Tendinopathy & Neuroscience with Dr. Patrick Vallance

I'm sitting here with Dr. Patrick Valance and we are going to talk, oh, we're going to talk tendons, but I came across your Instagram page. I think it's tendon opathy circuit breaker. Yeah. Came across like three months ago. You had some really interesting posts and then I just kind of got busy and lost it. And then someone else posted about it recently and I'm like, I'm going to go back and look, so I look for a few hours and you had a lot of things that are questioning basically the conventional wisdom that we have with with a patolar tendon opathy, Achilles tendon opathy. We're going to get into all that today. So tell people who you are. Yeah, thanks Jake. Yeah, so I'm a Melbourne Australia based researcher to knock the neuroscientist I'll call myself. I am really lucky. I'm working with some really well-known researchers here at Monash University. Professor Peter Malios, Malios has been a real mentor to me and whatnot. But yeah, just really, really interested in researching that space between tendon opathy, function of the motor nervous system, pain nervous system as well. So we can get a better idea of what's actually underlying the mechanisms in tendon opathy. So we can hopefully come up with better rehab because at the moment, our outcomes aren't necessarily fantastic. So I think if we can learn a bit more about that, that'd be great. But yeah, physiotherapist by trade. So worked as a physiotherapist for a while before then stumbling across a PhD, which the repeat twist mom and end up going down that pathway and haven't looked back, really enjoy all things to do with tendon opathy. So it's been great. So I think that really well. Okay, so I'm a strength coach who got into tendons because I had patellar tendon opathy for like a decade or it just never got better. And then strength and conditioning solved it. Why did you get into tendons? Yeah, I think that's. I was listening to Seth O'Neil's podcast with yourself and he said he developed in the Achilles tendon opathy as well. In my undergrad, so I was studying physiotherapy, developed a nice insertional Achilles tendon opathy and then yeah, that's a sprue to my interest. I remember reading lots and lots of papers at that stage and took a bit of a clinical interest in it in that area. So tendon opathy management, Achilles tendon opathy in particular when I graduated and actually started my PhD in Achilles tendon opathy and then COVID hit and there's a bit of an opportunity, a bit of funding that was available to do some sort of quite technical stuff in the patellar tendon region. So I moved up however many centimeters to the patellar tendon, we ended up in patellar tendon opathy and so I'd say I've used myself as being across those two spaces Achilles and patellar but yeah, a nice Achilles tendon opathy for me to manage early on, got on top of it eventually but yeah. What did it come from? So I played Osirul's football, I did play Osirul's football, I still sort of trudged around a bit here and there, I got talked out of retirement for this season and was not going to flash out but yeah, just heavy grounds, lots of running very poor load management. I also, I've got a running style that yeah, they call me gumboots down at footy sort of trudged around so I don't know that bi mechanically on the most efficient so quite a bit of ankle dorsi flexion as I'm running around so that probably doesn't help as well but yeah, it'd just be the load management running around in heavy fields. Okay, so you started in Achilles and then what was this opportunity in patellar? There was just like a yeah. Yeah, we just had a small pot of funding that was available internally at Monash to run a functional magnetic resonance imaging study in patellar tendon opathy and yeah, it just made sense to take that on. Someone else had successfully got access to that funding and they weren't going to be able to utilize it so we had a chat and they jumped on board as an extra supervisor and in the PhD and yeah, we ran, they got me to run that study so that was really cool. So moved up, got some really interesting data on patellar tendon opathy and then explored further from there. So what was it the PhD? Yeah, so the big title was neural deficits in pain and functional deficits or functional impairments in Achilles and patellar tendon opathy. So bit of a word scramble there for you, but essentially I was looking at the what's going on in a nervous system sense in people with Achilles or patellar tendon opathy. So we're looking at or are there signs of central sensitization and those sorts of features and then from a function or force output perspective, what could be what could be driving alterations in force outputs. So super, super interesting with the the function output side of things, we were able to use some cool technology. So we used transcranial magnetic stimulation, which it's sort of like a think of it like a portable MRI. We've got this really strong magnetic pulse that we hold this portable device that outputs that pulse. We hold it over the top of the head and it stimulates the area under it, which is the motor cortex. So you can sort of potwire the brain to produce a contraction in the saying the quality for looking at patellar tendon opathy and then based on a few measures that we can take with that, we can start to pick apart. Well, if there are alterations to drive from brain to muscle, where are they, which could give us some good clues for what rehab could consist of if we're trying to target them more directly. Okay, let's, so these whole, this whole like, you said that term central sensitization. Yeah, so could you get into, I mean, I guess for the sinners, maybe for myself as well, could you cover the one or one central sensitization and then, yeah, with tendons, what does that mean? Yeah, yeah. So this whole idea of in persistent pain and tendon opathy is a persistent pain state. You have pain for a long period of time. There had, well, there's been a big debate in this space and there's lots of research and probably we haven't landed on a clear answer yet, but this idea that because you've got ongoing sensory activity at the tendon, so our nosy septus fire, they're responsible for that pain experience. That neural, I guess, drive from the tend goes up to the brain and produces pain. The, the thinking is like some other painful conditions like low back pain or osteoarthritis, the efficiency of that signaling could become enhanced and therefore pain should be magnified as a result of that. In tendon opathy, we look at these in a few different ways. We've got some of pretty sort of laboratory based scientific ways of looking at it and then we've got a more straightforward, clinically friendly way of looking at it where we actually just get people to do exercise and look at their pain before and after. And that's something that I'm really interested in with the lab stuff, though, that often is a little bit more technical and that's where there's a bit more conflict in the literature. So the debate is when you compare people with tendons opathy overall to healthy controls. So people with out tendon opathy, it looks like there's not necessarily differences, but the, I guess the key there would be actually going a bit deeper into the data and looking at the variable response. And this is something I'm really big on. There's actually people or subgroups potentially. This is getting a little bit into the Sean Hanlon world where he looked at the subgroups, but there are people that have this profile where it looks like they essentially they've got that central sensitization or nocy plastic pain is another way we look at it or determine, but their nervous system is geared in such a way that they're more efficient at carrying that signal from the tendon up to the brain to produce pain. And then there's other people that their sensory system doesn't seem to be enhanced in that way. And I think it's really important that we start to