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On today's episode, healing chronic scar tissue in tendons with Keith Barr. Welcome to the only podcast delivering and deciphering the latest running research to help you run smarter. My name is Brodie. I'm an online physiotherapist treating runners all over the world, but I'm also an advert runner who, just like you, have been through vicious injury cycles and when searching for answers struggled to decipher between common... myths and real evidence-based guidance. But this podcast is changing that. So join me as a run smarter scholar and raise your running IQ so we can break through the injury cycles and achieve running feats you never thought possible. I just had an extremely fascinating conversation with Keith Barr, who is at the University of California, Davis in the Department of Neurobiology, Physiology and Behaviour. And I need to start changing how I talk about tendons, because after chatting with Keith, he just gave me a masterclass in the cutting edge research for tendons. He is... talking about tissue engineering, which we're gonna talk about, he is essentially growing tendons and ligaments outside of the body and then putting them through certain stresses and seeing how they behave and how they adapt. And for a long time, I have had this understanding of if a tendinopathy becomes chronic and is mismanaged for months and months and years, there forms some portion of the tendon that becomes degenerative, that's like scar tissue kind of appearance, the tendon collagen becomes quite disorganized. And if you leave that to be disorganized long enough, and if it gets worse and worse, that tissue damage becomes permanent. And our goal is to treat everything else around it, the surrounding healthy tendon. is what we're aiming for, is what we're getting stronger and adapting. And we have this analogy of, you don't treat the hole in the donut, you treat the donut. Don't treat the hole, which is the degenerative scar tissue portion, treat everything else around it. And it builds up the capacity, symptoms start to settle down. And now you have this strong resilient tendon that picks up the slack of the degenerative portion. And the scar tissue just goes along for a free ride and settles down because we're no longer putting load through it. But Keith has flipped the script on this. I want you to have a listen to what he has to say. Extremely knowledgeable, communicates hopefully in a way that everyday runners can understand and you don't have to have a science background. He comes up with some great analogies and some helpful tips. And I didn't really know what direction this was gonna take. He released a paper titled, Using Load to Improve Tendon Ligament Tissue Engineering and Develop Novel Treatments for Tendonopathy. I reached out to him to see if he'd come onto the podcast and chat about this paper. And this conversation took a completely different direction than I thought it would. All for the better. You're going to absolutely love this episode. Let's take it away. Keith, thank you very much for joining me on the podcast today. Absolutely. It's a great pleasure to be here. I want to get to learn more about you. So can we start off by talking through your academic background and what got you interested in attendance and in this paper that we'll discuss shortly. Yeah, sure. So I started predominantly as a muscle physiologist. So I did my PhD in muscle physiology. There we discovered kind of the mechanism, the molecular target for how your muscle responds to resistance exercise and gets bigger and stronger. And then I did a postdoctoral fellowship with a guy named John Holizy, who is, you know, thanks to him that a lot of the people that you have on your podcast do, which they do, which is to run because he was the first scientists actually show that endurance exercise was actually good for the heart. Because when he started in the 1960s, they would take chest x-rays of endurance athletes and they would have a big heart and they would take chest x-rays of people who had heart failure and they would have a big heart. So people were worried that by doing them by running a lot that you were in fact damaging or potentially damaging your heart. And he was one of the first, he was a cardiologist, but he then went into kind of He did his career as an exercise physiologist, and he showed that sure enough, when you do endurance exercise, when he had rats run, they got better mitochondria in their muscles, and they had a bigger, stronger heart. And so that was kind of the first real demonstration of that. And then when I was there, I actually found kind of the molecule that exercise was hitting in order to get those endurance adaptations. So more mitochondria, more blood flow by increasing capillaries, so that you can produce more energy. I helped him find that kind of the target of your endurance exercise, and that's a protein called PGC-1-alpha. It doesn't really matter. It just means that that's the molecule within your muscles that you're trying to turn on when you do your endurance exercise, because that's going to then give you all of the things associated with endurance adaptations, at least within the muscle component. And then, you know, I did postdoc. in Michigan where we were trying to engineer muscles. So we thought we had total control and then we were gonna just attach these to machines and they would run machines and we would be able to produce really cool robots. And the problem was that the robots always failed at the interface between the muscle and the machine. And so we had to start learning about that, how that worked in physiological systems. And so we started looking at tendons. And so, and you know, that took me then to my first position at the University of Dundee in Scotland. And there I was doing still a lot of stuff on muscle mass and strength and I was brought down to the English Institute of Sport or to British Cycling and they were saying, well, you know, we want our athletes to get stronger. And I was like, well, you got to get bigger muscles. And they said, actually, you don't because here's 10 years where the data where we have a lot stronger athletes and their muscles are getting smaller. So how does that work? And I was like, no idea. But we went back and we tried to work out what we call force transfer, which is how the motors in the muscle are actually transmitting the force to the bones to allow us to move. And that's both the connective tissue, but also the tendon. So the connective tissue within the muscle, the gristle within your stake, that's gonna be good for transmitting force. And that tendon, the tendon is absolutely essential to our ability to transmit force. And so we started looking at how the tendon worked and how we could improve it. over the last, say, 10 years, we've been doing a lot of stuff, trying to understand how exercise, nutrition, age, disease, hormones, all of these things are affecting tendon and what the outcome is for injury rate and for performance. Because the reality is that as most of your listeners understand, when you're at your best, Your tendon tends to be stiff because it can store energy and return it for free. So the energy it takes to run is less. But when your tendon is stiff, yeah, your performance is high, but when your tendon is stiffer, then your muscle is strong. That's when you pull the muscle associated with it. And so now what we have is we have this balance where we have to keep the tendon stiff to have high performance, but not so stiff that you're going to get injured. And that's really where I'm sure a lot of your listeners are. That's where most professional athletes are. is trying to figure out that, that razor's edge where you can get exactly the stiffness you need to perform well, but not so much stiffness that you're going to pull a muscle and that's what we've been working on for the last 10 years. The paper was titled using load to improve tendon, ligament, tissue engineering and develop novel treatments for tendinopathy. I