Transcription
Welcome to this webinar on better understanding exercise and pain. Thank you to everyone who has chosen to spend a little bit of time with me on this Tuesday night in September. Hopefully, we can learn together and understand a little better the problem of pain and exercise for pain as well, which is pretty interesting stuff. So, we can nerd out together and have a look at some of the things that we know.
Thank you to everyone who has let us know where they are from. Thank you very much; it's great to see people from all over the world. I am going to share my screen. Zoom has changed its layout all around, and I'm a little bit discombobulated.
This is our opening slide: "Exercise and Pain: How Does It Work?" I think that's a really important question. Of course, I can't let you know the exact answer for everybody, but the point of this lecture is to think about some of the potential things and ways that it could help people. Whether that's a causal variable, such as a mediator, or a less causal variable, such as a moderator, or perhaps it's some kind of mechanism that we can potentially think about and discuss a little bit more.
So, let's get into it. I wonder if you can do me a small favor. If you see an interesting slide or something that genuinely interests you within this lecture, please feel free to take a little picture of the slide, tag me in it, and put it in your Instagram story or wherever else. I would be really grateful for your support, which helps me continue to provide a little bit of free education for you. That would be a little job that you can do to make me happy and also eternally grateful. One day, potentially, I can return the favor for you.
Now, a big question: some people might ask, "Ben, who cares? Who gives a...?" That would be an absolutely fair question to ask. For some people, it doesn't matter why something may work; it just matters if it works. So, we could say, "Does exercise work for pain?" Brilliant! That's fine, and we may not want or need to go any deeper or further.
Unfortunately, that's not my type of character. I love to delve deeply into these things because I'd like to improve what I do. At the moment, we know that things we do aren't actually that fantastic for our patients. Sometimes they can have fantastic effects; other times, they have very little effect. In fact, sometimes even treatments make people worse, and that happens a lot more often than we probably like to admit.
But who cares why it works? I believe the more we know why, the more plausible we become. The better we are able to explain things to people, and if we know how these things work, are we therefore better at adapting, adjusting, and making them work better? I think that's really the key. If we understand a little bit more about whether this is related to descending inhibition, the immune system, psychology, biomechanics, or physiology, we can understand what makes it work and hopefully make it work better.
I know everyone on this call today cares deeply about helping people and probably also wants to make these things work a little better. So, we can work a little better by understanding a little better. So, who cares? I care!
There are probably a whole bunch of people that don't care and just think, "Ben, shut up. Don't worry; get on with your job." But I think if we can improve what we do and how we do it, we can do a better job. If I can be part of that, then I'm going to be really happy. So, who cares? Ben cares!
Something that I often say, and some people get their panties in a wad over this, is that exercise for fitness is not the same as exercise for pain. What I mean by that is if we think we're going to the gym to get big, strong, and fit, and the fitter and stronger we get, that's going to have more of an effect on people's painful problems. As someone who is evidence-based, I don't think we have the evidence to say that.
Now, does that mean evidence for fitness is useful for pain? Absolutely not! There are lots of people that benefit from using what we have currently in terms of reps and sets and these types of things. For some people, it works absolutely fantastically; for others, it might not work so fantastically, and they're the people we need to think about.
It's really important to understand that when I say exercise for fitness is not the same as exercise for pain, it doesn't mean exercise for fitness can't help people. It does, but it may not be for many of the reasons we think, such as the classic stretch and strengthen, motor control, or any of these other reasons that the evidence has kind of failed to help us understand.
So, why is that? Why do people not just get fitter, stronger, more mobile, etc., and then simply get out of pain? Well, that's because not everyone is the same. They don't have the same baseline characteristics, biosocial profile, or prognostic factors going on. A prognosis just means the likely cause of a problem, even with treatment. Natural history would be a problem without treatment; prognosis is the problem with treatment.
Some people may have negative prognostic factors, which leads to a poor prognosis. Here's a little model that I use for teaching, and there's the very famous George Box quote: "All models are wrong, but some are useful," much like the biopsychosocial model.
We see that different people have these different baseline characteristics. At one end of this spectrum, we have habituation, where we give people a stimulus, such as exercise, and that kind of desensitizes the system to that stimulus. Then, hopefully, it becomes less irritable, less reactive, and less sensitized. That's a win; that's absolutely fantastic!
Whereas, on the other side, we have a whole bunch of other characteristics, and on that side of the spectrum, we have sensitization. We keep giving people a stimulus; maybe it doesn't make them worse, but for some people, it might make them worse. We give them this stimulus, and they actually sensitize according to this stimulus and to other stimuli going on around them.