recognise those people that do have those signs and those people that don't have those signs and there's probably there's going to be some value in that. We've got to work out what that value is, but there will be value in recognising that in the future, so we can have a look at how we might manage them a little bit differently. Okay, so central sensitization that would fall into this nocy plastic idea, nocy plastic pain, you're getting changes in the nervous system instead of like local changes from at the tendon, which would be more of the nocy septiv, right? Nocy septiv would be at the tendon level. Yeah, yeah, so if we dig that big deeper for sure, so yeah, we have nocy septiv pain, which is just the production of regular signal from the tendon. That's regular, that would be if we say there was nocy septiv pain would be assuming that it's the same between people, any person, irrespective of like it's not upregulated or anything like that, you can have peripheral sensitization and that's upregulated signaling from the nerves at that tendon and then you have central sensitization, which is inferring that at the brain level, there's some upregulated processes that are amplifying that pain response. I say central sensitization because there, and you could look at the whole system, the definition nocy plastic pain, it's there's some criticisms about it because if you dig into the wording, it's sort of in first that there isn't a requirement to have that no-susceptive signalling at all, intent and opt for you when you look at people and when they get pain, it's when they're loading, so there would be a signal. So perhaps it's just me being a bit stubborn about the wording, but I think the sensitization phrasing makes more sense because there is this signalling, there would be signalling, we've got people loading, there'd be production of these sensory afference, we call them, so the no-susceptive signalling, but the response can be amplified. So producing a little pain. Okay, I have a few ways I want to go with that, but we're just going to go off a side tangent, so the main thing I wanted to chat about, because you had a really good analogy with the garden hose and the faucet, this idea of cortical inhibition, which would be from the brain. The brain is producing that inhibition to the tendon because of this pain, but then the other phrase was reticulose spinal, which would be that inhibition is coming further down from the spinal cord. If I have that correct, yeah, you can correct me on that. So does this fit nicely with this whole central sensitization would be from the brain, but more like maybe peripheral sensitization would be further down the chain. Sorry if I'm confusing that you can correct me and go into your main work there. Yeah, and it matters, we're looking at where it might be occurring. So I think we might, for example, if it was peripheral sensitization, we might address that differently to if it were central sensitization. If we're looking at intervention, the intending off the neuroplastic chain and concept has come up time and time again, potentially we're looking at producing more of a neuroplastic effect if it is central sensitization as opposed to if it's peripheral, we might be using interventions that target the sensation at that site more directly. So yeah, I think it does matter with the motor system, you let me know when you want to go through some of that. Okay, yeah, yeah, let me stop there then. Okay, because I, yeah, it's a lot of stuff to cover. Hopefully people aren't confused already. I'm trying my best to piece together, but the maybe to start like the understanding, maybe like the conventional wisdom or the understanding right now with this patellar tenonopathy is we have central sensitization. So the brain, is it the motor cortex mainly that we're looking at is like, there's something because of the tendon pain, our brain has changed and it's going to inhibit the quadriceps from firing in a way that we want. So this is where we do the neuroplastic training, the metronome is meant to help the kind of clear up that the motor cortex, the inhibition coming from the brain. But is that do we really have that brain inhibition in patellar tenonopathy? That's kind of the question you have, right? Yeah, yeah. So I guess, I'll touch on a couple of things. I guess we haven't necessarily made that connection between the pain system and the motor system so clearly. So they're there, I guess I've been considered in, as being distinct, you can make an argument that there absolutely would be interaction and my work has shown that there is an interaction that's just where that interaction occurs. So with the motor system, we look at the fact that in patellar tenonopathy, the known deficit when it comes to fourth output is your strength, max strength. So we've got some really good data to show that when we look at max fourth output, your respective of the motor contraction is reduced, be that isometric, isotonic, and so on. However, for a long period of time, you know, the better part of a decade, we've put that deficit down to this idea of cortical inhibition. So for the motor pathway to work to produce force, we've got drive from the brain first, the motor cortex, where we've got these neurons, corticospinal neurons, they carry signal from the brain all the way down to the end of the spinal cord where they then synapse or carry that send that communication, the signal, cross to a peripheral nerve, peripheral nerve, then takes it to the muscle, muscle contracts. So there's two sites at which that motor drive can be disrupted or altered. So at the very start of the chain, we have nerves that can input onto the motor cortex and make it more or less likely to fire. So that's our cortical inhibition. So we can have nerves within the brain that if they're more active, they're doing more, they're going to make it harder for the corticospinal neurons to switch on and therefore you're not going to get that drive that makes its way down the pathway to the muscle, it's not going to fire as well. Further down the chain, though, there is that that synapse, that communication between the bottom of that corticospinal pathway and the peripheral nerve, that's another site that can be altered. So we also have nerves at that site, that input there and if they're more active, they can also switch down the drive. So you can have all the drive in the world coming from the brain, it's making its way down to that spinal level, but it can be tuned down at that point and that could also result in forced deficits. Now, we thought for a long period of time, it was cortical inhibition, we thought for a long period of time, it was all happening at the brain, that stem, that whole tendon uroplastic training arc that was very, very popular using metronomes to help produce a motor training effect and therefore the brain will adapt and will overcome this cortical inhibition. That stacks up from a theory perspective, for sure, if it was cortical inhibition, that would be very effective. But what we didn't do is we didn't look at the spinal level. So that was my PhD, I looked at cortical level, I looked at the spinal level and I looked at what was altered compared to healthy people and cortical inhibition was fine. So cortical inhibition compared to healthy controls was unaffected, but at the spinal level, we found that that was where the problem was. So there was an increased activity of, we call them intonurons, but nerves that just erupt that synapse between the spinal cord and the peripheral nerve and we've been able to link that then to forced deficits. So we've been targeting the wrong thing. So yeah, it's super interesting. The way I like to describe it, I've got this analogy, the garden hose analogy and hopefully my Australian terminology stacks up for how you would describe it in the US, but so we've got, yeah, if you think of motor drives through the pathway as being like a garden hose where you've got water pressure at the