think tissue engineering, this is like the first time I've kind of heard of that term, would you mind explaining exactly what that means? Yeah. So, so what we do is we. We. try and make the tissue ourselves. All right, and so what a lot of scientists try and do is they try and understand, say muscle, or try and understand the heart, or try and understand it for us, tendons and ligaments. And the way that you can know whether you really understand it is if you can make it yourself. And my wife always tells me that she's a much better tissue engineer than me because she made our daughter and I can just make a little ligament in a dish. And she's right. because we don't really understand all the things that have evolutionarily happened over hundreds of thousands of years. But what we can do and what we do in tissue engineering is we provide kind of the ideal situation for cells to produce the tissue that they came from. And so what we do, we're in Davis, California, nobody knows where it is, it's in Northern California. And it's really nice because we're right between. the Sierra Mountains, where we have Tahoe and some of the best skiing in the United States, and the ocean, which is an hour in the other direction, San Francisco. And so what we have at this time of year, we just had big rain here in Davis last week, which means that there's been huge snow up in Tahoe. So everybody's coming up from down in San Francisco, they're gonna go up and ski, they're going up from this area, and a lot of them are gonna damage their ACL. they're gonna come down the mountain, get it repaired. And when they do, the surgeons call us up and say, we've got a surgery. We go and we get the remnants of their ACL that they ruptured. And we isolate all the little cells from that. So that's a human ACL cells. And then what we do is we put them into a dish and in that dish, we give them the same matrix or the same kind of environment that they have within a scar. And so what you do is we give them fibrin gel, which is the same thing you and I make when we make a scab. When we're trying to stop blood from oozing out of our finger, our body creates a blood clot. And that blood clot is this little protein that we call, or this little gel that we call a fibrin gel. So all we do is we put our ACL cells into a fibrin gel. That's the same environment that they had when they were in utero. So when you're inside your mom, you didn't really start with perfect ligaments. What you started with was a bunch of cells within this jelly-like material, and that's all we do outside the body. And then the trick is that we put two little calcium phosphate cements on either end. Just like our bones are made of calcium phosphate, we make a little cement that's made of calcium phosphate. And when we do that, now, as the cells contract on the gel and they're gonna form, you know, they're gonna pull it in. Now they're gonna form this linear tissue between our two little bone pieces. And because they're ACL cells, they're like, hey, look at this, we are in a tension. We know the tension, the line of tension is going this way. We're ACL cells, what do we do? We make collagen and we're gonna put it into alignment with the line of tension. And so they make over two to three weeks, they can make these really strong tissues outside of the body in a little. in a little incubator that we have in our laboratory. And then what we can do at any point in time is we can mechanically test them. We can pull on them until they break. And so everybody who's ruptured in ACL just flinched when I said that because basically it's the same thing. How much load does it take us to tear your ACL? And now what we've got is from every person that comes in and donates their cells to us, we can make almost a thousand little ligaments that we can then go in and say, I wonder what happens when we add you know, whatever to it. And then we have these really cool things, which I've got a bunch of engineers in the lab. They love to build machines. They build a machine that we can actually exercise our ligaments in a dish. And so now what we can do is we can figure out what's the best type of exercise for a tendon or a ligament. And that's where we started to revolutionize how we started to think about how these tissues respond to load. I guess. Tendons would be slightly different in the way that it goes from bone into muscle rather than like an ACL, which goes from bone to bone. How have you worked your way around that problem? So, so functionally, the tissue that goes between the tendon or the muscle in the bone or the bone in the bone, we call them different things. So when a muscle goes through a structure to a bone, that structure it goes through is called a tendon. And then when you have two bones that are attached, it's called a ligament. Functionally, the tissue, the tendon or ligament, looks pretty much exactly the same on a cellular level. They behave slightly differently. And the reason they behave slightly differently is one of them attaches two stiff structures together, two bones. The other one attaches a stretchy thing to a stiff thing. And that's the tendon. And so what that means is that our tendons actually are what we call a variable mechanical tissue. And so that's a little bit, that's a lot of words that people maybe aren't comfortable with. But if I'm trying to attach something that's stretchy to something that's really hard, that interface is going to always be the point where it breaks. So evolutionarily, what our bodies did is they developed a tissue that was stiff on one end and stretchy on the other end. And that's our tendons. The difference between a tendon and a ligament isn't the proteins or the other stuff that's in there. It's that mechanically, a tendon is stiff on one end and not stiff on the other. A tendon is, or a ligament is stiff on both ends. And that's really important because when we train, what we're doing is we're changing the stiffness on the muscle end of the tendon. So when we train by running and are doing lots of plyometric moves, what happens is the stiff, that compliant or the stretchy end of the. tendon becomes a little bit stiffer progressively over time. That's why when we go and we put on, say we do our first session on the track and we're in, we're in spikes. Now what we're giving is we're giving us much stronger stimulus to that muscle end of the tendon over time. It's going to adapt by getting stiffer. But the first time we do it, it's not quite stiff enough. So we're going to get little bits of, and that's one of the reasons why we get a little bit of a more injury when we go and do that first session. We have to be really protective of the first session because that's a huge overload to that muscle end of the tendon because now what we're asking it to do is we're asking it to be a lot stiffer. And so when we first do it, it's not really ready for that. And so progressively what we're doing is we increase our high velocity movements is we're making the muscle end stiffer and that's going to help us keep that system performing at the highest possible level. But... it's also going to push us towards a muscle injury. Yeah. It'd be nice for people to know this because when you're talking about tendon stiffness, we actually want tendon stiffness because that's what helps generate a lot more force and to do so a lot more efficiently. But when someone develops say a tendinopathy and they have pain in the tendon, all of a sudden, like their movements feel really stiff. I'm thinking of like a high hamstring tendinopathy where they bend over and they feel pain, like, Oh, everything just feels so stiff. And it feels like it's different, stiffer, the more pathological that becomes and the more sensitive that tissue becomes, would you say they're two different types of stiffnesses or at least they're very different things. Because one of the things is when I feel stiffness and it doesn't even have to be a muscle injury, if I do, if I do a heavy weight training session on my legs, I'm not damaging my