What we have here are some of the baseline characteristics that might be associated with that. That's why it's important to take a good history, listen to your patient, and understand your patient beyond just what their pathology or problem is. We need to understand their broader biopsychosocial profile and a little bit more about them as people as well.
On that sensitization side, we have high pain, high irritability, multisite pain, lifestyle comorbidities, negative psychological outlook, and all of these things may lead to the stimulus we give people, such as exercise, not having the desired result that we would like. That's because their systems may be primed for more sensitization versus more habituation or a positive response to the stimulus we're giving them.
Ultimately, with treatment, what is a stimulus? People's systems react to that stimulus, respond to that stimulus, and produce a response. For some people, that might be analgesic; for some, it might be very little; and for others, it might actually be hyperalgesic as well. That's really important.
So, let's think about how this exercise thing works. We're going to throw out some complex terminologies at you. I don't want to be too technical; my aim is always to make the complex more simple. Sometimes you need to understand to be able to do that, so let's see if I can do it right.
The first thing we have to think about is the idea of a mechanism—not if something works, but how something works. When we do research, we're looking to know if something works, looking at an outcome measure through a randomized control trial and then comparing that against another group.
How something works could be hypothesized, of course. We have lots of mechanistic hypotheses about how things work. In fact, a lot of the time, posture is a mechanistic hypothesis. We don't measure posture before or after; we just provide the treatment based on the mechanism.
But a mechanism is how something works. This is something from my friend Chad Cook, and he describes it as the process through which an intervention unfolds and produces change in an outcome variable. The outcome variable is if it works; that's the measurement variable. The mechanism is how that might work, and sometimes that's a little bit more complex to measure, especially when we think about things like the internal physiology and biology of the human body.
It's much easier to measure a measurement such as pain verbally rather than it is to measure some of the wonderful chemicals that are floating around our system and may produce hyper- or hypoalgesia. We also have mediators and moderators. A mediator is a causal variable; it's why something happens.
It's not always entirely causal; it could explain a percentage of an outcome. We also have a moderator, which explains the strength of a relationship between two variables. I think lots of treatments have a moderating effect. We give a treatment; it has an effect on pain; it moderates pain. But that change may not actually affect a causal variable.
We can't confuse a mediator with a mechanism. We might have a mediating variable and not know exactly what the mechanism is, and we might have a mechanism and not be able to see that as a mediator as well. But don't worry about this stuff too much. If you're a nerd like me and find it interesting, that's great. If you don't, it doesn't matter so much; it really doesn't.
But I do think sometimes we can have a better understanding of some of the basic terminology. When we talk about causal variables, I think there are three different areas that we should talk about: predisposing, initiating, and maintaining factors.
A predisposing factor is a risk factor. We could say that smoking is a risk factor for pain. We don't know exactly how it might cause musculoskeletal pain, but it certainly predisposes or increases our risk of developing it. The exact mechanism, we don't know.
It could be an initiating variable. I might bend over and feel pain. It might be that that has caused pain in that moment, but what has sensitized that structure may not be what has caused the problem. Then we may have a maintaining factor as well. This often happens with psychological variables.
We may develop a pain or an injury, and that may be nociceptive in origin, but maybe some of the things that maintain it could be plasticity of the nervous system and how our psychological status affects our behaviors as well. Again, causation is not just as simple as x equals y. Causal variables could be predisposing, initiating, or maintaining.
When people are talking about what has caused this, sometimes we don't know because the initial cause may have been and gone, such as tissue damage. But some of the plastic changes that occur after that might maintain that problem. So, again, just understanding the philosophy of causation a little better.
Let's think about exercise and pain and consider what some of these mediators and mechanisms are. I've lumped it all together because I don't want to make it too technical and have everyone fall asleep and get upset with me.
One of the things that I think we don't consider enough is the inflammatory system and the immune system. That's something that I think we may have, for some people, a pro-inflammatory environment within the body. When we exercise over a longer period of time, that can maybe have an epigenetic shift to a more anti-inflammatory part of the body.
Again, we probably don't have the sets and the reps for that quite yet, but we'll talk about that. Self-efficacy has been quite a well-described mediator. Our belief in our ability to do some things with pain, whether that's activity, exercise, or movement, would be a mediator, and we may be unsure of the mechanism currently.
Biomechanics might be that changing someone's biomechanics changes their tissue symptom modification, etc. That's a very plausible potential mechanism. Habituation is an interesting mechanistic concept, but it's a mechanistic concept we don't actually know the mechanism for, so it's quite a loose mechanistic concept.