tap, I think you call it a faucet. So the cortical inhibition, they'd be like the tap, if the taps close, the cortical inhibition is ramped all the way up and it's stopping motor drive from going down the pathway. Now in Patelotent Nocty, based on my research, our research, the tap's open, the cortical inhibition isn't disrupting drive. So water's still flowing along the hose and it's going towards the, would say, sprinkler, is that correct? So it's going towards the sprinkler at the end, water's going to come out, they'll be our force output. What we found is there's a kink further down the hose. So the hose is kinked over, so there's something further down, so they'd be the spinal level and that's stopping water flow. So you can have all water pressure in the world, the tap's open, so that's absolutely fine. Water's flowing to the point of that kink, but it's not going to get past that kink. So we need to do something about the kink in the hose. So garden hose analogy, that's what I'm running with at the moment. So hopefully that makes sense. Yeah, okay. Yes. So we have that metronome that, yeah, the metronome, like you're listening to a metronome at like 60 beats per minute and you're doing isometrics that way or you're doing like three up, three down with, or that's the typical, I guess, Patelotent Nocty rehab set up and you're just listening to kind of get that brain activity, I guess elevated or clear up the cortical inhibition. When it comes to the inhibition further down the chain, what's, yeah, what do we do, what do we need to do to help that? Yeah, it's very fortunate timing. There's a bit of research that's been happening, so in the last year or two within our lab as well, which has been really lucky because I've been able to so pick the brains of the people working on it. They've been looking at this alternate pathway, the reticulose spinal pathway. So I mentioned before and apologies for the terminology, but we have the corticospinal pathway and that's the primary pathway for motor output. That's confirmed. That's absolutely a known fact. It's the constant. It's the one that takes drive from brain to muscle and that's the pathway that we know that we've got this, this deficit in at the spinal level. But what we've been looking at is this alternate pathway, which is sort of like a supplementary motor pathway, you could think of it as called the reticulose spinal pathway. What it does is it carries signal and it doesn't go directly onto those peripheral nerves that we're talking about before. It actually uses a different peripheral nerve, a gamma motor neuron, call it instead of an alpha, but just think of it as a different, different nerve. And it has this loop where if the reticulose spinal pathway excitability is up, that then can help overcome the spinal inhibition. It's sort of like a bit of a bypass loop. So think of it over the garden hose as holding the hose straight so that water can start to flow back through. So in this lab that is here at Monash as well, they've been looking at how can we isolate that pathway to boost the excitability and what they looked at was metronome-based rehab. So pretty typical of what we're doing 10s and octaves, and I'll just preface that this wasn't in 10s and octaves, this was in healthy people, but they looked at, yeah, metronome-based rehab, and then they looked at self-paced rehab. And they then looked at the nervous system and what was changing. They also looked at function, so strength and power at the end of this block of training. And what they found was after the three weeks of training, which isn't much, but still as something. After three weeks of training, people that did the metronome-based, paste training, their cortical inhibition dropped, and they had a bit of a boost in strength. So they still saw some increase in strength. But those that did the self-paced training, no change to cortical inhibition, but their reticulospinal pathway excitability went through the roof, their strength went up, but their power went up as well. So that was a bit of a difference there. So if you're looking at peak force output, you'd argue that to power max strength, this self-paced training presents us a really nice way for us to access and target that spinal level inhibition, which seems to be the deficit in patellar tendonocleod that's responsible for force, max force deficits. So self-paced training is just you are, if you're doing a slow eccentric and car-centric, you just like are piecing that yourself. That's what that is. The local eye of control goes internal. So the idea with metronome-based training was that control goes external. You've got to focus on something and keep to pace with that. So it makes it more like a controlled task. When it's self-paced, you self-select pace. That doesn't mean that you can't provide instruction ahead of time to say, I want you to try to have this amount of seconds up or down or do it nice and slow, well, not, you can still instruct your patient or person with tendonocleod to do that. But the idea is that it's not listening to something external. It's an internal control. So by doing that, it becomes less of a motor learning task and more of an automatic task, which seems to be really important for the particular spinal pathway. Yeah. All right. You got to tell me how, if this is if this is dumb or if this even exists. So I was telling you that I did a I did a podcast Gabriel Fernandez who you've you've done some work with. We talked about the his paper on the lateral gastroc deficit in the Achilles tendonopathy and the term neurophysiology, neuroanademy, you know, these things that he's all and I I'm doing my best to understand it from him from you. There was this book I read Franz Bosch. He was a strength coach. He had a book strength in coordination and the little bit of me like dipping my toe on the water of the way things are moving is controlled. It was to me and I'm probably paraphrasing in its wrong was a lot of these like slower things can come from like the brain act brain down and then you activate the muscle but he was getting at like pre-tensioning muscles like very quick pathways of like the muscle has to work out immediately so it maybe it doesn't I don't know if this is right. It doesn't have time to travel up to the brain and then come back down or something along the side. Is there any yeah correct to me on all of that but it makes me think of what you're talking about with this max force deficit is it that because the way I'm thinking is like if it's a motor cortex thing a brain thing like is is that a slower pathway then like if we're doing something powerful or quick do we have time for this like control top down control from the brain. Anyways you're nodding your head so maybe it made sense and correct me on all that but yeah. Yeah it's the so the pacing when you actually look at the impulse we measure the the core latency so the time from yeah the time things take to get from brain down it's still the corticospinal path by that is quicker just because it has one less synapse I was talking about synapses that communication yeah between sites but the way the nervous system is is organized our reticular spinal pathway it's got a lot more dense innovation in low limb so it is got it's got a lot stronger input to the low limb and as opposed to the corticospinal pathway so the thinking is if you look at the upper limb corticospinal pathway is more important because we have a lot more control tasks with your hands the upper limb a lot of it is placing the arms the hands power max forces required less whereas if you look at the lower limb as a lot more about maximum output we have to produce bigger force and quicker force and a lot of it is a more lot more reactionary so this reticular spinal pathway it's considered to be a lot more I won't use the word reflexive because that's not the right word but it's yeah more automated in a sense as more of our if you they say it's really important to locomotion and movement and