tendons or muscles. If I've trained up. aggressively and I just go in and I do this week's session, but I go maybe a little bit harder. I get a little bit more kind of that feeling of a little bit pain. So when I push on my, so when I like go to sit down on something now, oh yeah, it's tight or I feel sore. If I go and I push on my muscle, it doesn't actually hurt more because my muscle doesn't have pain sensors. It has a length sensor in the muscle spindle. And then on the tendons, you actually have a tension sensor. pressure that's happening in the tendon. And so if I'm gonna do something that's gonna lead to inflammation by doing something that's maybe too much too soon, now what I'm gonna do is I'm gonna have more fluid in that tendon. That more fluid is gonna be higher pressure, and so that little sensory organ in the tendon, the Golgi tendon organ, is actually going to think that I'm pulling on my muscle more than I actually am. And so my body's gonna interpret that as soreness. Okay, so that's very different. That's not really stiffness. It's telling me that, yeah, the movement is stiff, but the movement is stiff because I'm actually stimulating this sensory organ sooner because there's extra pressure around it. And so that stiffness is coming from actually just that sensory organ. The stiffness that we're talking about here is actually within the matrix itself and how either the amount of collagen, how cross-linked the collagen is or the directional orientation of the collagen. So as my muscle gets bigger, my collagen actually gets more spread out and so by definition, it becomes less stiff. As my muscle gets smaller, my collagen becomes less splayed out. It becomes a little bit tighter and so now I can transmit force easier. So that's one of the other things that happens as we train, especially when we're doing a lot of high speed, low force movements, is our muscle gets a little bit smaller, so we get a little bit more directional orientation, and so that structure is stiffer. When we feel, oh, I'm stiff today, a lot of times that's because we're getting these senses, and we're getting reflex information from our Golgi tendon organs that are saying that, oh, I'm really stiff, and it's not actually stiffness per se. And if you actually go through and we warm that tissue up, and by warming that up, what that means is pulling on the tendon and relaxing in a rhythmic fashion. What we do when we do that is we squeeze out a lot of water. And then after you do that, you're like, oh, I don't feel stiff anymore. Okay, so there's two very different things that we would sense as stiffness. The thing that we actually sense as stiffness is much less permanent. it's kind of the fluid level and the pressure around the Golgi tendon organ. What we're talking about scientifically when we say we're gonna increase stiffness progressively of the muscle end of the tendon, is we're talking about fundamental changes to the actual tissue. Makes sense. I've never really had an answer when someone asks me, why do tendons have this analgesic effect? If I do load it... in my first set and it's a little bit sore. And then my second set is a bit easier than my third set. I'm almost symptom free. Um, I just like to say, you know, tendons love load and it just, you know, it makes things feel better once it's warmed up, but, uh, the explanation of pushing out the fluid would make a lot of sense. Would that be, would there be any other mechanisms for that analgesic effect? For the analgesic effect, there's, um, and this, you know, in Australia, you have the expert in Ebony Rio for talking about this. But so that would be something more like with because you're getting feedback, obviously from these sensory organs. And that's where some of the central innovation that she talks about a lot is coming from is that the feedback is giving us feedback and then our central nervous system, which is supposed to drive force through that tendon is going to be less likely to put as much force through it. The Golgi tendon organ is it it's important for what we call the autoinhibitory reflex. So what it does is it's supposed to sense tension and when it senses a lot of tension, it actually, there's a reflex that decreases the amount of stimulation our muscle gets that's attached to that tendon. And so the result is we can't stimulate that muscle as much as we would if there was less signal from the GTO. Okay, and so what that means is there's more, if you're getting more reflex, you actually can put less force through that and the result is what you see clinically is that, oh, you know what, you're not putting as much force or depending on where you're going, you're compensating with other things because you're producing less force using that muscle. The big difference between, say, an Achilles tendon and a proximal hamstring tendon, is the Achilles tendon is a beautiful tendon. It's got, it's. unidirectional, it comes up from the bottom, and then all the muscles come in from the top, and now I can get muscle on one side, bone on the other side. And what I can get is I can get this regional variation in stiffness that's really good for preventing Achilles tendon injuries. The problem with the proximal hamstring is that the proximal hamstring is what's called an aponeurosis, which means that it's a long tendon that goes up and into the muscle, and the muscle actually inserts on it at an angle. And because it's inserting it on an angle, I don't get as much of a long tendon where I can have a stretchy part and a stiff part. I have to go pretty quickly into the stiff part. And that's why muscle pulls at the proximal hamstring are much higher than calf pulls, for example. The other thing that's really important is when we, and we've done this in animals, there's a little bit of data in humans. When we look at quadriceps muscles versus hamstring muscles, The hamstring muscle actually has about half as much dystrophin protein than the quadricep muscle. The same is true for our tibialis anterior muscle, our shin splint muscle versus our calf. So the muscles we load all the time, we get a lot of dystrophin. Dystrophin's really important in preventing muscle injury. And so one of the reasons why hamstrings and shins get more injury than our calves and our quads is because, yes, we have different tendons setup, but we also have less of the protein that's actually going to help the muscles stay healthy. Interesting. In your paper, you talk about scar formation a lot in when it comes to tendon pathology. I want to get your understanding of those and your explanation as to what's happening within the tendon once it does develop into this tendinopathy and then the formation of this scar tissue. Sure. So, so what normally happens with a tendon is we have some sort of acute injury, we're overdoing something. And it's usually because there's a lot of high jerk movements. And again, jerk is a physiological property. It's actually a property of physics. So my location is where I am. My rate of change of location is my velocity. My rate of change of velocity is my acceleration. And my rate of change of acceleration is my jerk. And we know that jerk is really damaging, because a lot of the things that we know that cause tendon problems are the things that are highest in jerk. tennis elbow, golfer's elbow, all of these types of things, there's not a lot of force in a tennis ball or a golf ball. But when I'm accelerating really fast in one direction and then there's a quick little acceleration in the other direction, that is what's gonna cause tennis elbow. If I'm doing a lot of backhands all of a sudden and I haven't done it in a while, I'm gonna get an aggravation of my tennis, of that tendon that's attaching my extensor muscles. If I'm accelerating my golf club and coming through and hitting the golf ball or a little bit on the grass below it, now I've got the kind of the, the acceleration of the ball or the grass in one direction. I'm accelerating the other. I'm going to get that in my flexor, my flexor tendons. If I'm a