Habituation is just a decreased response to a repeated stimulus. It could be that we have tissue-related factors such as mechanotransduction. As we move and exercise, we have autocrine and paracrine processes occurring within the tissue itself. We have fibroblasts that lay down more collagen, and maybe that makes the tissue more robust, stronger, and more able to cope with things.
One of my favorite plausible mechanisms here would simply be the idea of blood flow and oxygen. When we look at research, we see that so many different exercise types can help people. There was the Jill Hayden paper from 2021 that looked at exercise for back pain. We see a range of movement, strength, motor control, McKenzie, everything in there, and all of them seem to exert some kind of effect.
Some were high dose, some were low dose; they had various different characteristics of the program, but they all shared some element of moving. The effect of exercise on pain could simply be that we are taking good metabolic stuff and pushing it into the tissue through moving.
Just basic pump mechanics, as we see with things like osteoarthritis, how we get into tissues through diffusion. The body works mechanically to get the transfer of stuff into tissues and out of tissues through mechanical factors. Could it be plausible that we bathe irritable acid-sensing ion channels in beautiful blood, which has a high level of oxygen within it, and that brings this calming effect?
We don't know, but for me, that's an exceptionally plausible mechanism: that it's simply basic metabolic activity or basic physiology occurring within anemic tissue. It could be descending inhibition. This is where we get into the idea of nonspecific effects. How many different treatments could activate the descending inhibitory systems?
We get opioids, cannabinoids, serotonin, all these wonderful things—manual therapy, exercise, dry needling, whatever you want to pull out of the bag. If we are getting acute changes within pain, it might activate what happens within the descending inhibitory systems.
Finally, could it also be psychological? Could it be that we are perceiving things differently, and the perceptual element of pain kicks in? Just thinking about stuff that happens at a perceptual level—our beliefs, our expectations, and how we may actually violate some of these things as well, which I think is really cool.
There are a whole bunch of different reasons that I could plausibly say could have an effect on someone's pain when I am using exercise or movement as an intervention. Now, it's important that we separate them in some way. We should separate them into acute changes and more chronic behavioral changes. I think that's really important.
If we're talking about symptom modification, that will often be an acute change, a short-term change where we've changed movement, maybe changed nociception from the tissue. If we do that enough, does that tissue calm down?
So, it might be there's an acute element and a chronic element, but initially, we would be reducing the amount of nociception coming from the tissue. We just talked about blood flow and oxygen again. That transfer of blood is going to be an acute thing, although if we do it enough times, does that provide desensitization or habituation?
Descending inhibition, getting those chemicals going and descending down the spinal cord and out into where they need to go, again, they are going to be acute changes. Maybe over the longer term, we see chronic changes in the rostroventromedial medulla. We have what are called on and off cells that either facilitate or inhibit nociception.
That might be a switch that gets flicked at some point towards a more pro- or anti-nociceptive system, if you like. Again, these perceptual elements are probably happening at an acute level as well or a short-term level.
Let me grab some water; it's hard to talk this much without getting a bit of a dry throat.
So, again, just highlighting what I'm talking about: changes in the chemical state of the tissue, decreasing acidity and decreasing acidosis, which likely sensitizes those peripheral nociceptors. Biomechanic symptom modification decreases nociception from the tissue, and our beliefs and expectations are perceptual changes.
Again, they may relate to treatment expectations, which will affect all treatments. That could be manipulations, mobilizations, ultrasound, exercise, whatever you want. They are all going to be affected by those.
When we talk about mechanisms of analgesia, they're not just tied into exercise. They are nonspecific, meaning they may be specific to a context and a person, but they are not specific to a treatment. Manual therapy and exercise could be very similar mechanistically; we just activate those mechanisms in different ways and may be mechanically different.
Descending modulation—again, this is something very technical. I do apologize for being all technical. This is our internal opioid mechanisms. The word we would use would be endogenous. Exogenous means external; endogenous means internal.
If I want some exogenous opioids, I have to find a man to sell me that. But I would love to activate my internal opioid mechanisms because they're going to dampen down some of that nociceptive stuff. As I said before, they're probably a really important reason for the effects of all interventions.
It could be stimulated mechanically, and it could be stimulated perceptually as well. It involves lots of different activation mechanisms. Actually, descending modulation—I talk a bit about descending inhibition and the positive chemicals. Could there also be chemicals that are turning things up?