and reacting to situations so if you start to fall you have to place the foot out to stop yourself from falling that's a reticular spinal pathway in action the other thing that's super important and interesting is that to produce max force output the reticular spinal pathway has to be active so it acts on the muscle spindle so it's it's really important to maintaining tension within the muscle which is important from a sensory perspective and I won't go into all of that but essentially to produce max force output this system has to be active as well as the corticospinal the main pathway so you can produce good force output if it's just a usual pathway but to get that max output and power you need this pathway to be firing maximally as well so okay the okay a couple of questions on that the maybe to the never-ending pursuit of me to understand on this the corticospinal like we have the motor cortex so that's what we're getting at with the corticospinal is the the cortex right motor cortex reticular spinal what is the reticular what does that what does that mean yeah so that's brain stem base so we've got the reticular formation which is in the it's just an area within the brain stem so we it's we still so technically it's the and I'm sorry about this the corticospinal pathway so we still have some input from the brain onto that area but it can it is somewhat just so there's an extra I guess a level of separation from the the cortex so that's why plasticity wouldn't affect it so much that's why that neuroplastic training wouldn't affect it so much the the main apparatus of that system is not located within the brain so it's within the brain stem so separate to the influence of the neuroplastic effects of all these other things okay and so they've they've arrived at that the the motor cortex training that's that TNT what does that acronym stand for yeah and the tendon neuroplastic training yeah sorry um I wrote it down I forgot it so they arrived at that so using the metronome like the first of all how did they arrive at that to know like this is how we're going to train the motor cortex and then with the reticular spinal pathway you're thinking like self-paced training is the thing but how do you arrive at that you know are there are there are there other modes of training that you would maybe you're speculating of like could we instead of the metronome what else could you do from motor cortex instead of the self-paced is there something else you could do for a particular spinal yeah yeah no completely about and really really important that yeah we would question how how I arrived at that I'm always looking for I guess I'm always looking at the least Sharon I'm always thinking about other ways we could potentially you know target the known deficit that spinal inhibition so with the tendon neuroplastic training that was arrived at it was based on the the Rio work back in I think 2016ish so about a decade ago what they they did is that group they looked at a few things in the same lab I use at the moment that was here at Monash and they they looked at people with patellar tendinopathy and and people without tendonopathy and they looked at the nervous system and they used transcranial magnetic stimulation like I use and they built what we call the response curve so they just looked at so amping up more and more of that magnetic pulse and what does the brain do in response to that the issue was only looked at so that corticospinal neuron level they didn't look at spinal inhibition and they found there was some alteration but they didn't localize or cortical inhibition in the first place but they also didn't measure the entirety of the pathway and the issue with that is force output is the so the net outcome of the whole pathway you need to look at all of the components if you're going to draw any conclusions about what's influencing the output so there were some big big gaps in terms of what they hadn't looked at. The other thing they did is they got people to do the isometrics. So that was where the isometrics for acute pain relief were born. They did look at cortical inhibition at that point. But they only looked in, they had the seven people with patellar tenopathy. That did isometrics for pain relief and then isotonics for pain relief. And they measured pain change and they looked at the change in the cortical inhibition. They found cortical inhibition reduced after the isometrics. But that's expected. Any time you do an exercise intervention, there is going to be some change to cortical inhibition in the acute sense. That's expected. That's not a shock. The issue there was that that was then used to say, well, okay, we've got cortical inhibition because we've changed it with this intervention. Therefore, it must have been maldaptive. That didn't necessarily show it was maldaptive. It was just a change with exercise. So therefore, if we've got cortical inhibition, what can we do about it? We should do some neuroplasticity training. And that was just based on the broader neuroscience literature. And that's where tender neuroplastic training was born. It was a more of a theory as opposed to a tested intervention. I don't want to misspeak. I don't know that. I'm not aware of any trials where it's actually been put into practice. That specific intervention that utilizes the metronome, that specifically isolates the effect of the metronome in tendinopathy compared to self-paced in patellar tendinopathy. But more theoretical. How I landed on the self-paced. Well, given my PhD where we looked at the different levels of the motor pathway and we worked out, well, spinal inhibition is affected. It stems down to sort of that understanding of neuroscience and the neurophysiology of the motor pathways. And this work of, I should give full credit. It's Jonas Akalu, was the author of that work I've spoke to before, where they looked at the self-paced versus the metronome-paced rehab. Importantly, with the self-paced work, through our knowledge of motor neurophysiology and what activating that particular spinal pathway would achieve. It would target the spinal level. Now, we haven't tested that in a formal sense yet. That's something that probably a few steps back from. You've got to work your way up to these things. But the theory stacks up fairly well. But I should really preface that it's theory. And if we were looking at other interventions, there's likely other interventions that could also target spinal inhibition. Something else we've been able to demonstrate is what could be driving that spinal inhibition. So it's all good and well to say we've got spinal inhibition. That's affecting false output. But why do we have it? Earlier this year, we published a paper, and it was a secondary analysis of some of my PhD work. And we demonstrated that it was increased activity of the pain system, that pain pathway, was linked to greater spinal inhibition. So in people that had enhanced pain system signaling, so they were talking before about the sensitization, they had greater spinal inhibition, and that was linked to false deficits. So before we used to think, when you reflect on it, it's quite an interesting thing, but we used to think patellotensinopathy, the mechanisms driving functional impairments of reduced force, where really you need compared to other conditions. We used to think I was cortical inhibition, and the rest of the pathway seems fine. But it's actually quite similar to a lot of other knee-based conditions. So what's happening, it appears to be much like arthrogenic muscle inhibition or AMI. So AMI is sort of well known in patello femoral pain after ACL reconstruction. It's one of the main mechanisms at blocks of maximal force output, knee osteoarthritis, and a lot of these conditions. So what happens there is you have pain going up towards the brain, and as it goes up, as it passes sort of the spinal level, it activates those nerves I was talking about before, which then sort of make it harder for the motor signal going