Practical Science on Movement and Pain
Practical Science on Movement and Pain
Foam rolling is very popular. Athletic trainers use it as a part of the warm-up. Physical therapists use it as part of their treatment strategy, often to improve extensibility of “short” tissues.
There is very limited evidence about what benefit, if any, foam rolling confers. But there are at least a few studies showing that it leads to short term increases in range of motion that are not accompanied by strength loss. (This is interesting because stretching interventions tend to show increased range of motion that are associated with a loss of strength and power.)
The purpose of this article is not to question whether foam rolling is effective for anything. I’m willing to assume that it is effective in some way for some people. It is hard for me to believe that so many intelligent trainers such as Mike Boyle would be singing its praises unless it was good for something. So I’ll give it the benefit of the doubt for purposes of this article.
The question that I want to answer in this post is the following: if foam rolling does work to reduce pain or improve mobility, what is the mechanism? I do not find the common explanations very convincing. But there is one (less commonly heard) explanation which I really like. Here’s my critical analysis of the different theories for why foam rolling works, including my favorite one.
This is one you will hear quite frequently, usually without any specifics as to which “qualities” are at issue. I think some people imagine that foam rolling can somehow smooth out bumps or incongruities in their tissues like a rolling pin over pizza dough. Of course, this explanation is usually intended for lay people and not scientists, so perhaps we can cut some slack about the lack of specifics. Perhaps the qualities to be improved involve the presence of fascial adhesions or trigger points. I’ll address those claims specifically below.
For some reason people just tend to assume that foam rolling works by changing the fascia. I honestly have no idea why. A foam roller puts pressure on all the other tissues in the body, and they all communicate with the CNS, which controls how we move and feel. Isn’t the CNS the most obvious place to look for changes after foam rolling?
No, it always has to be the fascia!
But fascia is tough stuff. Sure it has some interesting adaptive properties, but at the end of the day its purpose is to form a solid structure for the body. Is it really plausible that we can significantly change our structure just by leaning on a foam roller a little bit? We must be made of stronger stuff than that. If fascia started to break down, or elongate, or “melt” every time it felt a little sustained pressure, we would be pretty fragile creatures. Every time we sat on a rock our posterior chain would lengthen. So for me the idea that foam rolling lengthens or melts some important structural stuff in our body does not pass the common sense test.
And, more importantly, the research does not support this idea either. There are a few research studies (here and here) which try to determine the degree of pressure necessary to cause permanent deformation in mature human connective tissue. The upshot is that if you want permanent change, you better be prepared (as Paul Ingraham notes) to “get medieval.” Steam roller maybe, foam roller, no. It’s not going to happen in any of the places where the roller is most commonly applied, which are usually the strongest parts of the body – the ITB band, lumbar fascia, plantar fascia, etc.
Maybe a foam roller can’t lengthen the IT band, which is stronger than steel, but could it break up some little fascial adhesions that prevent sliding between different muscle groups? One of the studies I referenced above show that manual pressure might be enough to deform nasal fascia. Now I don’t see many people foam rolling their nose, but maybe there are tiny little adhesions between large muscles groups that are as weak and deformable as nasal fascia.
Again this seems highly speculative to me. How do we know where these adhesions are, or what angle will help break them? A foam roller is a blunt non specific instrument that delivers force in a diffuse manner into the tissue. Smash! Part of the job of fascia is to diffuse force, so it would be hard to target a specific point here. Also, the angle of pressure is always straight in. The foam roller would have limited ability to provide the kind of precise oblique force that might be able to slide one layer of tissue with respect to the other.
Another problem I have with the idea that foam rolling breaks up fascial adhesions is that the effects are often temporary. People do some foam rolling, they feel better for a while, and then tomorrow or even later that same day, they feel the need to roll the same area again. If the mechanism of effect is breaking fascial adhesions, then why do we need to repeat the process? Did the fascia knit itself back together again? The temporary nature of the results strongly suggests a nervous system mediated mechanism for efficacy, not a structural one.
Many foam rolling proponents explain that proper procedure involves finding a “trigger point” and staying on that point for a while. Is foam rolling a way to treat trigger points?