We could have things like GABA, which turn things down, so that's an agonist for NMDA, which would be something that turns things up. That is the modulation; it's not just inhibitory; it's modulatory. This means that these mechanisms could be placebo or nocebo.
When we look at the chronic changes, these are probably a little bit more long-term based. Why does Ben even bring this up? Well, doing a couple of exercises probably is not going to create a chronic change.
This is where we talk about behavior change. The sets and the reps of a deadlift probably don't matter very much, but how much you go to the gym and actually do stuff, or how much you play sport with your friends, or how much you just go out in the garden and dig up the weeds, does matter.
This is more about chronic, longer-term behavioral change mechanisms. We can have shorter-term or longer-term, and sometimes shorter-term leads to longer-term. But again, it's so important that we understand that a big part of the power in exercise might be in the behavior change, not how you teach a deadlift.
The inflammatory system, again, we know that takes time to change its function. When we look at activity, self-efficacy, again, you're going to need to do things enough to create changes in someone's belief and violate their expectancy.
Habituation literally requires a repeat stimulus, so you have to repeat it. Then again, something like mechanotransduction, laying down new collagen, is going to take a repeated action.
So, we have the kind of shorter-term acute changes that we might see modulated by all of those funky chemicals, and then we see these more chronic behavioral change mechanisms that probably require quite a lot more engagement.
Actually, we focus too much sometimes on the thing itself and not enough on the behavior change aspect. The power of chronic exercise changes isn't in finding the best exercise program for everybody; it's about intrinsic motivation.
It's about helping people find their values and their goals, but there are mechanisms here, such as the immune system, that underpin why that may help. Mechanotransduction is about tissue adaptations to load that doesn't require the brain. This is localized; this is actual cellular responses to load.
Self-efficacy, again, another way to describe it would be reducing pain interference. Habituation is a decreased response to a stimulus, whether that's a stimulus we give people or an aggravating stimulus occurring within their world or their context themselves.
This is fascinating work by Katherine Sluka, just looking at sedentary versus active people and looking at some of the mechanisms there. They created changes, and I think you could probably describe them as epigenetic changes—changes to our gene function according to exposure to a stimulus.
Here, the stimulus would be exercise. Over, I think it was a six-week period, they found that there were changes within the opioid system, switching to more of an inhibit kind of default rather than a facilitatory default mechanism.
That might involve, as we see, NMDA receptors and various other things, and how certain mechanisms block the uptake of some of those chemicals. That's the idea of the agonist and the antagonist; they kind of block each other.
We do have really good information here, but we don't know what type of training does that. We do know it's much more behavioral than it is finding the perfect exercise. It's about finding that thing for the person, not just what did your favorite internet guru say was the best exercise.
Really interesting here as well, again from Chad Cook. What they were looking at here was the immune system and some of the cytokines that are floating around. We have things like interleukin, which are part of our immune system function.
What they found here was that manual therapy really didn't influence in the same way as exercise this chronic anti-inflammatory cytokine profile. Chronic exercise leads to a long-term shift in our behavior. It changes our immune system function towards one that is anti-inflammatory.
How powerful is that? It's not about whether strength training is better than exercise for lower back pain; engagement in both of them over the longer term at a level that is enough to stimulate whatever creates these shifts in our immune system function. How cool is that?
I think that's ultra cool, but again, it takes us away from the idea of sets and reps back to the idea of changing behavior towards a more active lifestyle. That would fit with a biopsychosocial approach rather than a corrective exercise approach.
As I have you here, if you are interested in these kinds of discussions and talks, we have the Core Kinetic mentorship coming up in a few weeks. It's eight weeks of really in-depth learning. We're going to talk about things like research interpretation, communication, the biopsychosocial model, pain science, exercise prescription, clinical reasoning, and common conditions.
We're really going to get into the weeds with someone who knows how to talk about it. We're going to have live sessions, research papers, special guests, case studies, and practical exercise stuff. I've already got a whole bunch of people signed up from all over the world.
If that's something that might tickle your fancy, if you want to get deep learning—not just Instagram slides—and want to get really into this type of stuff and improve yourself in that way, please think about joining me. As you've come to this lecture, I might even include a special gift for those who sign up.
Anyway, advert over; I do apologize, but you are a captive audience. When we look at the immune system, we have to understand this is longer-term. This is about epigenetic changes. The change comes from exposure to exercise, and what we want is an anti-inflammatory environment that comes from a better lifestyle and more engagement in physical activity.
This is a little bit about behavior more than the sets and the reps. This is one of the little tools that I use, one of the little models that I use for teaching. It is about how we get to where we want to get to with our patient.