runner and I'm, and I'm just getting back to running and now I'm going to go at high velocity moves, or I'm going to do a bunch of running when I've been off for a while. That impact force. I'm trying to draw the gravity is pulling me down. I'm trying to drive up. I get jerk every time I hit the ground. That's where I get jerk. If I go faster, the jerk is higher because my acceleration in both directions is higher. So at those points where I have lots of that principle of jerk, now what's gonna happen is, and we can see this experimentally, if I pull really hard on something, a tendon, what's gonna happen is the collagen backbone of the tendon, is gonna denature more. And what that means is it's gonna become screwed up, to use a scientific term. And so what happens is you screw up the collagen that's supposed to be acting like the spring there. And what I do is I screw up a little bit of it. And now what happens is, now I've got a little bit of a screwed up tendon. Evolutionarily, what would have happened if that then resulted in tendon failure? is that we would have been eaten and our genes wouldn't have gotten into the next generation. So what we've evolved is we've evolved the ability to kind of protect that damaged area. And we use this, we use the healthy remaining part of the tendon to protect the injured part and in a process that we call stress shielding or it's called stress shielding. that makes up our tendon, we've got a little tear in it. And we don't want to tear it all the way through. So instead of going through that little damaged parts, all the load is going to go through the healthy part. And that's going to protect the injured part from injury, from catastrophic injury. This is what we think is causing tendinopathy and especially scar formation. And this comes from this beautiful work from a Japanese investigator called Hayashi. And what they did in his lab is they actually took a perfectly healthy patellar tendon in rabbits and they put a metal wire between the patellar, the bottom of the kneecap and the top of the shin bone. And all they did was they took the load off of that perfectly healthy tendon. And within two to four weeks, the collagen content was way down. The size of the collagen fibrils was much, much smaller. The direction was all over the place and the mechanical strength had decreased massively. He'd produced a scar from a perfectly healthy tendon. So what that tells us is that we need load to get through the tissue in order for us not to get a scar. When we stress shield, either with a piece of metal, in his case, or the healthy tissue is protecting that little area that we hurt. Now what we're gonna get is we're gonna get a scar. And what a scar is by definition is a weaker tissue. The weaker tissue doesn't get load through it because the strong tissue takes the load. The only way that I can actually fix that weak tissue is if I get load through it. And that's what our body is trying to prevent from happening. And that's why it's really hard to get rid of scars from tendons. Is this? different from someone who might've had the explanation of you have scar tissue, or if someone has a tendinopathy or some sort of pain and they say they have a therapist say, Oh, you have scar tissue that's emanating away from the tendon and is impacting your sciatic nerve or like something that's moving away from the tendon. I don't actually know if scar tissue in that matter is actually true, but that's what a lot of people are being told with that. Are we talking about two different things here? No, we're talking about the same thing. So now if you have poor quality tissue, but you wanna actually have the same overall quality. So there's two things you can control. You can control the quality or the quantity. And when the quality is low because it's not high quality tissue, it's a scar because there's not good low going through it, what your body tends to do is produce more quantity. And so it produces more, and we see this a lot of times in Achilles tendons, you'll see people who have a localized injury, you'll actually see a little bump in their Achilles. Okay, and so that is because the quality of the Achilles of the matrix of the collagen, the collagen gel that your tendon is, it's low so the strength is actually decreased. But in order to compensate for that, we've made a lot more of it. It's much more common when there's been a relatively big tear. So if you've had a relatively big injury, If you've been somebody who's had an Achilles tendon, but you didn't get it surgically repaired, you actually did it conservatively, then you're gonna get this huge amount of tissue that they make initially, or if you've had a repair, you'll get this huge rim of tissue. You'll get this big old callus, but the reason the callus is so big is because every inch of it, pound for pound, it's really, really weak. So what does your body do? Makes a lot of it, okay? So what we want in order to have a highly functional tissue is we want it to actually have high quality. We don't necessarily worry about the quantity. We want the quality to be as high as possible. One of the things that we always see in the laboratory when we do these, when we do direct measurements of tendon, when we say run an animal or we say do, we run train them for a long period of time, is we actually see that the Achilles tendon gets a little bit smaller. Collagen contents the same, so the relative collagen is higher. And what we've done is we've actually got very high quality tissue versus moderately high quality tissue. And so in a healthy tissue, if I train it, I actually improve the quality of the tendon. And so I don't need as big as tissue. When I have a scar, the quality is lower. So I'm gonna produce more. And the idea is that that's why you would get a callus or something like that. Same thing happens in the bone. When we break a bone, the first step is to make a lot of bone. lot of low quality bone. And then what happens over time is once you get load through that, then what happens is the bone reshapes itself and you get better quality bone over time. And the result is that callus goes away. Okay, the problem is that people don't get load through the scar. And really that's the fundamental component of what has to happen. Because what's happening is I have low quality, so low stiffness. tissue right beside high quality, high stiffness tissue. So everybody knows this just from personal experience. If I take a wire and I take a small piece of thread, the thread will tear really quickly, the wire wouldn't tear at all. The thread has got low stiffness, the wire has high stiffness. If I put them at the same length and I pull on both of them, the piece of... thread doesn't rupture the way that it did when I pulled on it without the wire there. That's really weird. Well, no, because it all went through the wire. Everybody knows that instinctively. We don't think about it, but that's exactly what's happening in our attendance. And so when we go to load, what's happening is all going through the strong part. It's not going through the weak part. We're going to get this scar that has no load through it, and that's going to be low quality tissue that can maybe get bigger, cause some pain because there's more pressure. All of those things are going to be what you're seeing in your patient population. Such a good analogy with that wire. No one's really been able to answer this question. And I'm wondering if it's probably impossible to answer for sure, but when someone has a scar formation with a tendinopathy, they haven't had any major ruptures. It's just been a overuse tendinopathy that's developed into something quite chronic and quite painful and really debilitating. How much of that... tendon, do you think is actually scar formation? Because you can imagine with someone in a lot of debilitating pain, they think it's like 90% of the tendon, they think it's like almost their entire tendon. If you were to put a percentage on most, you know, chronic tendinopathies, where would you place that