back down. So they might be activating, they might be the pain system might be the clue, it's potentially activating the nerves that are blocking that signal from coming down a strong at the spinal level. So AMI. Yes, yeah. Okay, so the techniques for people with AMI are. Yeah. You could use similar ones then for patellar tendonopathy. Potentially, potentially. So it's a space that again needs to be explored, and where the first group to suggest AMI and patellar tendonopathy, so it's really, really early on. We could lean on that literature, and I think it's worth looking closer at it, for sure. So yeah, potentially, potentially. So you'd be looking at what they use in those populations. It's interesting when you look at what could work there, but a lot of it is targeting that. It's either targeting, so I'm trying to enhance the signaling of the motor pathway at that level, so I'm trying to boost the activity of the muscle, neuromuscular electrical stimulation, that type of pathway, that type of approach. Alternatively, it could be trying to tackle that nosy-ceptive, so the pain signaling, so looking at. That's more your tens type approach, which. If you'd asked me five years ago if I'd be recommending tens for tendonopathy, I would have laughed, but maybe there's a bit in that, maybe. It seems like a lot of that comes from swelling, right? The AMI swelling? Is it even from range of motion deficits, or is it mainly swelling? What is it from when you post ECL? Yeah, so it predominantly, it's still nosy-ception, so still the pain signaling. So if you pick up up the term after a genic, so we're talking about the joint surface, and that's. So we've got really dense sort of pain of distribution through the joint surface. Now, in this is the difference, so tendonopathy, we're not talking about the joint surface, we're talking about the tendon, and the surrounding tissue that would be producing the nosy-cept of the pain. So potentially we have to come up with a slightly different framing, but quadriceps muscle inhibition might be another way to frame it, or after a genic-like muscle inhibition might be the way to frame it. So essentially we're looking at something that's setting off those sensory nerves, the pain nerves. Yeah, that would be the way to frame it. Okay, so this idea, this cortical spinal is more important for back more of an upper body thing. So, yeah, when you look at. Yeah, okay, when you look at rehab of upper body tendons versus lower body tendons, yeah, anyways, what are you differences in a rehab? Yeah, potentially, potentially. And this is where. You're really important that we're viewing these tendal fatigue conditions as being distinct. So, yeah, quite possibly if we think. We're in that corticospinal pathway in upper limb tendinopthes where is the deficit, where is motor, pathway, activity, effected if it is affected. I'm less across the literature in the upper limb in a definitive sense. Up the leave in lateral elbow, tendinopthes, so tendinopthes, there's some evidence of cortical inhibition. So potentially still targeting cortical inhibition is a good idea, so still using the metronome. Another thing I guess I should flag there is Achilles tendinopthes compared to Patela. So, there's differences. There are differences in that motor pathway and what's going on. Gabriel's work, so he demonstrated there was cortical inhibition, sort of elevated cortical inhibition in Achilles tendinopthes. And I guess the other thing to flag there is we don't have the full knowledge of that pathway as well, so we haven't looked at the spinal level in a great level of detail in Achilles tendinopthes. There's some gaps there for our understanding, but at a minimum we know cortical inhibition is higher in Achilles tendinopthes. So in theory the metronome could still be a good intervention there, the metronome based training in Achilles. So just sort of highlights the fact that we probably should be looking at these conditions as being their own entity, Patela tendinopthes, self-paced Achilles may be metronome. Yeah, you can carry that. Even though you said this whole strength and power thing is like this particular spinal and that's what I would be thinking with the calves and the Achilles, but there is this cortical. Yeah, so we're still looking at where the, I guess where the neural deafness is. Corticospinal pathway acybilia will always matter, irrespective of the body region as just the reticular spinal pathway seems to be so enhanced in terms of its importance to the lower limb. So plays a great role. a role relative to the ophthalm. Okay, one more thing before we go on to more with the patellar and Achilles, but so I don't know what organization, they have these three components of like pain, musculoskeletal pain, the noseyplastic, noseyceptive, and then neuropathic, and neuropathic, I guess you look at the definition and it's like disease or something with the nerves, but then there was that one paper, I think it was last year on, I forget the title, but it was on neuropathic pain and I believe it was Achilles tendonopathy, so they were talking about this nerve in growth and kind of these changes to nerves. Anyways, you have any thoughts on this, like do we have this, when it comes to pain, do we have this neuropathic type of response? Yeah, I don't know necessarily that it's neuropathic, so neuropathic pain, I guess one of the defining characteristics is that it's sort of very very constant, sort of unrelenting, the I guess the characteristics as well, being sort of, yeah, when we look at nerve pain per se, it's sort of disease of tendon lesioning of tendon, sorry, of nerve, yeah, so you're thinking sort of that sharp, so electrical type pain, these sorts of characteristics, so that's not typical of tendonopathy, but with some of the main outcome measures that we use for neuropathic pain, they can still detect certain changes that are somewhat consistent with our sensitization states, and just so potentially there's a little bit in that that there might be some sub-element sort of picked up in our, with those outcome measures, I think the pain detect is the main outcome we use there to detect neuropathic pain, and I guess we're also considering there will be individuals that there might be multiple drivers behind their pain, different things happening, with the nerve in growth, so that's definitely an arm of research in tendonopathy, I believe there is a bit of substance behind that concept of, we do have increased nerve growth within the tendon, so we've got a greater range of, greater volume of nocyceptives to produce more pain, so naturally if you've got more nerves to produce more sensation, you're going to get more sensation, whatever that sensation might be, so that's definitely something that I, when I'm talking in our trials, people with tendonopathy, with patellar tendonopathy, that's something I touch on, the fact that it makes sense that you're going to have more pain, elevated pain, because you've got greater apparatus to produce that pain in the first place, so yeah, that's definitely something that we need to consider. I guess the other thing to consider as well is, and this is where, I don't know if you've come across the work of Neil Miller before, over in the UK, he's, I'd love to spend some time in his brain, he's just such a switched on, guy, and he's done some really, really cool work in tendonopathy, and looking particular, particularly at that sort of molecular level, what's going on, and if you look at the, what's happening at a sort of chemical level around the tendon, it's super, super interesting in that, it's this self-sustaining loop where those nocyceptives, the pain nerves, at the tendon, they, when they're activated, they release certain chemical substance P, but yeah, this certain chemical and CGRP, they release that, what that then does, that reactivates that same nocyceptive, so it just keeps firing in this loop, it's, it's cruel, it's really cruel, but at a, at a chemical level, it's