee sport that can make almost anyone wickedly sore.

I have an example of sleep-deprivation induced DOMS from personal experience: The first ultimates games of the season have always been an ordeal. They are followed by 3-5 days of harsh DOMS. But in 2011 I started the season in unusually good physical condition, thanks to months of sprint intervals and strength training. For the first time ever, I was not sore after my first games of the summer. And my DOMS-immunity continued in week two, so it didn’t seem to be a fluke. That was then followed by some nasty sleep deprivation and jet lag. I suffered a great deal of it for two weeks — before, during and after a holiday to Amsterdam. When I returned to Vancouver and played ultimate again, I was really blasted sore. Quite extreme.

Coincidence? I think not!


“Percussive therapy” is widely regarded as stimulatory, often with the implication of subtle but exotic effects on healing, much like ultrasound (which is basically just another vibration therapy at much higher frequencies). Low-frequency vibration — AKA “jiggling” — may have some intriguing effects on biology. For instance, it really does seem to boost flexibility, which is a nifty effect.105

The effect on soreness is much less certain. These are mostly uncharted waters. As of spring 2021, the only available scientific review of vibration for DOMS is junk science, completely useless.106 There’s a handful of scraps of evidence showing some signs of slightly reduced soreness.107108

A massage “gun”

One of hundreds of similar products, trending strongly since the mid 2010s, almost all of which are being marketed as exercise “recovery” tools.

It’s just not enough. While it’s conceivable that vibration is useful, but it hasn’t actually been demonstrated yet, and it’s very unlikely that it’s a dramatic effect. Meanwhile, the massage gun industry is raking in the profits, selling massage “guns” mainly with recovery-themed promises. For a more detailed review — but no additional evidence, because there ain’t any — see Vibration Therapies, from Massage Guns to Jacuzzis: What are the medical benefits of vibrating massage and other kinds of tissue jiggling?

Meanwhile, I wouldn’t hesitate to vibrate my sore muscles, because it’s kinda fun and obviously harmless (other than the time/cost of the gadgets).

About Paul Ingraham

Headshot of Paul Ingraham, short hair, neat beard, suit jacket.

I am a science writer in Vancouver, Canada. I was a Registered Massage Therapist for a decade and the assistant editor of for several years. I’ve had many injuries as a runner and ultimate player, and I’ve been a chronic pain patient myself since 2015. Full bio. See you on Facebook or Twitter., or subscribe:

Appendix A
Dueling massage anecdotes: A typical testimonial versus my own personal experiment with massage for delayed-onset muscle soreness

In early 2012 I made one of my once-in-a-while appearances on I’m in their roster of reserve guest myth busters. This time Scott Gavura (the Skeptical Pharmacist) recruited me early one morning for some short-notice debunkery of a sloppy Globe & Mail piece on delayed onset muscle soreness (DOMS). I felt like the Batman getting the bat signal, but instead of being a billionaire martial artist gadget freak called to fight crime, I’m a middle-class amateur athlete gadget freak called on to fight … bad science journalism. An endless chore. Just like Batman’s.

The Globe & Mail recommended Epsom salts, massage, and light exercise for muscle soreness. None of those will do anything or much, just like every other alleged treatment for DOMS. As covered thoroughly in this article, there really is no cure for DOMS but time. Inevitably, we saw some anecdotal evidence to the contrary in the comments. OCTriathlete stood up for massage with this story:

I was lucky enough to receive a leg massage from a family member who is educated in massage but not a professional. However, I was unlucky in that the massage was interrupted after only one leg was complete!! The next day the leg that received the attention was only hinting at the sensation of the heavy workout the previous day. The leg that missed out? It was DEEPLY sore for 2 days. So there you have it—my own little scientific (however unintentional) experiment.

Lucky him! I’ve done that experiment intentionally and casually a half dozen times in my life before getting a little more serious about it — see the section “From the Lab of Me” — and I’ve never observed the slightest difference. If only. And in the early days I did it with the greatest of optimism and the full-on mental bias of someone paying his rent by selling that therapy. I love massage for many reasons, but recovering from a harsh workout has never been one of them.

O anecdote — how I want to strangle thee

I wonder what would happen if we took Occam’s razor to OCTriathlete’s anecdote. What is more likely?

I know which bullet point I’d bet on.

Maybe OCTriathlete truly got a benefit. I’m being very skeptical, yes, but I’m not actually saying that he couldn’t have actually enjoyed a nice effect. Physiology differs. The evidence on massage for DOMS isn’t entirely negative — just mostly, and distinctly underwhelming where it’s positive. There could be interesting cases on the edge of that bell curve, and OCTriathelete could be one of them — slightly pulling up an unimpressive average.

But … Occam’s razor cuts hard and deep on a story like his. If anecdotal evidence like this were actually reliable, then most folk medicine would still be the best medicine available today. If there are a lot of testimonials for something, people like to say that there “must be something to it,” but not only is that not true, it’s practically the opposite of true: testimonials are actually a sign of the wrong kind of thinking about medicine. The history of anecdotal evidence has given us almost every silly belief you have ever heard of: every naked superstition and outrageously dangerous quackery has had its zealots, converts, and emphatic testimonials, sometimes in extremely large numbers. People have sworn that snake oils work even as they were being (literally) destroyed by them. For a whole bunch of wonderfully entertaining examples, spend a happy hour listening to Caustic Soda’s terrific Quackery episode.

And what are those all beliefs are based on? Exclusively?


Perhaps a personal experiment like mine — an antimonial — is just a little bit of an anecdote antidote. I love massage, but I’m not kidding myself: if it helps DOMS at all, it doesn’t help most people much.

I am not anti-anecdote. I am against giving anecdotes too much weight as a form of evidence. But I always want to hear patients’ stories. They are an amazing source of important questions and inspiration … and both the telling and the listening are inherently valuable.
Cartoon of two people arguing. The caption reads, “How to make a scientist’s head explode.” The guy says, “Anecdotal evidence isn’t valid.” The woman responds, “Yes it is! I once used an anecdote as evidence, and later it turned out I was right.

Illustration used with the kind permission of Zach Weiner, of Saturday Morning Breakfast Cereal. Thanks, Zach!

Appendix B:
Radu’s rhabdo: a story of intense exercise gone wrong

Radu Simion kindly granted permission to use his story and his real name. It’s a story of true rhabdo: he was hospitalized with a creatine phosphokinase level of at least 60,000, which is quite severe. But how did he get it?

It wasn’t from a massage, so it might seem like a strange choice for this article, but the point of the story is that rhabdo can come from surprisingly minor physical stresses. In this case, a seemingly ordinary spike in exercise activity — the kind of spike that would make anyone extremely sore, but you wouldn’t really expect it to put anyone in the hospital.

Radu is a Romanian software developer. Sedentariness is the main occupational hazard of that line of work, and after a lazy patch, he decided it was time to hit the gym.

I was trying to push myself as hard as I can, and it did not feel bad while working out. I was sore in the evening of the first day, though.

The second day I was extremely sore — all movement hurt. But due to "manning up" and terrible advice from friends, I just pushed through. I went back to the gym, this time working the core, back and legs, but chest and arms were also involved in these exercises.

In the evening I couldn’t lift my arms up all the way anymore because of the pain.

And on day three, the exhaustion was severe, and not only was his urine cloudy and dark brown, but he could barely produce any — a sign that his kidneys were clogged with protein, and a medical emergency. Fortunately, Radu recalled reading something about this problem years ago, and went to the hospital, where he was to stay for twelve days, on IV fluids the whole time, his CPK levels dropping slowly but steadily. Quite dramatic.