What we see here is, let's pick the most likely area that this exercise is going to help this patient, and then we can program it accordingly. Again, all models are rubbish; some are useful. I describe this as imprecise precision, where we are trying to be a little bit more precise while still understanding the individuality of the patient.
When we are trying to get more engagement for some of these chronic elements, we are thinking about what are the barriers and facilitators for their engagement. We are thinking about what is intrinsically motivating them. We are thinking about what their values are and what they want and need from doing this, and how we tap into that.
Secondary to gaining a value, we're also thinking about how we can get people to do things that they enjoy. Sometimes, again, it does boil back down to that behavioral change element that I think is super important.
Now, let's actually look at a little bit of research. This was looking at a recent trial into Pilates exercise with my great friend, Lean Wood. I met Lean many years ago at an Explain Pain course, way up in York, up in the north of England. I can't remember when that was—2014 or 2015—but she'd gone on to do some really fantastic stuff, and I always remember the great chats we had there.
Here, they did a mediation analysis of a Pilates intervention for chronic lower back pain. What they wanted to find out was what were some of the things that mediated this. This isn't the mechanism; this would be a mediator.
What they actually found here was that one of the things that mediated pain intensity— the variable we're all interested in—was pain catastrophizing. So, having less extreme reactions or worry about experiencing pain or the future. The other was kinesiophobia, or fear of movement.
A lot of the time, we think that Pilates is about activating the core and stabilizing so there aren't these damaging micro-movements, etc. But actually, one of the mechanisms was pain catastrophizing—decreased worry about pain—and the other was decreased worry about movement.
Certainly, we would describe these as psychological variables; they are psychological mediators. If something is mediated, even in part, psychologically, does that mean we should maybe focus on some of those elements or create some techniques or ways of interacting that may take advantage of that mediation?
So rather than thinking Pilates is all about activating that core and getting those toned abs to stabilize the spine, maybe it's about making people feel safer to move and actually worrying less about pain. They did a nice little diagram that explains some of the pathways and effects they looked at.
There we see the intervention mediator effect. Pain catastrophizing at six weeks had an effect on pain intensity at six months. I like the way they describe Pilates exercise: once, twice, or thrice—it sounds like a Shakespearean novel.
This was another paper from an Australian group led by James McCoy and Aiden Cashen. They had an education and graded sensory motor retraining program in people with chronic lower back pain. They started off with simple spinal movements, and they had a psychological approach that said finding it was safe to move, understanding that it was safe to move through education, and feeling it was safe to move.
We could describe that a little bit like an exposure kind of embodied approach, which sounds really good. Cognitive Functional Therapy may use that type of approach as well, and just general exposure therapy may use these types of approaches as well.
But what mediated their outcomes? The two at the top would relate to these motor control variables—motor coordination, tactile acuity—and actually, we see that the effect on the outcome was very low. Back perceptions had an effect, kinesiophobia, pain self-efficacy in there, which I think is a really important one, pain catastrophizing, beliefs about back pain, and then all of these things stuck together.
We see some quite wide confidence intervals, and that's completely to be understood, although back beliefs didn't have wide confidence intervals and certainly confidence intervals that didn't cross zero. In fact, the two top variables had confidence intervals that crossed zero, so we could say maybe they don't have much of a mediating effect.
I think that's pretty cool to look at. We would probably see those more as psychological variables as the major driving force in that intervention versus the accuracy and motor coordination.
If we look at research interestingly from the CFT guys, this was from Kevin Worley, and they did a mediation analysis of one of their trials. What they wanted to know was movement associated. I used the word association, not causation here, but association is the first step to causation in some ways.
If we look at here for some of the patients, their biomechanics—the way that they bent their spine in terms of the amplitude and the range—these types of things were associated for the two on the left. If we look on the right side, they weren't associated so much.
What this slide really highlights is that what may be associated with change or a mediator or a mechanism of change for one person may not be the same reason something changes for another person. But it is good to know, on average, is it likely to be more mediated by the mechanics? Is it likely to be more mediated by various other variables as well?
They did another mediation analysis here, and they actually found one of the big mediators changed about 48% of the total effect on disability, which was increased pain self-efficacy. This idea of being a little bit more okay with having pain and actually doing some things with pain.
One of the other little sayings I have on my course is "zero pain is not the goal." What that means is sometimes we have this idea we always have to take pain away. Sometimes a role of exercise might be not to have pain or give pain per se, but sometimes we have pain, we move, we still have pain, and maybe that's an opportunity to change our relationship with pain.