It should be noted that the term trigger point means different things to different people. For some it just means a sore spot, but for others it refers to a specific pathology. The technical definition involves several elements such as a hyperirritable nodule within a palpably taut band that elicits a twitching response to snapping palpation. Trigger points are thought to be caused by some sort of metabolic crisis in the muscle cells which causes chemical irritation in the local area and for some unknown reason refer pain to other areas when pressed.
Trigger points are controversial to say the least. There is substantial debate as to whether they even exist. Whether they can be reliably identified is another debate. And whether they can be effectively treated is another. There are many recommended treatments – stretching, post-isometric relaxation, sticking needles into them, pressing on them, etc. I definitely don’t have the time or anything approaching the knowledge to address all these debates.
But given all these uncertainties, I’m disinclined to believe that foam rolling works by getting rid of a trigger point. There are just too many unanswered questions here. The experts in trigger point therapy will tell you that not every sore spot is a trigger point, that not all trigger points are clinically relevant, and that their identification and treatment takes practice and expertise. So I don’t think shotgun fascia smashing with a foam roller is a plausible trigger point treatment (assuming they exist and can be treated with pressure.)
I often hear claims that foam rolling works by proprioceptive enhancement – stimulating mechanoreceptors in the muscles and/or fascia, such as golgi tendon organs, or muscle spindle fibers, or ruffinis, or pacinis, or Pacinos or DeNiros. This could have some beneficial effect of encouraging relaxation of muscular or fascial tone, or causing the brain to reorganize its sensory or movement maps in the local area.
I think this is a very plausible explanation and definitely on the right track. But I doubt it is the main mechanism which explains why people like to foam roll. If stimulating these mechanoreceptors explains the claimed benefits of foam rolling, then why wouldn’t you just stretch and move around, and get probably even more stimulation to these organs, but within the context of functional movements? Can the foam roller, which doesn’t really provide that much movement or stretch to the target muscle or fascia, provide more proprioceptive stimulation then functional movements like the squat, lunge or reach? I think not.
Perhaps what foam rolling has to offer over movement is novel proprioceptive stimulation. I think novelty is great and of huge potential benefit. It helps get the brain’s attention, which is what you need to do if you want the brain to change. But here’s something else that you need to do. You need to provide the brain with information that is relevant to something that the brain cares about. The brain cares about how to move your body through functional patterns such as squats, lunges and hip hinges. How is the information derived from foam rolling relevant to these tasks? The brain is not interested in information just because it’s novel. The information must also help it solve movement problems. Why would the nervous system be interested in how it feels to have a lacrosse ball jammed into your butt?
This is my favorite explanation. And this is probably the mechanism with which readers will have the least familiarity. Here’s a description of what it is, how it works, and why I think it’s the major reason for the potential efficacy of foam rolling (and many other forms of manual therapy).
Diffuse noxious inhibitory control (DNIC) is one of several varieties of “descending modulation”, by which the brain adjusts the “volume” on nociception (danger signals which originate in the body). DNIC means that the brain inhibits nociceptive signals from traveling up the spinal cord to the brain.
DNIC is reliably triggered by a sustained nociceptive input, such as immersing your hand in cold water. The inhibition is diffuse – it suppresses nociception not just from the local area, but distant areas as well. In other words, if your leg hurts, and you stick your hand in icewater for a while, the resulting DNIC will cause both the hand and the leg to hurt less. This dynamic of fighting pain in one area by creating it in another likely explains the success of many therapies, and is sometimes called counterirritation. The effect is temporary of course.
How powerful is the effect of DNIC? Very powerful. When a soldier loses a limb in battle, he will often feel no pain so long as the emergency persists, and DNIC is a major reason. David Butler refers to DNIC as the “drug cabinet in the brain.” Here’s a video where he explains this idea in a little more detail, including the fact that some of the drugs in the brain are stronger than morphine.
Pain expert Lorimer Moseley views descending modulation and DNIC as a way for the brain to “second-guess” the periphery about the threat posed by a particular stimulus. For example, if the periphery is communicating information suggesting there is a large amount of mechanical threat in a particular area, the brain, which has access to a wealth of additional information about what is actually going on in the periphery, may decide that the problem is not so serious, and therefore inhibit the transmission of nociceptive signals to the brain.