sort of this self-sustaining loop, so we need, I think we need to move a little bit away from our traditional understanding of pain and start to consider this idea of, that's molecular inflammation, you refer to it as, and so there might be these further definitions that can be sub probed in future. Yeah, okay. All right, you said earlier, because I was trying to, I was like conflating the two, you were talking about the, the pain, and then I was talking about the motor system, but you're saying like there's, there's probably a lineup with the pain, the pain system and the motor system are two separate things, but they also have this kind of like, they're involved together overlap. Yeah, could you go more into that? What are you, what are you thinking? Because like I would, I get what you're getting at that, like they're, yeah, the two different systems, but it would seem like someone who has a patellar chronic patellar tendon pain, they're going to be seeing these, these deficits and, and strength, which would be like the motor output is going to be much worse, probably because of that sustained pain state, but this whole thing of like the, how they're different, maybe like practically, what does that mean? Yeah, it's, I think it's, it's, it's an interesting area. It's picking apart how they relate to each other, because they are related. They're going to, there's going to be interaction there. Yeah, and that, that was that, that paper I was talking about before the fact that we, we had a closer look at spinal motor inhibition and the interaction there with our, our, our sub pain signaling and we found that that, that, that was a, an intersection that was a point where they, they did interact. There, there would be an, an argument that could also occur at the, yeah, the brain level. So, you know, produce, produce pain, pain being an, an experience, you know, you get that signaling up to the brain, produces, pain for you to experience. You then do have some, some shared inputs from the somatosensory cortex, which is the area that, you know, is primarily response for producing, producing pain in the motor cortex. So, there can be some interaction at that level, and certainly in, um, AMI, I mentioned that term AMI before, as more time passes, there can be greater interaction at that brain level as well. So, um, if you've got, say, central sensitization, amplification of, of pain, um, you can have greater communication between the area of the brain that produces the pain and the area of the brain that produces motor output. So, there's some, some interaction with, but we're still mapping exactly how they interact, and at this stage, the only thing I could concretely speak to is the fact that the, at a spinal level, it does appear to be some interaction in, in patellar tendonopathy. Eoretically, you can make a case for elsewhere as well there. Yeah. Okay. So, this, you said, with patellar tendonopathy, that main deficit there, yeah, the big one is the max, maximal strength. Um, I want to go on to Achilles, like, how does all this, and you kind of touched on it with the Achilles, you had that kind of side, the cortical inhibition is probably a part of it. But, uh, outside of that, everything we've talked about, um, with the patellar tendon, patellar tendonopathy, all of this, does it pertain to Achilles tendon as well? Um, I, I think when I talked to Gabe, he was talking about the whole, like, the soleus deficit, not being a thing across the board, but like lateral gastroc being there. And then even like, maximal strength, maybe as questionable, but endurance is one thing where it was a big deficit. I could be wrong, misremembering. But yeah, anyways, with Achilles tendonopathy, how does all of this, your findings relate to the Achilles? Yeah. And this is where, um, yeah, I'll, I'll be up front, you know, the PhD and my research today, I've done some work in Achilles, predominantly, Patelus. So this is where I'm, I'm more digesting literature and, and trying to engage with literature as well. Um, there's some really, really interesting concepts that have connotations, or have implications, um, for how motor pathway changes would manifest. So I, I, I agree with, with Gabe and, and that, that, that idea that muscular endurance, so sub-maximal force production seems to be, um, seems to be more the problem as opposed to max strength output. Um, so we've got some really good literature, a systematic review I was involved in, we've fat met lead by fat methani, a few years back. We looked at Achilles tendonopathy functional outputs and, um, strength, max, strength output wasn't consistently affected. It's, there was some individual examples, but when you sum all that, that data together, and there was a lot of variability in how it was measured and that might matter as well. Um, but overall max force output didn't seem to be affected. What was affected was muscular endurance. Um, so if we're leaning that way and thinking okay, muscular endurance sub-maximal force output, we can start to think about how, how the calf works. So we've got the three muscles of the calf, medial lateral, head up the gastroc in the soleus, or how, how do you say it over there? It's soleus. Yeah, soleus. Yeah. Um, so we've got these three muscles. Now, how they activate, how they function is really important because it differs to the quads. So at the quads, all the quads muscles seem to fire together. We've got this, this idea that it's called common synaptic inputs. So it's this idea that all those peripheral nerves I was talking about before that the spinal cord puts on to that communicates with. They all seem to switch on together. So we can produce really good max force output quads. If the muscles are switching on together, concurrently, um, naturally going to be able to produce more force because all the muscles are contributing at the same time. Um, and it makes sense for the quads because for quads, if you think about how we're going to use them, the extensors, it's going to be more power-based work. You're thinking about the jumping athlete, um, so producing more force, jumping, um, squatting, uh, or getting back got from us. a seed of precision, et cetera, et cetera. Whereas when you look at the CAF, the difference area is the CAF is more important to emulation mobility. So walking, running, sub-maximal force production, we don't have that same common synaptic input for the CAF. So what happens there, instead, is particularly when we're running, the SLEES seems to be the workhorse. It's active throughout. It switches on, and it just runs its own race. And then we have this sort of synchronization between the medial and the lateral head of the gastroc. So the medial head switched on first, and as it starts to fatigue, then the lateral head kicks in, and so picks up the slack. And then I'd imagine there'd be a cycling effect from that point. We don't really know beyond that point, but it'd be likely as the lateral head starts to fatigue, medial kicks back in, and so on, and so forth. So naturally, then, if we've got altered motor drive coming down, it's probably going to be more isolated to one of the three muscles, because we don't have that common activation route. And this is where Gabrielle's work is really interesting, because he picks up the lateral head of the gastroc. There seems to be some deficits there in terms of how it switches on relative to the other muscles. And it probably checks out, it sort of fits quite nicely with that systematic review that we ran, where if it's muscular endurance, we're thinking, well, when you start doing that submaximal task, the latest runs that's own race, medial head, it's doing its work, it starts fatigue, and then if the lateral head was kicking into gear, we'd be able to do more work. But if it doesn't kick in, we're going to see that submaximal force is going to peter out at that point. Whereas if it's about that maximal force output, it's only going to be one of the heads raven, all of it