And yet for the most part Radu just felt worn out — like he’d really overdone it, but not “sick.” It might seem like a trivial detail, but I want to emphasize that even serious rhabdomyolysis can basically just feel like exhaustion — and if you can feel merely “very tired” with a CPK of 50K, then it seems likely that many people have had lesser rhabdo without any symptoms more striking than a sense of having overdone it.

Extreme rhabdo demonstrates that mild to moderate rhabdo can be subtle.

Radu’s doctor didn’t buy the exercise story

The rhabdo itself was undeniable, but Radu’s doctor was skeptical that it could have been caused by a workout. He suspected some other unseen injury or pathology, and that’s part of the reason Radu was kept in the hospital for so long — just in case the real issue was that something else was wrong with him, and the reaction to the workout just exposed it.

If there was any such underlying issue, it has never emerged. Radu has been healthy for years since these events, and has never again experienced anything like it. If he has a vulnerability — certainly still possible — he has never again provoked it, because ever since he has been “very careful, almost paranoid when doing any kind of exercise.”

His doctor’s skepticism is not surprising, and his caution was justified. Exertional rhabdo is a well-documented phenomenon, but also fairly obscure, and the average doctor can’t really be expected to know about it. But others did!

There was one resident at the hospital that was genuinely interested in what happened to me and he brought up the white-collar rhabdo thing — he thought it’s something that happens more often than we think and usually just flies under the radar and solves itself. I had forgotten in the meantime, but your article reminded me of that chat with him.

Maybe Radu’s rhabdo was produced by an unusually overzealous attempt to push through soreness, a second hard workout when his body hadn’t even begun to recover from the first. That could be enough. Or maybe almost anyone else would have gotten away with it, but he ended up hospitalized due to some relatively subtle biological vulnerability — something that makes him more likely to get rhabdo, but minor enough to go unnoticed ever since.

Related Reading

The major myths about massage therapy are:

The complete list of dubious ideas in massage therapy is much larger. See my general massage science article. Or you can listen to me talk about it for an hour (interview).

And massage is still awesome! It’s important to understand the myths, but there’s more to massage. Are you an ethical, progressive, science-loving massage therapist? Is all this debunking causing a crisis of faith in your profession? This one’s for you: Reassurance for Massage Therapists: How ethical, progressive, science-respecting massage therapists can thrive in a profession badly polluted with nonsense.

What’s new in this article?

Twenty updates have been logged for this article since publication (2007). All updates are logged to show a long term commitment to quality, accuracy, and currency. more When’s the last time you read a blog post and found a list of many changes made to that page since publication? Like good footnotes, this sets apart from other health websites and blogs. Although footnotes are more useful, the update logs are important. They are “fine print,” but more meaningful than most of the comments that most Internet pages waste pixels on.

I log any change to articles that might be of interest to a keen reader. Complete update logging of all noteworthy improvements to all articles started in 2016. Prior to that, I only logged major updates for the most popular and controversial articles.

See the What’s New? page for updates to all recent site updates.

Aug 30, 2023 — A variety of modest improvements to the sections on active recovery, particularly the evidence.

2022 — A minor (but particularly interesting) science update: Roman et al. on muscle nuclei migrating to sites of microtrauma for repairwork.

2022 — Minor science update, added a citation to Aidar et al. about the effect of ibuprofen on strength and fatigue.

2021 — Added a major new section about active recovery.

2021 — Important corrections and clarifications, acknowledging ongoing debate about the relationship between lactate, lactic acid, and acidosis. Importantly, however, this is only relevant to the biology of fatigue, not soreness.

2021 — Substantial upgrade to the debunking of the lactic acid myth, from a sidebar with a couple key points to a new section of the article.

2021 — New section: “Waiting it out or working through it: the role of rest and more exercise in DOMS treatment” in which I address two key questions I should have answered here long ago: “Should you exercise while sore?” and “Can exercising while sore actually help?”

2021 — Added a fun image of Anti-Stiff, an old-timey snake oil for muscle soreness (good historical perspective, too). Added discussion of worst-case scenarios, especially rhabdomyolysis, and DOMS that’s out of proportion to overexertion. Added examples of pathological vulnerability to DOMS, and some speculation about mechanism (neuroinflammation).

2020 — Correction: new evidence suggests that the phenomenon of non-local muscle fatigue isn’t quite as well-established as I thought (see Behm).

2020 — Added an unimportant but really interesting citation about non-local muscle fatigue.

2020 — Added more information and references about protein supplementation, especially the branched-chain amino acids.

2019 — New section about vibration.

2018 — New section about “That troublesome 2018 study that declared victory for massage therapy” (Dupuy et al.).

2018 — Very short new section about the modest potential of fish oil to help with DOMS.

2017 — Major science update about a series of Japanese rat studies that suggest DOMS is basically “neurological growing pains,” summarized by Mizumura et al. It’s a fascinating potential solution to the DOMS mystery.

2017 — New sections dedicated to inflammation and the effects of non-steroidal anti-inflammatories on healing. Elaborated on the bizarre findings of Deyhle et al. and integrated evidence from a major new review (Morelli et al.). Some re-organization of the article for clarity.

2016 — Added new sections about vitamin D deficiency and the general concept of excessive DOMS as a symptom of other health problems.

2016 — Added a particularly high quality mobile-only article summary.

2016 — Short new section: “DOMS timing: just how delayed is it?”

2016 — Added citation about compression garments (Beliard et al.).

This article was updated regularly for many years at least before I (finally) started logging the updates with a minor routine update on Jul 8, 2016.

2007 — Publication.


  1. Post-exercise muscle soreness (PEMS) is probably a better term, but DOMS definitely dominates — you can pretty much use the acronym DOMS as a word unto itself, certainly with health and fitness professionals. I will use it that way for the rest of the article.
  2. The “delay” effect is strong in me. I often have no symptoms at all on day one, and peak on day three.
  3. Knochel JP. Catastrophic medical events with exhaustive exercise: "white collar rhabdomyolysis". Kidney International. 1990 Oct;38(4):709–19. PubMed 2232508 ❐
  4. Luetmer MT, Boettcher BJ, Franco JM, et al. Exertional Rhabdomyolysis: A Retrospective Population-based Study. Med Sci Sports Exerc. 2020 03;52(3):608–615. PubMed 31652234 ❐
  5. Hopkins BS, Li D, Svet M, Kesavabhotla K, Dahdaleh NS. CrossFit and rhabdomyolysis: A case series of 11 patients presenting at a single academic institution. J Sci Med Sport. 2019 Jul;22(7):758–762. PubMed 30846355 ❐ “CrossFit participation poses significant risks to participants including exercise induced rhabdomyolysis.”
  6. Acutely and chronically painful patches of soft tissue are a real phenomenon. However, exactly how they work is still mostly mysterious. Conventional wisdom says they are tiny spasms stuck in a metabolic vicious cycle, but they could also be a more pure neurological problem. So-called “muscle knots” are definitely not knots, and probably not limited to muscle either — it’s just that most of our soft tissues is muscle!
  7. It was rarely (if ever) the main reason for the appointment, however. “Help, I’m sore from my workout!” is not really a common thing for people to say when they book massage appointments. This will come up again below.
  8. Well, not nothing. A gentle, soothing massage can be quite nice when you have bad DOMS. However, the niceness lasts not much longer than the massage itself.
  9. There are many massage myths, like the idea that massage increases circulation, or detoxifies, or reduces inflammation. Massage can be a lovely experience, but it is extremely unclear how medically beneficial it is, and a great many massage therapists drink deeply from the well of pseudoscience and quackery.
  10. This comment was provoked by a really awful mainstream article about muscle soreness in the Globe and Mail: I’m sore after weight-training. How can I recover?
  11. An eccentric contraction is an interesting type of muscular contraction while lengthening — an apparent contradiction! Eccentric contraction is a bit mysterious, and is known to be a bit “harder” on muscle and a strong stimulus to adaptation. For more information, see The Role of Eccentric Contractions in Rehab: A weird bit of muscle physiology, and what it has to do with recovery from injury.
  12. Parr JJ, Borsa PA, Fillingim RB, et al. Pain-related fear and catastrophizing predict pain intensity and disability independently using an induced muscle injury model. J Pain. 2012 Apr;13(4):370–8. PubMed 22424914 ❐ PainSci Bibliography 54315 ❐