percentage? So it all depends on the injury. We know this most from our from our athletes who are basketball players who have jumpers knee, we can actually get MRIs, we can actually see the size of the of the tenonopathic region, because you can see it on MRI, you can sometimes see it on ultrasound. And realistically, you can get up to 50% of the tendon being a whole. And that is what can happen, especially with a central tendinopathy. A central core tendinopathy is different than something that happens on the outside. Because if there's an injury on the outside of a tendon, Basically all the load goes around it, nothing goes through it, yeah, we get a scar. If you get an injury in the middle of a tendon, what happens is now, yeah, all the force goes around it, but as I pull that tendon, it has to get skinnier because it's what we call isovolumetric, which means that as I pull on it or stretch it or my muscle contracts, what happens is the strong parts are all around the core. And so as they get... stretched out, yeah, the load's going through them, but then what happens is they have to come together. Think of the finger trap toy that you had as a kid. When you'd stick your finger in the hole between all of that little mesh, you try and pull your fingers out, your fingers get stuck in there. Because as I pull it, the fibers get closer together and that holds onto your fingers. That's great for my little finger. but it's horrible for your tendon because now instead of getting tension across that area in the middle of the tendon now what happens Is it's getting compressed? And when you compress the cells in a tendon they actually start becoming more like cartilage like cells And cartilage like cells are gonna have more of the proteins that suck water into the tissue to prevent compression And so that's why we can see it on an ultrasound or an MRI because you actually have this Region where there's actually fluid within the tendon because what we've got in that center of the tendon is now it's been compressed as I've been taking, I've been stress shielding that core, but as I stress shield from tension, the strong parts come together and now I get compression of the core and I get this area where I have a little bit of fluid. And that's really what drives a lot of the long-term central core patellar tendinopathies. That's why the the injuries at the center of the tendon are much more devastating than ones that happen on the outside. Because the outside ones, yeah, all the loads going around, I'm getting a scar here on the outside, but I don't get the compression that I would do if it was in the middle and I'm getting squeezed by everybody around it. So I don't get the compressive phenotype that I would in those central cores. And so that's why the injuries to the center of the tendon are much more devastating long-term than the ones that are to the outside. Makes a lot of sense and kind of makes me think of why if someone does have proximal hamstring tendinopathy, why symptoms might vary from person to person. Cause we're, we're looking at like multiple tendons and it could affect any one of the three major tendons, but even in one given tendon, it could be on the outside, it could be in the middle. It could be like in a different portion of that tendon, which would then slightly change someone's aggravating factors or, um, you know, what makes things feel better. And there's going to be a lot of problems with the central with the proximal hamstring as well, because there's multiple muscles coming in at different angles. So there's going to be a lot more other forces there that can easily change based on one injury versus another. And so that becomes, again, it's a really difficult part of the body to, to deal with, but there are ways that you can get load through there properly and you can fix those proximal, proximal hamstring tendon. What's the hope for someone who say is in a major case of like 50% of the tendon has become a tendon opsy or scar and they're in a lot of pain in terms of like rehab for return to running return to sport, return to function, return to sitting. What's their hope in those like severe cases? Absolutely. There's there's great hope. So we've published a paper On a case study from a professional basketball player in the NBA, he had about a 50% central corpateller tendinopathy. We put him onto a program that supplemented. So he was still playing, he still played 50 to 60 NBA games. He still did his normal training. We just put in a program that supplemented that training designed really to specifically load the damaged part of that tendon. the next imaging we got was 12 months later, the hole was almost completely gone. We've got the hole was gotten so and healed. Yeah. And so we've actually got faster data where we've got a discus thrower from the from New Zealand, and he had a central core patellar tendinopathy, he was using ultrasound, so we get more frequent measures within 50 days, the hole within his central patellar tent that hole within his the center of his patellar His patellar tendon had gone bigger, stronger, more striated. So we know that this turns over, this tissue turns over pretty quickly. There's this traditional feeling that you treat the donut, not the whole. I always tell people that I'm Canadian. Canada, we have Tim Hortons. Tim Hortons, their best donut is the donut hole. So my whole thing is all about the donut hole because of my Canadian roots. And so what you just have to do is you have to change the loads and that's really what we're talking about in that paper is to how to control the load that goes through these different structures. And what we do is we use either stress relaxation of the tendon, but really what we try and do is we try and use creep. All right, so those are two physical or bio, they're bioengineering terms. So let me explain them to you and try and get them out. So tendon. When we load it quickly, it's stiffer than we load it slowly. We all know that because, you know, if you're going to try and touch your toes, what we do is we go into the movement slowly. If we're just gonna let gravity take us, we're just gonna hang there. What's gonna happen is the tendon over time is going to go through an exponential decrease in its stiffness. The strong parts of the tendon relax first. And that's why after about 10 seconds, you can reach further towards your toes. Okay, that's stress relaxation. Creep loading is basically what you did in gym class. I'm assuming you did in gym class. I had a gym teacher who was a little bit sadistic. I'm sure that most people did. They played a lot of games where you're trying to pick off the small person, but basically what you'd... what you did in gym class, one of the things that they had you do is a wall sit. Did you guys do wall sits? And we did. Yes. Yeah. So wall sit is a classic example of creep. You're not moving. You're not doing anything. You're just sitting there. Why the hell are my legs burning so much? And again, what's happening is your tendon anytime where we're keeping the tendon longer than it's normally kept. It's going to slowly relax and get less stiff. And as it does that. In the wall sit, what I have to do to maintain my position is I have to contract my muscle more and more. When I'm just reaching or stretching my quad, if I pull my foot up to my butt, yeah, my tendon is gonna get longer a little bit for a second, it's gonna get shorter because it's going to decrease in stiffness. Sorry, it's going to get longer as it decreases in stiffness, but it's not really going to have the same tension across it. When I do the wall sit, I have to use my muscle. to contract, to keep the load, so that the tendon is actually under the same load. So what happens is the tendon lengthens a lot while I do that. You can call it either stress relaxation or creep. So as that happens, now if we go back to our analogy of the wire and the thread, I'm pulling on that, at the beginning, all the load goes through the wire. But in reality, Our collagen isn't wires and