There is significant research showing that many chronic pain conditions such as fibromyalgia, irritable bowel syndrome, and TMJ are characterized by relative failure of the DNIC mechanism.
The effectiveness of DNIC in suppressing pain is highly dependent on the expectation that the counterirritant will have an analgesic affect. In this interesting study, researchers immersed the hands of participants in cold water, shocked them with an electric blast to the sural nerve, and then measured the level of nociceptive activity in the spine, as well as the self-reported pain level. Importantly, the participants were divided into two groups. The first group, called the “analgesia group”, was told that the cold water immersion would reduce the amount of pain they felt from the shock. The other group, called the “hyperalgesia group” was told the opposite – that the cold water immersion would make the pain in the leg worse.
The analgesia group experienced 77% less pain, and less spinal cord nociceptive activity than the hyperalgesia group, who experienced almost no reductions in pain or spinal cord nociceptive activity. In other words, expectation of relief was a huge factor in determining whether DNIC worked.
Now let’s put this all together. DNIC is a powerful but temporary way to reduce pain in one area by creating pain in another. It depends on a decision by the brain to ignore danger signals from the body. Expectation of benefit from the irritating stimulus plays a strong role.
There are several aspects of foam rolling that are very consistent with the hypothesis that its main benefit is achieved by creating DNIC. Rule number one in foam rolling is to find a sore spot and stay on it for some time. You need to create some pain. Of course, the pain is often a “good pain”, which is exactly the type of feeling that would correlate with the brain’s conclusion that the irritation is somehow beneficial – which is what gets DNIC going.
Foam rolling often creates pain relief, not just in the area of pressure, but in other areas as well. People also tend to feel more freedom of motion, which could easily be explained by suppression of nociceptive activity, which tends to create muscle guarding, stiffness, and compensatory patterns of movement.
Further, the results of foam rolling are often temporary and need to be repeated (and often repeated harder the next time- are people becoming addicted to the drug cabinet in the brain?) This suggests a CNS mediated mechanism.
So here is the story I tell about foam rolling. You put a foam roller into your butt and create some significant nociceptive signalling. The brain receives it and says something like: “OK, the butt is telling me that there is some danger down there right now. But I happen to know that this is a therapeutic situation because my trainer said so. So, let’s send some drugs down the spinal cord to block all this talk about danger. And, we’ll make this feel like a “good” pain, not an injury.” The drugs reduce pain and thereby improve movement temporarily.
Now some people will read this and say “well who cares about how it works, all I care about is that it works.” And in some sense that is fine, but this lack of curiosity ignores the potential improvements one might make to a therapeutic regime by understanding the real mechanism of effect.
If foam rolling really works by nothing other than DNIC, then perhaps it would be easier to get the same effect by just pinching yourself or putting your hand in ice water. Or maybe this would mess with expectations, which we know are important to get the effect.
Here’s another interesting question that arises from the consideration that foam rolling may work purely on the basis of DNIC. If the results are only temporary, can there be any progressive benefit? I think the answer is: it depends. Pain relief and improved movement open a window of opportunity that one might climb through. If you are feeling better only for an hour, this provides enough time to train movements that would not normally be accessible, learn new skills, develop new capacities, and reduce the perceived threat associated with certain movements. This could have permanent benefit. But of course if you just sit on the couch, the benefits would probably be temporary.
Here’s another question I have in regard to foam rolling. If the major reason it works is release of the drug cabinet in the brain, then can one become addicted? I have no real evidence of this, but I swear I’ve seen a disturbing pattern. Someone gets relief from a foam roller, and then graduates to the lacrosse ball, and then to the wooden ball, until they are bruising themselves with steel in an effort to get that fix! Avoiding this type of situation is one reason it’s a good idea to know why something works.
Well there’s a lot more to be said here, but I am out of time, and if you have already read this far you are a champion!
I’m sure some of my readers will point out that I missed one or two great explanations for why foam rolling works. If I did, then please post in the comments and I’ll try to address it in a further post.
One way or the other, let me know what you think in the comments. And pass this around!