    The fear of pain was assessed in 126 brave volunteers with a questionnaire before — yikes — “inducing muscle injury to the shoulder.” (Don’t worry, nothing too awful for the subjects: they just did a workout with a lot of eccentric contraction that made them super sore.) The results were not what the researchers expected. This study is interesting because it found evidence that fear of pain before injury can predict recovery time. In other words: how well you respond to injury and recover is affected enough by fear that it can actually be predicted by measuring fear beforehand. That’s profound!

  13. Pyne DB. Exercise-induced muscle damage and inflammation: a review. Aust J Sci Med Sport. 1994 Sep-Dec;26(3-4):49–58. PubMed 8665277 ❐
  14. Pollak KA, Swenson JD, Vanhaitsma TA, et al. Exogenously applied muscle metabolites synergistically evoke sensations of muscle fatigue and pain in human subjects. Exp Physiol. 2014 Feb;99(2):368–80. PubMed 24142455 ❐ PainSci Bibliography 53975 ❐ Surprisingly, this fairly unsurprising result is brand new information: “the first demonstration in humans that metabolites normally produced by exercise act in combination to activate sensory neurons that signal sensations of fatigue and muscle pain.” more below about lactic acid myths.
  15. The key indicator molecule is creatine phosphokinase (CPK, which is not myoglobin but a molecule that increases in concentration along with myoglobin). Rhabdo is “official” when kidney damage starts around 20,000 U/I of CPK. Myoglobin itself is not toxic, and can circulate more or less harmlessly through your blood. It doesn’t become a problem until it dissolves in acidic urine in the kidneys, because one of its molecular parts poisons the kidneys on its way through. It’s the kidney damage that particularly makes rhabdo a medical emergency.
  16. Lai MY, Yang SP, Chao Y, Lee PC, Lee SD. Fever with acute renal failure due to body massage-induced rhabdomyolysis. Journal of Nephrology, Dialysis and Transplantation. 2006 Jan;21(1):233–4. PubMed 16204282 ❐ PainSci Bibliography 54301 ❐

    Interesting, short, and readable story of an elderly man who collapsed after an unusually strong massage.

    This is one of three case studies of massage-induced rhabdo in my bibliography: see also Chen and Tanriover.

  17. Knochel 1990, op. cit.
  18. As opposed to, say, doing it because you’re a peasant farmer and you’re really screwed if you don’t get the harvest in.
  19. Olerud JE, Homer LD, Carroll HW. Incidence of acute exertional rhabdomyolysis. Serum myoglobin and enzyme levels as indicators of muscle injury. Arch Intern Med. 1976 Jun;136(6):692–7. PubMed 1275626 ❐ PainSci Bibliography 54278 ❐
  20. Degrees matter. Ice and steam are both made of the same stuff, but they have fundamentally different properties. Mild rhabdo might be too different from acute rhabdo for the label to be meaningful.
  21. 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. PubMed 1499133 ❐

    From the abstract: “The myofibrillar and cytoskeletal alterations observed in delayed onset muscle soreness (DOMS) caused by eccentric exercise are generally considered to represent damage. By contrast our recent immunohistochemical studies suggested that the alterations reflect myofibrillar remodeling (Yu and Thornell 2002; Yu et al. 2003).” In other words, these researchers found evidence that what previously looked like microtearing of muscle tissue is actually probably just muscle tissue doing microscopic renovations — an adaptive process, not a repair process, and probably not painful in and of itself.

  22. Malm C, Sjodin TL, Sjoberg B, et al. Leukocytes, cytokines, growth factors and hormones in human skeletal muscle and blood after uphill or downhill running. J Physiol. 2004 May 1:983–1000. PubMed 14766942 ❐

    From the abstract: “Eccentric physical exercise (downhill running) did not result in skeletal muscle inflammation 48 h post exercise, despite DOMS and increased CK.” Inflammation is the hallmark of tissue damage, so this evidence tends to suggest that muscles are not damaged by hard, unfamiliar exercise.

  23. Roman W, Pinheiro H, Pimentel MR, et al. Muscle repair after physiological damage relies on nuclear migration for cellular reconstruction. Science. 2021 10;374(6565):355–359. PubMed 34648328 ❐ PainSci Bibliography 52199 ❐
  24. Ibid. More from the abstract: “It is suggested that exercise can induce DOMS by activating inflammatory factors present in the epimysium before exercise. Repeated physical training may alter the content of inflammatory factors in the epimysium and thus reduce DOMS.” The italics are mine. Inflammatory “factors” refer to molecules that mediate inflammatory processes, and note that these are not “metabolites” (products of metabolism). Activating them does not necessarily mean that an inflammatory process occurs, just that they may be implicated in DOMS pain. These researchers believe that DOMS may be related to molecules that are present before exercise, not after — or, more likely, to a combination of molecules present before and after — which suggests that “metabolic stress” is almost certainly much more complex than simply finding the molecule, or even the set of molecules, that cause pain after hard exercise. It’s much more likely to be dependent on several variables over time, which means that we’ll need pictures of muscle chemistry, and not just metabolites, before and during exercise and throughout the onset and resolution of DOMS, before we’ll get a clear idea about what might constitute “metabolic stress.”
  25. See also the discussion of metabolic complexity in Why Drink Water After Massage?
  26. Close GL, Ashton T, Cable T, et al. Eccentric exercise, isokinetic muscle torque and delayed onset muscle soreness: the role of reactive oxygen species. Eur J Appl Physiol. 2004 May:615–21. PubMed 1468586 ❐
  27. Ibid.
  28. What we refer to as lactic acid in muscle metabolism is actually lactate, which is not an acid. Lactate production is associated with acidosis, but is not itself an acid. Lactate differs from lactic acid only by an ion, but that missing ion defines an acid, and lactate doesn’t have it, and so it isn’t an acid. Lactic acid is a Brønsted acid, the main type of acid, a molecule that can donate a proton (a hydrogen ion, H+). If you can’t donate a proton, you aren’t an acid. Lactate is not an acid, because it has no H+ to give.
  29. This came up earlier. We know from Pollak et al. that it takes the presence of three metabolites, including lactate, to cause that sensation… and they are not the mechanism of the limits of muscle endurance, but rather a warning sign for the brain that the true limits are approaching. Fascinating. Muscles do get tired, of course, and lactate production is going on when it happens… but lactate is not an acid, and it’s not “the fatigue molecule.”
  30. [Internet]. Kolata G. Lactic Acid Is Not Muscles' Foe, It's Fuel; 2006 May 16 [cited 21 Oct 23]. PainSci Bibliography 54387 ❐
  31. Robergs R. Nothing ‘evil' and no ‘conundrum' about muscle lactate production. Experimental Physiology. 2012 Oct 1, 2011;(96):1097–1098. PainSci Bibliography 54384 ❐
  32. Hutchinson A. Endure: Mind, body, and the curiously elastic limits of human performance. First edition ed. William Morrow; 2018.
  33. Robergs RA, Ghiasvand F, Parker D. Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol. 2004 Sep;287(3):R502–16. PubMed 15308499 ❐

    “Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production.”