affected. So it kind of makes sense. It all fits quite nicely. Mm-hmm. Yeah, yeah. OK. The other thing I wanted to get into was the back. You've kind of talked about the study already, the isometrics for patellar tendon pain. And then how it was taken, and then like, this is going to-- yeah, I mean, people got to the point where it's like, I mean, you talk to the average person, and they think it's the key for patellar tendon pain relief. And then they even have that number of 45 minutes. It'll last for 45 minutes, the pain decrease. I don't know if that was in that study or not. And that's always been so dumb for me, because I'm like, what happens to have 46 minutes in? Your pain's back. Like, come on, this 45-minute window. But anyways, what have you made of this, getting into the patellar tendon, and then this whole isometrics are going to be the thing for pain relief. Yeah, what have you found? Yeah, it's interesting, because it just has stuck, hasn't it? It's this idea that isometrics are awesome for pain relief. They can use it. You can bank on it. It's going to be amazing. But it's probably not. So yeah, no, it's based on that original work, the RIO work, 2016 around that range where they had the seven individuals. They did five by 45 seconds of isometrics at a relatively high intensity. I think you're in that 75% of max isometric force. And they all got traumatic improvement in pain. It went from like a seven out of 10 to a zero for all of them. So naturally, then everyone jumped on board and used isometrics for pain. Patellar Achilles, everything, any condition-- I've seen clinically it's been used for everything under the sun, every condition. However, there have been multiple studies that have retreated that intervention, including in patellar tenopathy, but also Achilles, multiple other body sites as well. And the results are much, much, much more modest and variable. So in Achilles, tenopathy-- I don't know that it was significant, but there was actually an increasing pain on average as opposed to a decrease. Patellar tenopathy, it was the Holden group. I think they're in the US, possibly. They found that, yeah, much, much more modest and hugely variable response with isometrics. So some people did get better. Some people got no change, and some people got worse. And that seems to be the trend across the board irrespective of which site it is tested out in terms of tenopathy. And really interesting with the Holden work as well, they also looked at an isotonic intervention. And it was much the same again. So much the same as the isometric where some people got better, some people no change, some people got worse. So this idea that we could use isometrics as a cure-all for acute pain. Yeah, I think that one's been disproven pretty well at this point. What that response to pain is useful for, and this is something I think we're just starting to get into now, in tenopathy, but it's been done really well in some other musk conditions and persistent pain conditions is it might be a really good assessment tool for us. It doesn't need to be isometrics necessarily. We've seen already that response to isotonics and isometrics is comparable. And you can chuck a ruby exercise in there as well for that response as well. But there's been some work. I think it was the Lemley was the author back in the mid teens. They looked at our more laboratory-based tests that we use to work out if people have signs of sensitization. So they're called they're endogenous pain profile. So whether they're geared towards pain going through the roof or not, they found that the acute response to exercise corresponds with those lab tests that we have. So there's a nice connection there. They utilize some of the same pathways to produce this reduction in pain if you are prone to a reduction in pain. So we could in theory use these tests to gain a window of insight for what the likely pain profile of the person in front of us is. So we might be able to determine why are these tests? Do you see pain reduction? Do they get more pain? Yeah. Whether or not they're going to be in that sort of the heightened pain group. I guess the implications of being in that heightened pain group and this still has to play out in the literature in tendinopathy, but it might be that in time we can give them alternate or adjunct interventions beyond our usual rehab. And that's Kirsty Bannister is a brilliant researcher. US as well, I think potentially. She's got some good researchers over there. And she's been big on identifying this variability in pain profile and using it as a tool for precision intervention. So sort of the holy grail in rehab, but this idea that we can individualize people's rehab down to a final level based on a few key markets. And one of those would likely be, do they have these kinds of changes to their pain system or not? So it could be a really good tool there. Yeah, okay, yeah. Yeah, okay, it reminds me of Lauren Pringles. He has the intratent and the pressure paper. A bunch of them in his PhD is like about five, seven studies or something like that in it. But I'm going to do a podcast with him soon, but it reminds me of that because I've had a conversation with him and I've had some people that do the isometrics and immediate pain relief, you know, they feel amazing. But it's like, I'm going to say that's like 10% of people, maybe 20%, you know, because it's not like that for everyone. And I wonder if that's like an intratentious pressure type thing is like, maybe are we getting some of the fluid out of the tendon is maybe the pain system, maybe there's something with the nose receptors that are happening, maybe the tendon doesn't like being in gorge with this fluid. Yeah, but then generally I say, people come to me all the time. Should I do isometrics? Like, yesterday I just had a guy who did my paternal tendon rehab. He's back 100% and is like, do I still do isometrics before I play basketball? And I'm always like, if you want to go ahead, but otherwise you could just warm up, just go and do a general warm up. And if you have some pain, you're probably going to feel better after a general warm up. But I've always had this and I want to ask you, if there's any like validity to this, because when we talk about these people with the tendon pain and then they have this deficit in the maximal force of their quadriceps, or their knee extensors, I guess would be all of them, but the quadriceps in the main, the force producer there. In the strength world, we have this idea of potentiation, doing something and seeing an immediate benefit or maybe activation, quote unquote, activation and activating a muscle. Is there any validity to like, okay, someone has a history of paternal tendon pain, we kind of are thinking that they have this problem with their quads, they're not working right, they're not activating properly. If they did something like an isometric beforehand, would that potentially be better for them when they play, because now their quads are more active, or is that just like reductionist and super? - No, no, no, that's completely valid. I touched on, I think I sort of grazed over it earlier, but the idea that, yeah, I was talking about isometrics and how we get a reduction to cortical inhibition with them, but that'd be expected across activity, it could be isometrics, it could be isotites, it could be whatever, but movement. Yeah, so as soon as you engage in activity, there is going to be a response from the nervous system and it would be along the lines of potentiation. it's the idea that you're waking up the nervous system more or less. The reticulospinal pathways are also going to, depending on if it's lowlym, in particular, you expect a greater response there, but you're engaging those pathways so they're going to get a bit more excitable, and that's going to mean you can produce more force. So for sure, absolutely. But do you think there's anything special with asymmetrics versus just general activity? I don't think so. No, at this