Updated: Jan 4
Delayed Onset Muscle Soreness (DOMS) and pain share many characteristics. For one thing, we’ve all experienced it at least once in our lives. They are occasioned slightly differently, however, and maybe that’s the key. We’ve all experienced the feeling of aching legs, which comes on a day or so after squatting for the first time in a while, or the aching forearms after playing your first game of tennis of the summer (of course after the racket has been under the stairs for the previous 8 months). We’ve all also stubbed a toe or sprained an ankle. Most people intrinsically understand the meaning and are happy to ‘ride out the wave’ of DOMS; it is typically subclinical and doesn’t cause too much of a stir (if that is, you experience what we understand as the current phenomenon of DOMS - not something else like muscle damage). This is not so with pain. Through this blog, I want to show you that these phenomena are potentially more similar than you think. There’s a lot we still don’t know about both phenomena, and although there are certainly some important differences, understanding the links may help us develop strategies for both in therapeutic environments.
In people with pain, movement is troublesome and can be avoided or become different - sometimes for many years. These are precisely the kind of breeding grounds for a good case of the old DOMS, and we can be safe to assume that it is - sometimes - an unavoidable consequence of returning to the kinds of movement that people in pain once used to enjoy.
What causes DOMS - it’s complicated, kind of like pain.
What has become very clear over recent years, is that DOMS - like pain - is necessarily explained by multiple different theories, which is indicative of its complex nature. Before proceeding, it is necessary to define a few things. DOMS is not ‘muscle soreness’ - as they differ both in their temporality and aetiology (Ref). DOMS is characterised as resulting from a bout of movement or exercise to which you are unaccustomed, and is theorised to be predominantly the result of eccentric, or muscle lengthening, contractions (Ref, Ref, Ref).
DOMS has historically been proposed to be caused by microtrauma of muscle cells and subsequent inflammation (Ref). We’ve been fairly certain of this for many years, the key to this pandora’s box was all but locked away; until a brave group from Japan started to ask some questions - biomedical model and ‘pain scientists’ sound familiar to anyone? This microtrauma and inflammation may be sufficient but are not essential to create DOMS. Meaning, it’s more complicated than what we originally thought. There can be DOMS without muscle fibre trauma and inflammatory markers are an unreliable soup not related to the amount of exercise performed (Ref, Ref). Add to this that anti-inflammatories rarely work to manage DOMS (Ref). It is likely associated with ‘upregulation’ of neurotropic factors, which reduce the threshold of thin nerve fibres A- delta and C fibres (nociceptors) to mechanical stimuli (Ref). We don’t quite know why this upregulation occurs, and the authors of this scientific work have been wise to not draw too many grand conclusions, but it may be related to adaptation to the next bouts of exercise (Ref). This acute, subclinical muscle soreness could be another wonderful example of the body’s singular focus of adaptation - to get better at this movement the next time you do it. There is data to show that brain regions involved in controlling movement are modulated as a result of DOMS, which can be both protective and adaptive (Ref). The body learns how to do everything better. If this all sounds familiar to elements related to the experience of pain, that’s because it is.
The similarities with pain
Starting with the peripheral events, these are same nociceptors and the same pathways involved with pain (Ref). We have seen striking similarities between the ever evolving tendon pathology models by pioneers in the field and DOMS theories (Ref). There potentially being a role for many mechanisms going on, not just one or two ‘reductionist’ mechanisms. Meaning, things like ‘microtrauma’ and associated inflammation are probably insufficient to explain the entire response (disruption of tendon collagen is probably not going on, whereas in DOMS disruption of muscle fibres may be questionable), and we have a larger role for satellite cells in creating some kind of response, something that isn’t what we would typically call ‘inflammation’ (Ref). Put this together in a rough way and we get, ‘less damage, more adaptation’ - the damn body at it again, adapting to stimuli.
Upstream, we also have the same cortical areas involved in DOMS that are involved in pain (Ref, Ref). The same brain regions and matrices that are involved in controlling and predicting movement are impacted, which would seem to make sense intuitively. So much so, that inducing a state of DOMS has been proposed to safely (and ethically) study pain states more closely (Ref, Ref). What seems to be missing, however, are the brain regions involved in fear and emotion - our lizard brain if you will - that are oh so active in pain states (Ref).