  34. There were vigorous rebuttals and rebuttals to the rebuttals, and a rather technical debate continues to this day: Robergs published again just a few months ago. Robergs’ position might be largely unopposed, or the reverse — I have no way of knowing. All I can do is report the debate! However, even if Robergs is wrong about this point down here in the biochemical weeds, it doesn’t really impact the broader point.

  35. See Gina Kolata’s clear overview in the New York Times, or a concise professional summary by Robergs in Experimental Physiology. For a deeper and geekier, but excellent read, see Dr. Goodwin’s entertaining rant about the prevalence of the lactate myth in the 2012 summer Olympics coverage. Alex Hutchinson’s book, Endure, delivers a lot of great detail about the history of lactic acid and lactate research, and then a bit more on our modern understanding — putting it all in a much broader context, too, which is fascinating.
  36. Semark A, Noakes TD, Gibson SCA, Lambert MI. The effect of a prophylactic dose of flurbiprofen on muscle soreness and sprinting performance in trained subjects. J Sports Sci. 1999 Mar;17(3):197–203. PubMed 10362386 ❐

    Experimenters tortured sprinters’ muscles with a savage workout, and the painful results were identical with or without an anti-inflammatory medication. “In conclusion,” they wrote, “the aetiology of the DOMS induced in the trained subjects in this study seems to be independent of inflammatory processes … .”

  37. Mizumura K, Taguchi T. Delayed onset muscle soreness: Involvement of neurotrophic factors. J Physiol Sci. 2016 Jan;66(1):43–52. PubMed 26467448 ❐ “ … we have observed mechanical hyperalgesia in rats 1-3 days after lengthening [eccentric] contraction without any apparent microscopic damage of the muscle or signs of inflammation.”
  38. Deyhle MR, Gier AM, Evans KC, et al. Skeletal Muscle Inflammation Following Repeated Bouts of Lengthening Contractions in Humans. Front Physiol. 2015;6:424. PubMed 26793125 ❐ PainSci Bibliography 54082 ❐ If DOMS is caused by inflammation, then there must be less inflammation after repeated workouts than initial workouts (repeated bout effect). These researchers tried to confirm that reduction, and found (“overwhelmingly”) the opposite. There’s no less or even more inflammation after subsequent workouts. Therefore, exercise soreness is probably not caused by inflammation, but by something else that inflammation actually prevents. •mind blown• Here’s a jargon-free version of the authors’ explanation of what might be going on:
    Overwhelmingly, our data undermines the idea of a muted inflammatory response after a second bout of exercise. On the contrary, the data suggest an neutral or increased inflammatory response! … We saw that inflammatory indicators only increased after a second workout. This suggests that the initial workout may have sensitized the muscle toward a stronger, longer inflammatory response after the second workout. In other words, the muscle seems to “remember” the stress of the first workout, and responds with a stronger recruitment of immune cells when the stress is repeated — much like the way our immune system responds to an invader by preparing for an even stronger response the next time. Furthermore, muscle soreness goes down when the inflammation goes up, indicating that’s unlikely the soreness is caused by inflammation.
  39. Ayles S, Graven-Nielsen T, Gibson W. Vibration-induced afferent activity augments delayed onset muscle allodynia. J Pain. 2011 Aug;12(8):884–91. PubMed 21665552 ❐

    For this study, young men exercised one leg hard enough to make it good and sore. Pressure pain thresholds and sensitivities were measured a day later in the sore muscles, but also in other muscles that send their sensory information to the same part of the spinal cord — that’s unexercised and non-sore muscles on the sore side, that just happen to be connected to the same area of the spinal cord.

    Not surprisingly, pain thresholds were lower in the sore, exercised muscles. But — and this is cool — vibrating the sore muscles caused soreness in other muscles that should not have been sore! So soreness effectively “spread” to other muscle groups, via the central nervous system. This raises interesting questions about how people with brain-regulated pain dysfunction might react to exercise soreness: could the pain spread to unaffected areas by the same mechanism? It seems likely.

  40. Halperin I, Chapman DW, Behm DG. Non-local muscle fatigue: effects and possible mechanisms. Eur J Appl Physiol. 2015 Oct;115(10):2031–48. PubMed 26330274 ❐ Wear out your glutes or pecs … feel it in your cloits n dloits? Some experiments have been able to demonstrate this weirdness, others have not, and so it’s ontologically ambiguous (see Behm). If it exists, it seems to involve multiple pathways: “neurological, biochemical, biomechanical, and psychological.”
  41. Behm DG, Alizadeh S, Hadjizedah Anvar S, et al. Non-local Muscle Fatigue Effects on Muscle Strength, Power, and Endurance in Healthy Individuals: A Systematic Review with Meta-analysis. Sports Med. 2021 09;51(9):1893–1907. PubMed 33818751 ❐

    This paper presents some compelling evidence of absence: “Overall, the findings do not support the existence of a general non-local muscle fatigue effect.”

    The authors do make a concession, though: a non-local fatigue effect might crop up specifically when measuring endurance. If so, that certainly counts as one kind of non-local muscle fatigue. So it’s fair to say that the question remains open, even if NLFM isn’t quite the “known unknown” that I used to think it was.

  42. Murase S, Terazawa E, Queme F, et al. Bradykinin and nerve growth factor play pivotal roles in muscular mechanical hyperalgesia after exercise (delayed-onset muscle soreness). J Neurosci. 2010 Mar;30(10):3752–61. PubMed 20220009 ❐
  43. Urai H, Murase S, Mizumura K. Decreased nerve growth factor upregulation is a mechanism for reduced mechanical hyperalgesia after the second bout of exercise in rats. Scand J Med Sci Sports. 2013 Mar;23(2):e96–101. PubMed 23134144 ❐
  44. Murase S, Terazawa E, Hirate K, et al. Upregulated glial cell line-derived neurotrophic factor through cyclooxygenase-2 activation in the muscle is required for mechanical hyperalgesia after exercise in rats. J Physiol. 2013 Jun;591(12):3035–48. PubMed 23587883 ❐ PainSci Bibliography 52961 ❐
  45. Mizumura K, Taguchi T. Delayed onset muscle soreness: Involvement of neurotrophic factors. J Physiol Sci. 2016 Jan;66(1):43–52. PubMed 26467448 ❐


    Delayed-onset muscle soreness (DOMS) is quite a common consequence of unaccustomed strenuous exercise, especially exercise containing eccentric contraction (lengthening contraction, LC). Its typical sign is mechanical hyperalgesia (tenderness and movement related pain). Its cause has been commonly believed to be micro-damage of the muscle and subsequent inflammation. Here we present a brief historical overview of the damage-inflammation theory followed by a discussion of our new findings. Different from previous observations, we have observed mechanical hyperalgesia in rats 1-3 days after LC without any apparent microscopic damage of the muscle or signs of inflammation. With our model we have found that two pathways are involved in inducing mechanical hyperalgesia after LC: activation of the B2 bradykinin receptor-nerve growth factor (NGF) pathway and activation of the COX-2-glial cell line-derived neurotrophic factor (GDNF) pathway. These neurotrophic factors were produced by muscle fibers and/or satellite cells. This means that muscle fiber damage is not essential, although it is sufficient, for induction of DOMS, instead, NGF and GDNF produced by muscle fibers/satellite cells play crucial roles in DOMS.