threads. What it is, is it's strong collagen, and it's weak collagen. So what happens is the load goes through the strong collagen and over time that relaxes. And as it relaxes in the strong parts, what happens is it becomes less stiff than the weak part. Okay, so when I pull and I hold and I do my wall sit, or I do an isometric leg extension, or if I do an isometric lunge, What has to happen is initially when I go into that movement, all the load is going through the strongest parts of the tendon, the healthy parts. But as I hold it there, those healthy parts start to relax and they actually become less stiff than the scar. And when they become less stiff than the scar, the scar actually feels the tension of load that it hasn't been feeling because you've been running and you've been jumping and doing all those things, fast movements only. So now as I hold it for longer, load goes through that scar. And now what I get is I get the signal that those cells need in order for them to know what they're supposed to do, which is to directionally orient along the line of stretch and start producing a strong collagen matrix. And so if I use that kind of isometric contractions where I'm pulling on the tendon and I'm holding the tension, the tendon is slowly relaxing and getting longer, what I'm getting when I do that is I get a 10, I get a a signal that is more evenly dispersed across the tissue. When I move quickly, all the load goes through the strongest bits and the strong gets stronger. But none of the load goes through the weak bits. When I hold an isometric hold for longer, now what's happening is I'm getting a more equal load through all the cells. And so now what I get is I get more cells within that tendon, get the signal that would... they were loaded so more cells respond in the way that we want them to, which is to start making more collagen, to align it in a certain direction. And now what we can do is we can regenerate that, that tendon. I'm learning so much here. Um, and some of it's kind of reflecting on what's worked with rehab in the past, but other things that are like, Oh, maybe I should try this with rehab as well. Because when it comes to something like proximal hashing tendinopathy, I love assigning a deadlift to someone. And it's like eccentric, it's slow, it's heavy load if they can tolerate it. But that is extremely different to something like a kettlebell swing where it's the same movement, but explosive and powerful and that sort of thing, which would only just stimulate, like you say, those rigid healthy portions, but. I'm also thinking like, well, maybe I should spend a lot of like the tempo of the exercise that I advise is like, okay, three seconds down, two seconds up for a deadlift if it's, you know, depending on the range, but I used to think that's good time under tension, but maybe someone has a progression might, or maybe through trial and error, maybe try like a slightly longer eccentric phase. Maybe we're looking at like five seconds down, six seconds down, two seconds up, I guess, pending the weight, but what do you think on that? So, so the thing, the thing here is, is quite easy. So, so classically everybody says, Oh, you've got tenonopathy do eccentric load. Michael Kerr has shown that concentric loading is, heavy concentric is just as good as eccentric. The similarity between the two of them, you don't say do eccentric load by doing it really quickly. You say do it on a three second down, two second up. The good part of the load has nothing to do with the eccentric. It has to do with the length of the contraction. So when I hold a contraction for three seconds, I'm getting a little bit more stress relaxation. We wouldn't even do that for the first three to four weeks of if you've got a significant proximal hamstring injury, we would do isometric holds at the proximal hamstring. We would do them, we would build up to 30 second hold at a pain threshold below two out of 10 in pain. Once we've done that and we can do, we can produce good force and we can get maybe a little bit of the leg coming up. So we do this laying on the back. with one leg bent, straight leg in the other one, we're gonna increase the range of motion without getting glued by anterior tilt of the pelvis. I can get load directly through the proximal hamstring and only through the proximal hamstring using that isometric. I would use that for the first two to four weeks and then now I'm gonna come in and I'm gonna start to increase the amount of load that's going to be more of a dynamic load, so more of a isotonic load. So now I can bring in, start to bring in my light, my light deadlifts or other things that are designed to get load through the proximal hamstring. That's perfectly good. And then now I'm gonna progress then up to plyometric type of movements that are gonna get load through that. And then I'm gonna progress that way. There's a study out of Nijmegen in the Netherlands where they've done this for jumper's knee. They've used the kind of system that we talked about, which is... how we filled in the central core of that basketball player. They took a group of 150 young athletes who had anterior knee pain, patellar tenonopathy, and they did either they did standard of care, eccentric load through the patellar tendon, just like is prescribed normally, or they did the first four weeks as an isometric, basically used our four times 30 seconds with two minutes of rest of isometric load going through there. They then said, okay, once after the four weeks, then they went into the progression of the increased load through the patellar tendon. What they found is that the VISA-P score, so the pain in the patellar tendon, was much lower in the ones who did the four weeks of the isometrics. The return to play was much faster in the ones that did the isometrics for that first four-week period. So what we're trying to do when we do this is that... We have to understand that what we're programming when we program load is that we're programming velocity. So what you said there was that depending on their strength, we're gonna do a heavier, heavy, as I go heavier, my velocity goes down. As my velocity goes down, I get a little bit more stress relaxation within that, within the tendon, I get a little bit healthier move for my, for my tendon. So when I use a heavy, concentric move or a heavy slow isometric move, I'm getting a little bit of stress relaxation. When I do that isometrically, I get much more stress relaxation and that's why we see a bigger benefit from the isometric component. And then it's really about how do you progress back into the dynamic moves to get yourself back. For most people, you can do them together. So you don't have to do the exclusive four week of isometric. So what we would do with somebody who is still training but has chronic niggling pain in the hamstring or Achilles tendon or whatever, what we're going to do is after they've done their training, we're gonna do specific isometric contractions that are designed to target the area that they've got tendinopathy. So in the proximal hamstring, after I do my run, especially any kind of higher velocity run where I'm using my hamstring more, now what I've done, Remember, I've got the healthy part is shielding the weaker part. So as I've run, the healthy part has gotten tired because it's been shielding the weaker part the whole time. Now, when I go to load it, the healthy part is easier to get through because it's already tired. So if I wanted to relax, it's already tired from doing all that run that I just did. So now it's going to relax much easier. Now I can get, it's easier for me to get load through the, the injured part and start to fix it. In my basketball player, the example that I told you about or in the disc is throw that I told you, they were continuing to train at an elite level. So they're training nine times a week. We didn't take out training. We actually added in specific time to training that was designed to get load through that scar. And by doing that, what happens is the scar can start