Maybe we can dethreaten it and change its interference on what we do and how we do it. Pain self-efficacy, I think, actually has some really strong research around it. One of the basic things we need to do sometimes with some people is change their relationship with pain.
Sometimes taking pain away or never doing anything with it that causes any pain attached to it, I think that might be doing some people a disservice, even though everyone feels like it's actually doing a service. We may be perpetuating pain-related behaviors and pain-related interference and disability.
In fact, here in this paper back in 2003, so 21 years ago, just as old as I am, they found that self-efficacy was actually the most important predictor of disability, then fear avoidance, then pain intensity. I think that's really important.
We often say, "Well, pain intensity is the reason people aren't doing things, and if you took their pain away, then that would be fine." But actually, it doesn't just seem to be the pain; it seems to be the self-efficacy associated with that pain as well, which I think is really interesting.
Here's a little tweak from myself—a little bit of self-promotion, well, not really self-promotion per se, but just getting my point across. If we want to improve pain self-efficacy through exercise, then we have to have an element of discomfort involved.
I'm not saying cause pain, but often there is discomfort. Just not stopping when there is discomfort and being able to talk about that and reframe that and maybe recontextualize that. If we want to change pain self-efficacy, we need variables associated with pain self-efficacy.
One of the big complaints is we don't know if strength mediates pain. If strength doesn't change, we can't say that those two things are not associated, even though we have evidence they're not that well associated.
But we would never expect strength to change without actually emphasizing load or effort. We cannot expect pain self-efficacy to change without an emphasis on pain and self-efficacy of pain. That would just be nonsensical, and it is nonsensical.
We're going to do a little thought experiment to finish tonight. We are going to think about taking one exercise and adjusting it and adapting it according to different mediators or mechanisms. We often like to change the exercise to change the effect or the outcome.
I actually believe we could keep an exercise the same but change the variables and emphasis around that exercise to take advantage of potential mediators and mechanisms that we identify.
So, let's take pain self-efficacy. If we wanted to do a deadlift and we thought pain self-efficacy was low, maybe you measured it using the Pain Self-Efficacy Questionnaire (PSEQ). The first thing is that we might not stop if there was some discomfort or some pain.
We might want to discuss pain pre-deadlift. We might want to think about pain post-deadlift. Was it as bad as they thought it was going to be? What does that pain actually lead to? Is it a bit sorer, but is it still safe?
I love that terminology: "sore but safe," because that allows us to do a few more things and stops pain from interfering so much, as long as it doesn't increase sensitization. That's the balance, isn't it? We want to be a bit better off with pain.
We still want to be able to do the things that we want to do or need to do or value, but without reens or without more sensitization of that painful problem. If I want to do a deadlift that has an effect on pain self-efficacy, there may be specific variables that I need to engage with.
So, strength with a deadlift—of course, we're going to have to focus on low reps and higher load. If you want to get stronger, you probably need to pick up heavier, and the deadlift is a great exercise to do that.
I would like to pick the equipment that allows me to pick up the heaviest load. I would measure changes within that strength, and as that load becomes greater, I'm probably going to be a little bit stricter on the performance of that exercise simply because I want it to be the most effective and efficient to increase someone's strength.
One might focus on pain; one might focus on strength. I actually believe the most common variable that we have an effect on for patients is simply confidence to move. Rehabilitation creates a positive environment for people to use their bodies.
What they're going to do is build their confidence. Maybe that leads to a little bit of lifestyle change where they're going to use their bodies a bit more. They're going to go back to the gym or go back to doing activities that they enjoy, and that's going to have a positive effect.
So, confidence is much more generalized than self-efficacy. Self-efficacy is a quite rigid concept in that it relates only to a specific domain, whereas confidence is probably much broader and wider.
If I want to improve my patients' confidence to use their body through a deadlift, I'm thinking about not over-coaching. I'm thinking about giving positive feedback. I'm making sure that they're successful, so not making it so hard that I have to over-coach.
I'm going to consider their concerns, their worries, and answer their questions, making a very open environment for that person to ask their questions and make sure they feel heard.
Still the same exercise, let's think about movement variability. A deadlift, again, doesn't have to be done with a barbell; that seems to be the most common thing. Could you do it with a kettlebell? You could do a kettlebell deadlift—no problems! A dumbbell, a bag, or whatever.
Movement variability with a deadlift might be using different objects. It might be taking a non-linear approach. If you're interested in movement variability, something people don't talk a lot about is what's called nonlinear pedagogy—looking at ways that we change the environment and ecological dynamics to create an environment that requires change and adaptation.