  46. The infamous “PACE” trial was a big British study that concluded that graded exercise therapy was helpful for ME/CFS. But the PACE trial was tainted by scandal, and harshly criticized as “uninterpretable” at best. There are good reasons to believe that PACE got it disastrously wrong, and exercise actually hurts ME patients. See Shepherd, Rehmeyer, Tuller, Coyne.
  47. Lyon P, Cohen M, Quintner J. An evolutionary stress-response hypothesis for chronic widespread pain (fibromyalgia syndrome). Pain Med. 2011 Aug;12(8):1167–78. PubMed 21692974 ❐
  48. It’s pretty silly that this one was tested!
  49. Cheung K, Hume P, Maxwell L. Delayed onset muscle soreness: treatment strategies and performance factors. Sports Med. 2003;33(2):145–64. PubMed 12617692 ❐
  50. Torres R, Ribeiro F, Alberto Duarte J, Cabri JMH. Evidence of the physiotherapeutic interventions used currently after exercise-induced muscle damage: systematic review and meta-analysis. Phys Ther Sport. 2012 May;13(2):101–14. PubMed 22498151 ❐
  51. Hasson S, Mundorf R, Barnes W, Williams J, Fujii M. Effect of pulsed ultrasound versus placebo on muscle soreness perception and muscular performance. Scand J Rehabil Med. 1990;22(4):199–205. PubMed 2263920 ❐
  52. Brock TS, Clasey JL, Gater DR, Yates JW. Effects of deep heat as a preventative mechanism on delayed onset muscle soreness. J Strength Cond Res. 2004 Feb;18(1):155–61. PubMed 14971967 ❐

    From the abstract: “Increased muscle temperature [by ultrasound] failed to provide significant prophylactic effects on the symptoms of DOMS.”

  53. Rodenburg JB, et al. Warm-up, stretching and massage diminish harmful effects of eccentric exercise. International Journal of Sports Medicine. 1994;15:414–419. PubMed 8002121 ❐

    Although the title sounds positive about massage, the article is actually much less optimistic: results were equivocal, showing that the treatment regimen had some benefits, but was conspicuously ineffective when it came to, for instance, reducing pain. “DOMS on pressure ... did not differ between the groups.” Although it’s nice to see that this combination of therapies probably had some beneficial effect, it’s hardly persuasive if they didn’t reduce the pain of DOMS. I think it’s reasonably safe to assume that none of them alone are definitely effective.

  54. Ibid. Exercise or “working it out” as a method of reducing DOMS was also studied in the previously cited paper. The method was “upper body ergometry,” which basically uses a machine to exercise the upper body. It had no effect on DOMS.
  55. Amino acids are the molecular components of protein, and there is a vast industry selling amino acids as supplements, primarily to bodybuilders. Lots of athletes take them — but lots of athletes wear scammy Power Balance bracelets, too, and that’s blatant nonsense. There are way too many claims about the benefits of eating extra proteins to unpack here. For more detailed analysis, see Vitamins, Minerals & Supplements for Pain & Healing.

    Some amino acids are believed to have a greater role in supporting muscle recovery, and that which promotes recovery might also attenuate DOMS, which is not a safe assumption, but it is a reasonable hypothesis. Unfortunately, there’s only a little basic science suggesting the possibility that they work in this way, almost no relevant clinical studies, just a couple pathetically small positive ones that I don’t trust without replication (see Tajari 2010 and Legault 2015). From a scientific perspective (and I’m not sure what other perspective would be useful here), there’s just not much to go on here: supplementing amino acids for this purpose is still based on an educated guess.

  56. Branched-chain amino acids (BCAAs, or just “protein supplements”) are three of the six essential amino acids in human physiology, and they are widely believed to be more important to recovery than the others for more or less the same reasons: that is, they are allegedly better at promoting protein synthesis, and therefore may help muscle growth/repair after exercise, and that in turn might — in theory — also reduce DOMS.

    For several years there was a lot of excitement (and protein supplement sales) on the strength of promising preliminary evidence about BCAAs… which then failed to be replicated. Recent trials and reviews of this topic are mostly negative (see Pasiakos 2014, VanDusseldorp 2018, Estoche 2019). Fedewa 2019 is the only recent review to claim victory: “A large decrease in DOMS occurs following BCAA supplementation after exercise compared to a placebo supplement.” There’s always the possibility that certain people, with just-so biology, are benefitting way more than others. But clearly its benefit for the average human is not robust enough to be easily confirmed.

  57. Lund H, et al. The effect of passive stretching on delayed onset muscle soreness, and other detrimental effects following eccentric exercise. Scand J Med Sci Sports. 1998 Aug;8(4):216–21. PubMed 9764443 ❐

    From the abstract: “There was no difference in the reported variables between experiments one and two. It is concluded that passive stretching did not have any significant influence on increased plasma-CK, muscle pain, muscle strength and the PCr/P(i) ratio, indicating that passive stretching after eccentric exercise cannot prevent secondary pathological alterations.”

  58. Herbert RD, de Noronha M, Kamper SJ. Stretching to prevent or reduce muscle soreness after exercise. Cochrane Database Syst Rev. 2011;(7):CD004577. PubMed 21735398 ❐

    Does stretching help either before or after exercise to reduce soreness? Nope. This large review of eleven small scientific studies, and one huge one, wrapped up with a clear thumbs down:

    The evidence from randomised studies suggests that muscle stretching, whether conducted before, after, or before and after exercise, does not produce clinically important reductions in delayed-onset muscle soreness in healthy adults.

    The evidence was “low to moderate,” with “moderate to high” risk of bias, which means most of the researchers were probably hoping to find that stretching does help DOMS … but even with that likely bias, they still didn’t find what they were looking for.

    The big study was technically positive, finding an average drop in soreness of four points on a 100-point scale, which is basically meaningless. The variation between the results for individuals is undoubtedly greater than that.

  59. Howatson G, Van Someren KA. Ice massage. Effects on exercise-induced muscle damage. J Sports Med Phys Fitness. 2003 Dec;43(4):500–5. PubMed 14767412 ❐

    A small study showing no effect of ice massage on muscle soreness after exercise. The massage was not very “massage-y,” but non-ice massage for DOMS is also somewhat tainted by this evidence.

  60. Torres again: “inconclusive evidence to support the use of cryotherapy,” based on a review of 10 studies.
  61. Yamane M, Teruya H, Nakano M, et al. Post-exercise leg and forearm flexor muscle cooling in humans attenuates endurance and resistance training effects on muscle performance and on circulatory adaptation. Eur J Appl Physiol. 2006 Mar;96(5):572–80. PubMed 16372177 ❐

    It’s only one study, but … yikes! This fascinating experiment done by Japanese researchers showed that regular icing for a few weeks after workouts resulted in a significant reduction in training effects: ice users didn’t get as strong. This implies that icing may interfere with normal post-exercise muscle physiology and prevent the process of muscles adapting to stress. This finding is reinforced by Tseng et al.