to get the signals it needs to reform and to regenerate, and we can progressively improve functionality. Let me just reiterate a little bit. So you're saying that when there is a scar formation within the tendon, if we have like a fresh tendon and we apply a quick load, it's just going to go straight through that healthy portion and totally dismiss that it's going to shield away from that scar formation. But if we have a slightly fatigued tendon and we apply load. it's going to almost access, like it's going to have more availability to go through that scar formation. Or if we take advantage of this creep loading where it's slowly being nudged into more and more load and this healthy portion starts relaxing a little bit more, then we can sort of tap into that scar formation and therefore the scar tissue itself, like those collagen fibers that are really disorganized, they can slowly start. realigning themselves, they can slowly start healing, slowly start adapting to load. And that's why you start seeing that scar tissue start becoming less and less. Yep, and it goes away eventually. Yeah. And so basically that's what our research shows quite clearly, is that when you load and you hold. So we've done a bunch of experiments where we do the exact same time under tension, either as dynamic moves or as isometric holds on a central core tendinopathy. And then we took out the little core and we actually did, we measured RNA expression. And when we did that using the isometric, the genes that we turned on were tendon genes. And we did it using the dynamic, the genes we turned on were actually cartilage genes. Because that's the difference. You basically, it's a switch. The cells themselves, can respond if you give them the right load. And if all you're giving them is really dynamic moves that are really moving quickly, then all you're going to get is, especially if you have a central core tendinopathy, but even if you have an outer tendinopathy, so an outer edge tendinopathy, what you're gonna get is you're not gonna get any load going through the scar. So it's not going to get any indication that it's a tendon. Tendons need to be under tension. they're not getting tension, they don't actually act like tendons. It's not a surprise. If I don't give the right stimulus to the cells, they're not gonna behave in the way that the other cells get. And so just like every aspect of our lives, basically there's strong individuals and weak individuals. And as most of us know, the people who do most of the stuff, they take on more of the load. And the people who are kind of just hanging around, they... They're not gonna do anything unless you step away and you say, oh, it's up to you. You've gotta take the load. Then that person will step in. Same thing happens with our scars. All right, the cells within our scars, they're not getting the signal. So what we have to do is we have to get relaxation. So everybody knows that we don't really tear our tendons kind of at the beginning of stuff. What happens is we're going into the third quarter, we're going into the end of something, and that's when we get the damage. And that's because the healthy part, the shielding part is getting tired. And so it can't shield as much anymore. And so now the likelihood of carrying that whole tenant goes way up because we can't stress shield to the same degree. That's why in all of our basketball players who are rupturing their Achilles, it's like after they've done warmup, they're in the third quarter of the game. Now that's when they get their Achilles tendon rupture. Because the shielding part of the tendon has been fatigued. It's under. It's had fatigue loading and it stretches a little bit more than it should. And now more load goes through the scar and it's not strong enough to hold it. And that's when the whole tissue fails. We take advantage of that by using submaximal, sub rupture level. When we go out and we do our training, we've decreased the stiffness of the healthy part. So now it's easier for us to get load through the unhealthy part. And that's why we do a lot of our. isometric holds after we do our training, because now what we're doing is we're actually taking advantage of the fact that you already got that part tired. So I don't have to work even as hard. So I don't have to work at these big loads with big heavy weights that you do when you're doing your deadlift on somebody who hasn't done any training beforehand. Now what it can do is I can go with a relatively low intensity isometric, and I can get great load through that injured part, and I can actually give it the stimulus that it needs. Really good stuff. Um, I'd be kicking myself over to ask this question. Um, I get asked a lot about tendon, tendinopathy is, or someone developing a tendinopathy and they say, Oh, it's because I'm getting old or, um, hormones or menopause or like that stage of life and increasing risk and that side of things. Um, is there much of a correlation there? Is there much, um, guidance for someone who is in that stage of life? Sure. So there's lots of different ways that our hormones affect this. So we've published data on our little engineered ligaments where everybody kind of knows that the women suffer four times more ACL ruptures, four to eight times more ACL ruptures than men. One of the reasons for that, at least from our work, is when we take those little engineered ligaments and we put physiologically high levels of estrogen. So the kind of level of estrogen that would be in a woman at ovulation. when you've got a lot of estrogen there, they actually rupture sooner, they become less stiff. And what we found is that estrogen actually directly inhibits this enzyme that makes collagen gels stiffer. It's called lysoloxidase. So estrogen directly inhibits that. What we've also found and we haven't published is that testosterone activates it. So a lot of times back in the 80s in the US, a lot of the sports, there were people who were getting big muscles because they were taking testosterone. The problem was that they would all get injured. really, really quickly because what happens with testosterone, stiffer tendon, but it actually decreases collagen synthesis. So what happens is you have a stiff tendon that's small and it becomes brittle and it becomes easy to break. In women, you've got more collagen synthesis, but you've got less stiffness. And so it's a little bit more stretchy and that makes great suds evolutionarily because if you have to give birth to a child, In order to do that, you have to have ligaments that stretch a lot more at that time. And so what happens in young women is every time you're going through that ovulatory phase, now what happens is you get more stretchiness to your tendons and ligaments. That makes it so that you're four to eight times more likely to have a ligament rupture. It actually means that you're 80% less likely to pull a muscle. Because as we said early, muscle pulls happen when the tendon is stiffer than the muscle is strong. If estrogen is decreasing stiffness, you shouldn't get as many muscle pulls. And that's what the data shows from elite sport as well as most sport. Is it women pull muscles less frequently? They rupture ACLs much more. So if I have now a stretchier tendon, the likelihood that tendon is going to overstretch and maybe pick up a little bit more injury is gonna be higher. Okay, so again, that's going to mean that where we're having injuries, especially in young women, is we're going to have more injuries in the tendon itself rather than the muscle that's attached to it. In men, we're gonna have fewer necessarily injuries in the tendon, but we're gonna have more in the muscle. Okay, and then what we add to that is we add menopause. And now what's happening is we're getting this dramatic shift in the hormone levels. So estrogen's going down, testosterone levels are rising. And so now what that's gonna do is that's gonna change how we're synthesizing collagen, decreases collagen synthesis, but it makes it stiffer. So as people go through