Maybe we create a movement problem versus a movement solution. Rather than looking to reduce rep-to-rep differences, as we often do and might be good for something like hypertrophy for a repeat stimulus, we might actually promote rep-to-rep differences to create that variability.
There seems to be this idea that variability is like adding in something people don't have. I think a lot of the movement variability concepts now sound a lot to me like corrective exercise. If you can't pronate, I'm going to get you to pronate. That's corrective; that's not variability.
But anyway, moving on. Maybe I want to create some kind of expectancy violation. Making that person feel dethreatened around that problem. We don't always reduce fear when it comes to violation processes; sometimes, we build courage and build confidence.
We may aim at fear but build courage. Just a little kind of note if you understand anything about expectancy violation.
Thinking about identifying fears and beliefs—remember that graded exposure is a psychological concept. Graded exercise or graded activity is the process of the actual physical action. Graded exposure is actually psychological change, and that often involves a physical action.
What we're measuring is not the amount of exposure to the physical activity; we are measuring the amount of change in that person's belief structure. Sometimes we could call that cognitive restructuring, which is changing our beliefs around something.
To do that, to create change in belief, you might need to identify those fears and beliefs. We might need to create a reasonably safe environment around that deadlift. Maybe they have a fear of picking things up, for example.
One of the things we'd like to find out is the discrepancy between the expectation and the outcome. Was it as bad as you thought it was going to be? If you thought it was going to be 10 out of 10 pain and it was only 7 out of 10 pain, well, that's an expectancy violation—an uncomfortable one, but certainly something we can do.
Then think about how we use that information moving forward. What we've done here is adapted the same exercise, the deadlift, to take advantage of lots of these different mechanisms or mediators that we've identified.
Actually, that might be more powerful than just banging out those three sets of 10 reps. It might be that you could include little bits and pieces of different things here.
If we want to change engagement or adherence, maybe with the deadlift, we emphasize the relevance of that to the problem. We help people enjoy it. If we really think about enjoyment, maybe it's not even about enjoyment; maybe it's making it meaningful.
How do you relate the exercise to the problem and to solving the problem? Upping that kind of engagement, adherence, whatever you want to call it.
Also, how do I get the easiest possible deadlift going so that I can repeat it at home? I can do it in lots of different ways. The emphasis on the exercise might change according to the mechanism that we think is going to be most beneficial for the person we are working with.
One of the problems is people say to me, "Ben, what is the best exercise for back pain?" which is a pretty dumb question given the evidence that we have. But at the same point, we could take the same exercise, and it's not the exercise that matters; it's the way that you actually use the exercise that might be really, really powerful and might create that change for your patient.
I think we're at the end there. Yeah, so look, oh Jesus, we've gone dark. There we go. It went dark in my study while I was talking, so the nights are drawing in here.
I hope you enjoyed that little dive into pain, exercise, mechanisms, mediators, and all this nerdy stuff that some people may not be interested in. But we know that what we're currently doing isn't having the effect that we want it to.
Let's all be honest with ourselves. The effects that we are able to have on pain using exercise and movement aren't as good as we could make them. I think exploring the why—not just if it has an effect—can lead to having a bigger effect.
Also, just nerding out and understanding a bit more about human body physiology, etc. We get really nerdy about biomechanics, but actually, the biomechanics of the body aren't half as important as the physiology and the neurology and perceptual elements.
I think we need to move towards some of that stuff, even though it's a little bit more complex. We have a few minutes. I don't know if anyone has any questions that they would like to ask.
Ahmed says here there was a recent paper out of Australia by Matt Jones. I actually think Matt Jones was one of the authors, but we had the guy who was the lead author on the BCP to talk about that. I can't remember his name; it was a Middle Eastern name, I think—Gulani or Giuliana or something like that.
That was his paper, and what was really interesting about the paper was that barriers and facilitators for some people—the facilitators were the barriers, and for some people, the barriers were the facilitators.
Again, what gets people to adhere to stuff isn't always the same. If anyone's got a quick question they want to ask, then I'd be more than happy to answer it. If everyone has had all of their questions answered, I'm going to send out a recording for those people.
I'm going to send out something to you guys in the next couple of days, probably a little advertisement for my mentorship as well. That's the game we're going to play.
Britta, great question: how far do you think a client's mood can affect pain? Well, actually, if we look at the research here, I don't think there's a direct link between mood and nociception. I don't think we see a really strong change in measures of sensitivity, such as quantitative sensory testing.