  62. Tseng CY, Lee JP, Tsai YS, et al. Topical cooling (icing) delays recovery from eccentric exercise-induced muscle damage. J Strength Cond Res. 2013 May;27(5):1354–61. PubMed 22820210 ❐

    Bad icing news: a small study of icing for severe muscle soreness with “unexpected” results, according to the researchers. It seemed to do more harm than good. The icing victims had higher blood levels of molecules associated with muscle injury, and they felt more fatigued. Icing had no effect on recovery of strength, or any biochemical sign of inflammation. A small study, to be sure, but how good can icing be if it can generate this kind of data?

  63. Denegar RC, Huff BC. High and low frequency TENS in the treatment of induced musculoskeletal pain: a comparison study. Athletic Training. 1988;23:235–7. PubMed 10957699 ❐
  64. Weber MD, Serevedio FJ, Woodall WR. The Effects of Three Modalities on Delayed Onset Muscle Soreness. Journal of Orthopaedic & Sports Physical Therapy. 1994;20(5):236–42. PubMed 9512831 ❐

    Forty women were subjected to intense training of the biceps and brachilias muscles, until they were sore, and then treated with one of four treatments for DOMS: massage, TENS (electrical stimulation), and ergometry (basically light exercise, to stimulate metabolic activity), and rest. Treatments were given immediately after and then 24 and 48 hours after. There was no difference in the results for any of the women.

  65. Adding Epsom salts will not make that hot tub any more effective for your muscle fever. I cover this topic separately, and in great detail, in another article, all about Epsom salts. In a nutshell, using Epsom salts is just a bit of implausible folk medicine — a claim that dissolves into nothing when scrutinized. (If that gets your hackles up, please do jump over to the big salt article for all the details before sending me cranky email.)
  66. There’s no direct evidence about this, but there is some suggestive indirect evidence: in 2011, Schwellnus et al. showed clearly that there’s no strong link between hydration and cramping — the death of (yet another) myth about water. They found that dehydrated triathletes were no more likely to suffer cramps than their soggier comrades. Now obviously cramps are not DOMS, and it is possible that dehydration increases the risk of one but not the other … but I doubt it, and will err in that direction until the evidence leads me somewhere else.

    A common rationale for trying to wash your DOMS away with hydration is not that whatever prevents cramps must also prevent soreness, but rather the biologically illiterate notion of “rinsing” metabolic wastes from your system — which doesn’t make any more sense here than it does in other contexts. See Why Drink Water After Massage?.

  67. Connolly DAJ, McHugh MP, Padilla-Zakour OI, Carlson L, Sayers SP. Efficacy of a tart cherry juice blend in preventing the symptoms of muscle damage. Br J Sports Med. 2006 Aug;40(8):679–83; discussion 683. PubMed 16790484 ❐ PainSci Bibliography 53887 ❐ Click through to the bibliography for more detail, but the upshot is that black cherry juice only had an effect on the recovery of strength, not pain or range of motion. Whoop-de-do.
  68. Beliard S, Chauveau M, Moscatiello T, et al. Compression garments and exercise: no influence of pressure applied. J Sports Sci Med. 2015 Mar;14(1):75–83. PubMed 25729293 ❐ PainSci Bibliography 54151 ❐

    Maybe if I squeeeeeze my limbs, that’ll help? Improve athletic performance, ease soreness after exercise, reduce the risk of injury? Science says: “There are conflicting results regarding the effects of wearing compression garments during exercise.” There’s a few studies with slightly encouraging results — of course, there always are — but nothing remotely exciting: a classic example of being damned with faint praise. Results this tepid can be safely regarded as effectively negative.

  69. Connolly DA, Sayers SP, McHugh MP. Treatment and prevention of delayed onset muscle soreness. J Strength Cond Res. 2003 Feb;17(1):197–208. PubMed 12580677 ❐

    This is a review. From the abstract: “To date, a sound and consistent treatment for DOMS has not been established. Although multiple practices exist for the treatment of DOMS, few have scientific support. The reader will note that selected treatments such as anti-inflammatory drugs and antioxidants appear to have a potential in the treatment of DOMS. Other conventional approaches, such as massage, ultrasound, and stretching appear less promising.”

  70. Hasson SM, Daniels JC, Divine JG. Effect of iboprufen use on muscle soreness, damage and performance: a preliminary investigation. Med Sci Sports Exerc. 1993;1:9–17. PubMed 8423760 ❐

    An old and small but well-designed test of ibuprofen for muscle soreness, showing a modest but definite benefit for pain, but probably not function. In other words, ibuprofen reduced the soreness only, but had no significant effect on other outcomes, like muscle function and inflammatory markers.

  71. Tokmakidis SP, Kokkinidis EA, Smilios I, Douda H. The effects of ibuprofen on delayed muscle soreness and muscular performance after eccentric exercise. J Strength Cond Res. 2003 Feb;17(1):53–9. PubMed 12580656 ❐

    Another very small test of ibuprofen, very similar to Hasson 1993 in design and results: “ibuprofen can decrease muscle soreness induced after eccentric exercise but cannot assist in restoring muscle function.”

  72. Hyldahl RD, Keadle J, Rouzier PA, Pearl D, Clarkson PM. Effects of ibuprofen topical gel on muscle soreness. Med Sci Sports Exerc. 2010 Mar;42(3):614–21. PubMed 19952809 ❐
  73. Aidar FJ, Fraga GS, Getirana-Mota M, et al. Effects of Ibuprofen Use on Lymphocyte Count and Oxidative Stress in Elite Paralympic Powerlifting. Biology (Basel). 2021 Sep;10(10). PubMed 34681085 ❐ PainSci Bibliography 51979 ❐

    Ten national-level paralympic powerlifting athletes were assessed for post-training fatigue and oxidative stress with ibuprofen versus a placebo. (“Oxidative stress” is a general biological signature of a body under strain, measurable after bouts of intense exercise.) There were no differences in oxidative stress… but, surprisingly, the athletes with ibuprofen in their veins were stronger and had less fatigue.

  74. Nieman DC, Henson DA, Dumke CL, et al. Ibuprofen use, endotoxemia, inflammation, and plasma cytokines during ultramarathon competition. Brain Behav Immun. 2006 Nov;20(6):578–84. PubMed 16554145 ❐
  75. Pacific Standard [Internet]. Aschwanden C. Convincing the Public to Accept New Medical Guidelines: When it comes to new treatment guidelines for breast cancer, back pain and other maladies, it’s the narrative presentation that matters; 2010 Apr 20 [cited 19 Jan 10]. PainSci Bibliography 55203 ❐

    An excellent article about how hard it is to get people to accept new evidence. In particular (and most relevant to, Aschwanden makes an example of research showing that ibuprofen does not prevent athletes from getting sore muscles (see Nieman 2006). She also uses back pain as an example, focusing the disconnect between guidelines and practice, especially when it comes to imaging.

  76. Morelli KM, Brown LB, Warren GL. Effect of NSAIDs on Recovery From Acute Skeletal Muscle Injury: A Systematic Review and Meta-analysis. Am J Sports Med. 2017 Mar:363546517697957. PubMed 28355084 ❐
  77. Confusingly, “active recovery” also refers to lighter exercise between bursts of really intense exertion (high-intensity interval exercise). Although not settled science, the evidence on that may lean towards passive recovery (see Perrier-Melo et al.) — just catch your breath, that’s it.
  78. The stress of excessive loading could conceivably be a trigger for more generalized illness. The idea here is that it could disrupt homeostasis for months or even years, which is one way to explain how illnesses like fibromyalgia and ME/CFS work. It’s unlikely this would happen in someone who wasn’t otherwise teetering on the brink of that particular disaster… but for those people, significant over-exertion in pursuit of fitness might be a particular danger.
  79. Soligard T, Schwellnus M, Alonso JM, et al. How much is too much? (Part 1) International Olympic Committee consensus statement on load in sport and risk of injury. Br J Sports Med. 2016 Sep;50(17):1030–41. PubMed 27535989 ❐

    This is a detailed review paper about the risks of athletic training and competition intensity (load). The bottom line is that there’s not enough research to know “how much is too much” even on average, let alone for specific athletes. And this is for the much measurable and higher stakes risks of frank injury — not simply the risk of “soreness” and suboptimal training pace! Click through to the paper for more detail on what we do know — a few general principles, e.g. “loading spikes are definitely risky.”