stage, it doesn't seem to be the case, particularly if we, yeah. I guess if you look at it from a hard core neurofuse perspective, the more specific the task is to what the performance is going to be afterwards, the better, because there's going to be, you're going to access neurons, you're using those neurons, creating greater cybilin neurons that are corresponding with the muscle group and a task that you're trying to produce. So we activate neurons at a task and a muscle level. So it's not just, if I do a knee extension movement, I'm not going to access those neurons the same if it was knee extension while jumping compared to knee extension in sitting. So we engage neurons in a different way. It's quite a flexible network. It's really, really complicated as something that I'm trying to get my head around a bit. But essentially, the more specific the movement is that you're warming up with for the task that follows afterwards, the more likely you are to get the greatest sort of warming effect in the nervous system. Yeah, okay. Okay, this, I got maybe a couple more questions. The, you talked about the calves and the quad, like the quads all firing together in the calves, you can have this lateral gastroc deficits. When it comes to patellar tendon opathy, like we have these anterior fascicles and then I was, there was some research that was saying it was mainly like rectus femoris running over quad tendon and then it's turning into the anterior fascicles. Then you have the posterior fascicles that are just the patellar to the tibia. When it comes to like the muscle, so like the muscle deficit in the quads, you know, like the VMO is a big thing for all. You have a smaller VMO. We need to build the VMO and then we're kind of like, well, they all activate together. Is there anything you've seen with like, are there, are there certain heads of the quads that are like lose hypertrophy or lose their, their potential? Can you even measure like force output of a certain muscle or, anyways, is there any deficits to any of those quad heads with patellar tendon opathy or not? Yeah, I couldn't, couldn't speak to anything in like specifically, I couldn't, couldn't raise any literature or anything like that. I guess from a, again, from a theory perspective, this is where it's, yeah, with that common synaptic input, the fact that if all these muscles are firing together, you would expect effects, if it were say a nervous system, alteration sort of model, you'd expect it to be fairly global across them. It's going to be, if you've got inhibition of one, you've got inhibition of all the, at the moment, we're looking a bit more, so it's, I might be able to answer that question better in a few years time. At the moment, we're looking at the motor unit firing of VMO and Vasta Slahralis, so I'll have greater insight. Give me, get me back on in a few years time and I'll be able to speak to that, but it hasn't been picked apart. I think this is where there's a little bit of a lag in some respects with patellar tendon opathy research relative to Achilles. So I think, yeah, we'll have more answers for you soon on that, but my, I'm anticipating that the theory stacks up that it likely be an effect across all of the muscles in a fairly equivocal manner. All right, based on that, what is, what are you working on right now? What is your newest, your newest, maybe thing that's exciting to you and the research field or what are you, what are you coming up with next? Yeah, yeah, no, we just launched a troll in the last few weeks, which I'm, I'm really excited about. So we're, we, so PhD was very cross-sectional, you know, what is going on? What's also more or less? Now we're going that next step and looking at what actually changes we've rehab, who responds, who doesn't respond, and why might that be? So this is, it's a, it's a big question. Is it definitely a very ambitious question? There's one that I think we, we need to have a close look at. So we, with, with rehab at the moment, there's an infertility not the, if you look at the literature, the, the breeder trial was sort of the most recent, sort of gold standard rehab, depending on how you determine the sort of threshold for minimally, clinically important difference, you know, improvement if it's a percentage or a raw number, it's anywhere between 10% to 40% of people didn't achieve sort of the, the cutoff for what would be viewed as being minimally important from a clinical perspective. So there's this large portion of people that aren't getting better with rehab, despite it being so our gold standard. So we thought, well, some people are getting better, some people aren't, and we don't know why that is. Can we start to profile these people in a bit more detail and try to pick apart who's responding. And, and when we know more about who doesn't, we might be able to design more important interventions. So we're looking at nervous system changes in these people from a motor, pain perspective, looking at a whole heap of psych things, we're looking at function as well, adherence, of course, or these sorts of things. So yeah, we're really excited about that. The motor unit side of things as well. So it's a bit of a, we're trying to capture these people as best we can and track them as best we can so that we can see what actually changes. And it might be that we've leaned on a conclusion of, we don't know, but at least we'll be able to rule a few things out, but I'm hopeful that something in there, and we've got a few hypotheses, but hopefully something in there gives us a better clue for why people, some people do get better and why others don't, so we can help those that don't a bit more. Yeah, all right. Okay, so you have, you're online, you have an Instagram page, you have this 10 and up the course online that people can go through. Anyways, tell me, yeah, tell me about these things. Yeah, where people maybe, where people can contact you as well. Yeah, yeah. So it's a bit of a, yeah, side arc to the, so I've got the research stuff. I do it in my hatch, but separate to that, I'm, yeah, I've got the 10 and up the circuit breaker, find me on Instagram, and I've, yeah, I've got a course I offer. It's, so for those, I guess, I could do it abroad as well. So it can run, run courses online and whatnot, but I've got a self-recorded, self-paced course that people can work through, and what is it? So the neurofiz informed approach to rehab. So I lean on the research I've done, and also just picking a part of the literature to, so question what we're doing with rehab and try to offer a bit more of an individualized, yet neuroscience informed rehab approach. So I go through all the pain thing, the pain side of things that I was touching on. I go through all the, the motor side of things as well and offer some strategies that are a bit more targeted, but also methods to try to measure as best we can what's going on. Yeah, as well. If we, we're good with our assessment, we've got these sort of, for example, we've got these known deficits in Achilles and Patel attendant Opti. I offer ways that we can measure them so that then you can profile a person in front of you and then go about trying to address it with a really smart rehab that actually factors in the neuroscience as well. So it actually makes sense. Do you have like extensions with the metronome in there? I might talk about the metronome a bit. Metronome lives for Achilles, but the leg extension machine worth it's absolute white and gold. But I, you probably predicted on suggesting the self-paced leg extensions in that, that rehab. Yeah, okay. All right, Pat, we got your, your Instagram pages is new. We got to get you some more followers on there. I appreciate that. Your content is, I mean, I'm always looking for new, new ideas and new, new content. And I came across your page and it was like, I have not seen people post this type of stuff. So yeah, it's really interesting. Thanks for coming out, man. This has been fun. No, awesome. Thanks for having me.