But I think sometimes when we are down, when we are low, pain feels worse in the sense that we don't cope as well with it. It might still be 5 out of 10, but I don't cope as well with that 5 out of 10.
There's some work by Natalia Costa that looked at pain flares, and they find pain flares aren't always greater pain, but they're worse psychosocial features. The relationship between pain and psychosocial features might be coping, not increasing pain directly.
KLU, can you talk a bit more about self-efficacy and pain self-efficacy? Self-efficacy is my belief in my ability to do something. Pain self-efficacy is my belief in my ability to do things despite pain—so go dancing, play football, bend over, fill the dishwasher.
If I have very low beliefs in my ability to function with any pain, that tends to lead to worse outcomes. An anonymous attendee—that's an interesting name. What about exercising patients with high pain scores?
This is where dosage adaptation is really important. They're much more likely to sensitize than habituate, so I think the stimulus should decrease. I use the rule of 10, and I talk a lot about pain irritability and pain intensity in the relationship and how changing dosage is probably one of the keys.
So, changing the stimulus versus the response. Amir says here, does pathology like herniation affect exercise prescription? There are no exercises for disc herniations that are better than any others.
There was a recent paper that looked at physiotherapy intervention for things like sciatica, and they found there isn't a method. But I would say, you know, making sure that whatever you're doing is not aggravating the problem and creating a worse inflammatory environment.
Would you say your explained concepts apply to athletic lower back pain? Well, they can only explain that. I think we only have set physiology. If we look into athletic—athletes have the same physiology as non-athletes in the sense that we have the same systems.
They may have genetically better systems, but athletes may actually have greater anti-nociceptive ability. So absolutely, that would affect athletic low back pain.
Yeah, absolutely. Is it okay if I watch the whole webinar with my spine in not a neutral position? I hope you watch the webinar with your spine in not a neutral position. Whether you're here tomorrow morning, we don't know. You may be dead, but I hope not. I pray for you, my brother.
What is your opinion on the biggest way in which we influence the patient negatively? We tell them nocebo. Remember, we talked about pain modulation and behavior modulation. If you tell people their back is all up, they are less likely to use it, and therefore they are less likely to have a positive physiological environment.
What do you think about the self-confidence of the practitioner? I think that probably definitely has an effect—probably definitely, undoubtedly has an effect. How much effect? We think of context as around 20% of the overall effect that we see throughout the course of change.
About 50% tends to be natural history or just the cause of the problem. About 30% is specific to the treatment, and then about 20% would be contextual or what you just described.
Have an MSK B6 interview in two weeks. Will we receive a certificate for this? Absolutely not! There's no way I can write out hundreds of certificates.
If a patient has a 10 out of 10 pain scale, how to reduce it by exercise through a deadlift? I probably wouldn't use a deadlift. I would use something much, much more gentle. A 10 out of 10 reactive irritable problem, I'd probably start off with a very low stimulus, like something basic, a pelvic tilt.
Ahed asked another question: what about the use of dry needling? If you feel justified to use it, use it. I would call it a moderator of pain, whether that's mechanistic or perceptual. Whether it's kind of anti-nociceptive, I don't know, but I would definitely say it was more of a moderator rather than a mediator of the problem.
Would you recommend a book to learn more about pain physiology? Not so much a book; I think there are so many articles out there. Although I think some of the NOI guys have some interesting pain physiology in some of their books. The Sensitive Nervous System and the Louis Gifford books have great pain physiology in them.
Alright, I'm going to do two more. Is education or exercise more important when dealing with chronic non-specific lower back pain? I would say education, although education should hopefully lead to behavior change, such as activity and exercise. Not a lot of stuff outperforms education for MSK issues across the body.
How important is muscular endurance? No idea; probably about as important as strength, which doesn't seem to be that important. So, Ma said, can you repeat it? The overall change that we see from an intervention in a trial would be 50% natural history, 30% the specific effect of treatment, and then 20% relates to the context of what happens around us.
You've asked loads of questions. Thank you so much, Ben. Well, thank you for saying thank you. As I said, the best way to thank me would be to do a little Instagram story saying how much you enjoyed this pain lecture and how smart, funny, tall, and handsome Ben is. That would be absolutely fantastic!
So, guys, really, I appreciate you coming on and listening to me. We had a few hundred people from all over the world. It's my pleasure to be able to reach people and talk about stuff. I will send you a recording, maybe a little special gift if you sign up for the mentorship program. Love you; see you later!