  80. Querido SM, Radaelli R, Brito J, Vaz JR, Freitas SR. Analysis of Recovery Methods' Efficacy Applied up to 72 Hours Postmatch in Professional Football: A Systematic Review With Graded Recommendations. Int J Sports Physiol Perform. 2022 Sep;17(9):1326–1342. PubMed 35961644 ❐
  81. What methods? Massage and cold water immersion. Both of these are currently damned with faint praise by a bunch of “promising” trials that mostly aren’t very good quality, and have yet to smacked down by better trials. Ideas can persist in this semi-justified “promising” state practically forever.
  82. Boyle CA, Sayers SP, Jensen BE, Headley SA, Manos TM. The effects of yoga training and a single bout of yoga on delayed onset muscle soreness in the lower extremity. J Strength Cond Res. 2004 Nov;18(4):723–9. PubMed 15574074 ❐
  83. Nijs J, Kosek E, Van Oosterwijck J, Meeus M. Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise? Pain Physician. 2012 Jul;15(3 Suppl):ES205–13. PubMed 22786458 ❐

    Exercise is great medicine for many chronic pain conditions, but there is an important “but”: it’s unclear if it’s a Band-Aid or if it actually “has positive effects on the processes involved in chronic pain (e.g. central pain modulation).” This narrative review concludes that it’s complicated and it depends, and some patients definitely have a “dysfunctional response” to exercise, and thus “exercise therapy should be individually tailored with emphasis on prevention of symptom flares.”

  84. [Internet]. Rehmeyer J, Tuller D. Getting It Wrong on Chronic Fatigue Syndrome; 2021 November 18 [cited 23 Aug 30]. PainSci Bibliography 52219 ❐

    The huge but notoriously flawed PACE trial seemed to support the idea that chronic fatigue syndrome patients are just de-conditioned and therefore need to suck it up and exercise, slowly building themselves back up again. This was evidence-based medicine at its very worst: one low quality but influential study drowning out both contradictory evidence and patient voices. It has become the most extreme example of telling sick people that their illness is “all in your head.” Julie Rehmeyer and David Tuller’s NYT piece is the canonical summary of the whole debacle.

  85. Viitasalo JT, Niemela K, Kaappola R, et al. Warm underwater water-jet massage improves recovery from intense physical exercise. Eur J Appl Physiol Occup Physiol. 1995;71(5):431–8. PubMed 8565975 ❐
  86. Mayer JM, Mooney V, Matheson LN, et al. Continuous low-level heat wrap therapy for the prevention and early phase treatment of delayed-onset muscle soreness of the low back: a randomized controlled trial. Arch Phys Med Rehabil. 2006 Oct;87(10):1310–7. PubMed 17023239 ❐
  87. Tsuchiya Y, Yanagimoto K, Nakazato K, Hayamizu K, Ochi E. Eicosapentaenoic and docosahexaenoic acids-rich fish oil supplementation attenuates strength loss and limited joint range of motion after eccentric contractions: a randomized, double-blind, placebo-controlled, parallel-group trial. Eur J Appl Physiol. 2016 Jun;116(6):1179–88. PubMed 27085996 ❐ A small 2016 test of the effect of eight weeks of fish oil supplementation on recovery from weight lifting in 24 men. The researchers measured outcomes in many ways. Although they observed some benefits, the results were modest, and only for range of motion and strength, not for pain (or several other measures, such as various blood test results). There were an assortment of isolated minor wins for fish oil — e.g. less pain on day 3 after the exercise — but that’s to be expected in any set of data (especially when it comes from a group of subjects this small).
  88. Nicol LM, Rowlands DS, Fazakerly R, Kellett J. Curcumin supplementation likely attenuates delayed onset muscle soreness (DOMS). Eur J Appl Physiol. 2015 Mar. PubMed 25795285 ❐
  89. For instance, a 2012 review by Torres et al., which looked at the results of nine studies of massage, concluded that it is “ slightly effective” but “its mean effect was too small to be of clinical relevance.”
  90. Tiidus PM. Manual massage and recovery of muscle function following exercise: a literature review. J Orthop Sports Phys Ther. 1997 Feb;25(2):107–12. PubMed 9007768 ❐


    There is currently little scientific evidence that manual massage has any significant impact on the short- or long-term recovery of muscle function following exercise or on the physiological factors associated with the recovery process. In addition, delayed onset muscle soreness may not be affected by massage. Light exercise of the affected muscles is probably more effective than massage in improving muscle blood flow (thereby possibly enhancing healing) and temporarily reducing delayed onset muscle soreness. This paper reviews current scientific evidence on the use of manual massage to affect: 1) muscle damage caused by eccentric muscle action; 2) retention and recovery of muscle strength and performance following "eccentric-mechanical" muscle damage; 3) reduction of delayed onset muscle soreness following "eccentric-mechanical" muscle damage; and 4) recovery of muscle strength and performance following anaerobic exercise. Because manual massage does not appear to have a demonstrated effect on the above, its use in athletic settings for these purposes should be questioned.

  91. Cambron JA, Dexheimer J, Coe P, Swenson R. Side-effects of massage therapy: a cross-sectional study of 100 clients. J Altern Complement Med. 2007 Oct;13(8):793–6. PubMed 17983334 ❐
  92. Researchers would have avoided inflicting painfully strong massage on their subjects, but breathtakingly strong massage is quite common “in the wild.” Other, less specific studies have reported higher rates of complications. Carnes found that 20-40% of all manual therapy treatments — massage, chiropractic, physiotherapy — will cause some kind of unpleasantness: a side effect or “adverse event” in medicalspeak.
  93. Crane JD, Ogborn DI, Cupido C, et al. Massage therapy attenuates inflammatory signaling after exercise-induced muscle damage. Sci Transl Med. 2012 Feb;4(119):119ra13. PubMed 22301554 ❐

    This study is the source of a new massage myth that massage reduces inflammation. Inspired by the doubtful notion that “massage may relieve pain in injured muscle” after intense exercise, researchers looked for changes in the proteins that cells constantly make (“gene expression”). They compared muscle tissue samples with and without massage and concluded that “massage therapy appears to be clinically beneficial by reducing inflammation and promoting mitochondrial biogenesis.” Massaged muscle was found to be producing different amounts of five proteins related to inflammation and promoting the growth of mitochondria (cell power plants). It was an interesting, technically demanding, and worthwhile experiment, and it’s nifty that there was any difference in gene expression in massaged muscle.