What really isn’t clear, though, are the links (or lack thereof) between the affective and behavioural elements to DOMS and pain. We just don’t know what this relationship might be, or if there is one. Once again, though, we - as humans - can intuitively appreciate that these two phenomena are quite similar to experience and there is some data to show this.
There is some low level evidence that there may be similar fear and disability in experimentally induced DOMS in low back pain (Ref). In this study by Bishop et al (2011), 52 healthy volunteers were put through a trunk flexion and extension protocol and then asked to rate their pain, answer a disability questionnaire and a pain-related fear questionnaire (Ref). The results of this cohort suggest that patients going through a DOMS experience have similar pain, disability and other affective outcomes in comparison to LBP patients (at low levels) (Ref). In other words, they are similar experiences and people tend to behave somewhat the same. The difference, in the words of the authors may be that, “participants are told during the informed consent process to expect the pain that they experience to be of short duration”; no-one gets this assurance when in pain - no matter how much they are reassured it may go away.
So, these two phenomena are more alike than you may originally think at both the peripheral and central level. There also may be some similarities in the affective components - they are similar experiences - but there surely some important differences.
What’s the difference?
The differences between DOMS and pain, are significant, if not obvious. Being a human qualifies me to make the following inferences about what the key differences are, but a warning is included with this - this is not evidence based, simply human based:
DOMS has a defined cause and effect relationship, pain - typically - does not. This is easy to gather for the patient and professional; it makes sense. So much of what makes pain the biggest burden we live with today is that it mostly just doesn’t make sense.
DOMS has a defined end-point, pain does not. Even, as suggested above, the experience is impacted upon by the suggestion that it will have an end-point, we all know that DOMS finishes - it ends.
DOMS isn’t associated with the ‘lizard’ brain regions that typify pain responses (as far we know). There may be less ‘emotional’ overlay, and even if fear levels may be quite similar, the above two points may just negate that (maybe).
DOMS isn’t associated (as far as we know) associated with unhelpful beliefs, as with many pain states. Once again, number 1 and 2 on this list mean that whatever beliefs may be present or underlying probably don’t contribute to the outcome quite as much as they may in pain states.
These are key differences that contribute to the experience of both, and while similar phenomena, make them ultimately world’s apart for the person experiencing them. These are key differences that make our approach to pain all so important.
If DOMS is an experience, which sits on the same spectrum as pain, what if we could use the above differences to explain pain and its role in the body? Can we use even use DOMS to modulate the pain experience?
So, what do we do?
Firstly, and somewhat obviously, we need to know more - about both. But it is a common occurrence that when we have patients in pain, and when trying to get them on the path to recovery, we run the risk of inducing muscle soreness or DOMS. Ben Cormack has written extensively and eloquently about these topics, so I will direct the reader to learn directly from him on this. But there is a fundamental difference between programming exercise for someone in pain compared to someone not in pain; pain is complex and responses are variable. So it becomes hard to know where one phenomenon ends (muscle soreness) and one begins (pain). We would hope that with our knowledge of progressive overload, we would avoid inducing DOMS, but what if we did?
It isn’t new to utilise eccentric training for rehabiliation (Ref). But as with all things, it seems doing just one thing is probably not as good as doing many things - in other words, one kind of muscle contraction is probably not as good as doing many kinds of muscle contraction (Ref, Ref). And so, as DOMS is a response to an unaccustomed bout of exercise or movement, is there scope to use this therapeutically? If we understand some key differences (above), can we ‘set the scene’ for some truly monumental ‘experience tinkering’?
This probably depends, and should be taken on a case by case basis, but if the framing is something that contributes to the experience (I said if) then there is a potential that a bout of DOMS could modulate any other similar experience. There is evidence to show that induced DOMS in an ‘already painful state’ reduces activity in brain regions associated with creating new movement strategies (Ref). This is obviously not what we want to achieve in most people, but this is a small study and authors - like anyone, including me - should be open to questioning. DOMS may not be ideal to induce in painful situations, but it also hasn’t been proven beyond doubt to be harmful either.
I am not advocating for inducing DOMS, I just think we probably don’t need to be as scared of inducing it as some may be. Who knows, a little bit of knowledge about DOMS may not be a bad thing in our patients. So if DOMS does happen to occur, it may be a good chance to educate them on what we know about both experiences.