    Unfortunately, the results of this study were actually negative: the data showed that massage has no significant effect on gene expression in muscle cells. There are several major problems with the study: the sample size was extremely small; the number of changes they found was trivial (and dwarfed by what exercise causes); the size of the differences was barely statistically significant—and short-lived, too; they measured genetic “signals” and not actual results, and guessed about their meaning; and we already know from clinical trials that massage doesn’t work any miracles for soreness after exercise, so what is there for the data to “explain”? Despite all of these problems, the results were spun as an explanation for how massage works in general — in the paper itself, the abstract, the journal’s summary, the press release, and interviews. Consequently, the results have been widely reported and discussed as if it is now a scientific fact that massage actually does reduce pain and promote recovery, and the only question was “how?” It’s a debacle.

    For a much more detailed analysis, see Massage Does Not Reduce Inflammation, or a more technical analysis by Dr. David Gorski at, Does massage therapy decrease inflammation and stimulate mitochondrial growth?

  94. Ernst E. Does post-exercise massage treatment reduce delayed onset muscle soreness? A systematic review. Br J Sports Med. 1998 Sep;32(3):212–4. PubMed 9773168 ❐ PainSci Bibliography 57074 ❐

    From the article: “An effective treatment has been sought for many years … to date, none of these approaches has been fully convincing.”

  95. Just as a side note, Dr. Edzard Ernst has become far more skeptical than he used to be. There’s a strong chance that he wouldn’t be so casually optimistic about massage as a DOMS treatment if he were tackling the subject for the first time today.
  96. Connolly et al. again: “ … anti-inflammatory drugs and antioxidants appear to have a potential in the treatment of DOMS. Other conventional approaches, such as massage, ultrasound, and stretching appear less promising.”
  97. Best TM, Hunter R, Wilcox A, Haq F. Effectiveness of sports massage for recovery of skeletal muscle from strenuous exercise. Clin J Sport Med. 2008 Sep;18(5):446–60. PubMed 18806553 ❐
  98. Zainuddin Z, Newton M, Sacco P, Nosaka K. Effects of massage on delayed-onset muscle soreness, swelling, and recovery of muscle function. J Athl Train. 2005 Jul;40(3):174–80. PubMed 16284637 ❐

    This is a good representative example of research about massage for DOMS, and notable for how underwhelming it is. After acknowledging that “the findings about the effects of massage on DOMS and muscle function are inconclusive or contradictory in nature,” these researchers muddied the waters still more with their own inconclusive experiment. In an extremely small study comparing 10 massaged arms to their unmassaged twins, “Massage was effective in alleviating DOMS by approximately 30% and reducing swelling, but it had no effects on muscle function.” Those results sound encouraging, and they are to some degree, but there are major caveats. They are barely statistically significant, and one key measure of pain was not: in other words, the results could have been a coincidence. Also, the effect size — a 30% reduction in pain — is just not that great, but especially if it’s temporary … and the researchers don’t say how long it lasted (and yet they did provide graphs of how all their other measurements changed over time). Cynically I wonder if it means that the pain-killing effect was quite brief: wouldn’t it have been a nice thing to report if it had been lasting? It’s an odd omission. Finally, the failure to have any effect on muscle strength is consistent with all other studies of massage for DOMS, and it means that massage is only relieving a little pain at best — not actually “fixing” or promoting recovery.

    Bear in mind that this weak evidence is one of the stronger examples of a “positive” study of massage for DOMS. This is roughly as good as it gets.

  99. Dupuy O, Douzi W, Theurot D, Bosquet L, Dugué B. An Evidence-Based Approach for Choosing Post-exercise Recovery Techniques to Reduce Markers of Muscle Damage, Soreness, Fatigue, and Inflammation: A Systematic Review With Meta-Analysis. Front Physiol. 2018;9:403. PubMed 29755363 ❐ PainSci Bibliography 53216 ❐
  100. Confirmation bias is better known as “selective perception” and “selective memory,” but it goes deeper than that: many devious and largely unconscious mental tactics and thinking glitches that lead people to confirm their beliefs and pet theories. We not only tend to ignore, deny and overlook anything that contradicts our point of view, but we also invariably notice, inflate and or even fabricate anything that supports it. Confirmation bias is why amateurs and experts alike are prone to significant thinking errors. Everyone has confirmation bias: it’s just how minds (don’t) work! See Confirmation Bias: Confirmation bias is the human habit of twisting our perceptions and thoughts to confirm what we want to believe.
  101. Ioannidis JPA. The Mass Production of Redundant, Misleading, and Conflicted Systematic Reviews and Meta-analyses. Milbank Q. 2016 09;94(3):485–514. PubMed 27620683 ❐ PainSci Bibliography 53217 ❐
  102. Guo J, Li L, Gong Y, et al. Massage Alleviates Delayed Onset Muscle Soreness after Strenuous Exercise: A Systematic Review and Meta-Analysis. Front Physiol. 2017;8:747. PubMed 29021762 ❐ PainSci Bibliography 52834 ❐

    This is a flawed meta-analysis with a technically “positive” conclusion that is clearly actually a damned-with-faint-praise result, consistent with the body of evidence on this topic. This analysis of pooled data from a dozen mostly poor quality trials — “garbage in, garbage out” — establishes nothing except that there probably isn’t a strong benefit to detect.

  103. Manson JE, Patsy M B, Rosen CJ, Taylor CL. Vitamin D Deficiency — Is There Really a Pandemic? N Engl J Med. 2016 Nov 10;375(19):1817–1820. PubMed 27959647 ❐


    The claim that large proportions of North American and other populations are deficient in vitamin D is based on misinterpretation and misapplication of the Institute of Medicine reference values for nutrients — misunderstandings that can adversely affect patient care.

  104. Holick MF, Chen TC. Vitamin D deficiency: a worldwide problem with health consequences. Am J Clin Nutr. 2008 Apr;87(4):1080S–6S. PubMed 18400738 ❐ PainSci Bibliography 55028 ❐
  105. Kinser AM, Ramsey MW, O’Bryant HS, et al. Vibration and stretching effects on flexibility and explosive strength in young gymnasts. Med Sci Sports Exerc. 2008 Jan;40(1):133–40. PubMed 18091012 ❐

    Replicates the findings of both Issurin and Sands — “simultaneous vibration and stretching may greatly increase flexibility, while not altering explosive strength.”

  106. Veqar Z, Imtiyaz S. Vibration Therapy in Management of Delayed Onset Muscle Soreness (DOMS). J Clin Diagn Res. 2014 Jun;8(6):LE01–4. PubMed 25121012 ❐ PainSci Bibliography 52478 ❐

    This extremely poorly written review is published in suspected predatory journal and is glaringly simplistic and overconfident about vibration for DOMS, based on “very few researches.” It cannot be trusted at all, and only serves to highlight the poor state of the research.

  107. Broadbent S, Rousseau JJ, Thorp RM, et al. Vibration therapy reduces plasma IL6 and muscle soreness after downhill running. Br J Sports Med. 2010 Apr. PubMed 18812416 ❐

    This is a test of vibration therapy on sore muscles in runners. 29 male creational runners were studied after running a 40-minute downhill run. Half were given “once-daily sessions of vibration-therapy on the upper and lower legs,” and the other received no treatment. Vibrated muscles were less sore and had fewer blood markers associated with soreness Conclusion: “Vibration therapy reduces muscle soreness and IL6. It may stimulate lymphocyte and neutrophil responses and may be a useful modality in treating muscle inflammation.”

  108. Bakhtiary AH, Safavi-Farokhi Z, Aminian-Far A. Influence of vibration on delayed onset of muscle soreness following eccentric exercise. Br J Sports Med. 2007 Mar;41(3):145–8. PubMed 17138635 ❐ PainSci Bibliography 51829 ❐


linking guide

17,000 words

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