menopause, as women go through menopause, they're gonna find direct changes to the likelihood that they're gonna pull muscle or that their tendons become more brittle because testosterone is becoming dominant. And then you compound that on top of that is if you have individuals in your listening population who are women who are going through estrogen positive breast cancer, the treatment for that is to add what's called an aromatase inhibitor. Aromatase is just testosterone and estrogen, as much as men like to think that testosterone is this great thing that makes a man a man, nothing to do with it. You can convert testosterone into estrogen just through this enzyme aromatase. And it goes back and forth through that one enzyme. So if you have breast cancer and it's sensitive to estrogen, not only do you get rid of the estrogen from... say menopause, but you also prevent the conversion of testosterone into estrogen. And that's in women who are treated with aromatase inhibitors, their tendon injuries go way up, their musculoskeletal pain goes way up. And that's because this interaction has been dramatically changed again. So absolutely, there's all kinds of stuff that happens. Young women. are gonna go through periodic differences in the stiffness of their tendons. And that means that their performance is gonna go up and down a little bit. So their power is gonna change. Because as your tendon becomes a little stiffer or less stiff at ovulation, you actually lose a little bit more power. So you're gonna actually have to, you're gonna feel like you breathe heavier when you're running on those days at ovulation or a little bit after it, because you're actually having to do more muscle work because there's less energy stored within the tendon. For men, it's a little bit easier because our tendon stiffness doesn't vary the same as it does in women. And they start stiffer in the first place. And so what that means is it's easier for us to run because we get more free energy back. But it also means that we have to be a little bit more careful about muscle pulls if we don't do anything other than say run or do high plyometric load activities. If someone is in menopause, does it make their tendon rehab more or less successful, or is it just like a different strategy? So, again, there's almost no data on this. There's a beautiful paper by Jill Cook, who's also down in Australia. She did this lovely paper where she looked at runners in menopausal runners who are on estrogens replacement therapy or hormone replacement therapy or not. And what she found was that the... runners who are not on estrogen replacement therapy actually had bigger Achilles tendons than the ones who were. So that again suggests that there are some changes that are happening with menopause, that the tendon was bigger. Does that mean that it's healthier? I don't know, there's not enough data out there because unfortunately, as most people understand, a lot of the decision-making when it comes to what research gets funded is funded by a... bunch of old white guys who sit there and say, this is what's important. So suddenly, there's all kinds of research into prostate cancer or erectile dysfunction. There's very little on the other side, because they don't necessarily hear that because they're on wife 2.0 3.0, whatever it is, when they're making those funding decisions as to where the funding goes. So there's very little money that's gone into kind of trying to understand that. The other real problematic thing for those of us who try and research it. is that most of the animals we use to try and really understand what's happening at the level of the tissue, they don't really go through menopause in the same way that human women go through menopause. And so it's really difficult for us to get a really good understanding of what's happening with these transitions like in menopausal women or in men who have prostate cancer and have to take the anti-androgens because there's not really, that's easier for us to model. We just... cut out the testes in a rat, we can model that. It's really difficult for us to understand and to model what happens in menopause. Is there any other final takeaways that you think runners or someone who's rehabbing the tendon might get a lot of use out of or a lot of benefit from that we haven't yet discussed? Yeah. So, so the easiest thing, so, so I'll run every other day and the thing that keeps me the healthiest. So I get to apply my research and then, and what I've realized is over the years is that my research follows my point in life. So I'm in my mid fifties now. I'm like, okay. I'll be able to keep running if I stay injury free. So most of my research now is on basically preventing and recovering from injuries. And so what I find is that after every run that I do, I don't bother doing like a static stretching type of thing, but I have a mobility, what I call a mobility routine. And all it is isometric holds. So I'll do an isometric lunge on both sides. And what that does is on the one side, I'll get load through my quad and patellar tendons. On the other side, I'll get again, quad and patellar tendons as it's in the lengthened position. I'll do a side lunge where I really try and get my knee way over my toes because what I'm doing there is I'm getting load through my Achilles tendon. And my Achilles tendon is going to respond to that because I'm holding that isometric load in my Achilles. Now my Achilles is going to give me what I'm looking for, which is a little less stiffness in the muscle end. And then I'm gonna do an isometric squat through the back to again, try and get some of the things that are associated with like, hamstring and glute. And so what I'm doing is I'm actually using more isometric holds in my cool down or in my recovery period after I train. Because also as we said, I've just gone out for a run. My tendon, the strong parts of my tendon are as weak as they're gonna get. So this is a great time for me to check to see if I have any weak parts. And so by holding those for 30 seconds as I go through that. And I go through and I do my whole routine and I can do one to two bouts of that if I'm healthy. If I've got a specific area where I'm really, oh, you know what, my Achilles is getting tight on my left side, I'm gonna do two or three or four 30 second holds on that one spot. And now what I can do is I can use those long isometric holds as a prevention and a recovery tool for me. And so really that's the first thing that I would say. The second thing is that unlike our muscles, our heart, skeletal muscles and heart, they continue to adapt for as long as you're gonna go for your run. So if I go out for a three hour run, my heart and my skeletal muscles are adapting for three hours. My connective tissues, my tendons, ligaments, cartilage and bone, they respond very short periods of time. So within 10 minutes, they've gotten the whole signal they're gonna get. and they're already starting to turn off. I tell people this a lot like my 17 year old daughter. I try and tell her something and she's tuned me out after a couple of minutes. Same thing is true for our connective tissues. And so what we wanna do is instead of continuing, and all they're doing for the rest of that three hour run is for two hours and 50 minutes, they're picking up mechanical injury, they're getting fatigued, and they're getting more and more likelihood of getting injury. I only got a signal for the first 10 minutes. And so what you can do and what... you know, Camille Herron does, because in her other life, other than being the world's best ultra-marathon, ultra-runner, she's also, she did a master's degree in bone mechanobiology. So she understood that bone responded to short periods of load with about eight hours of rest. So what she does is instead of doing a three hour run, she does two one and a half hour runs. And what she's doing there, she gives the same stimulus for skeletal muscle and heart, but she's given two stimuli to her tendons and ligaments. So now what she's got is she's got twice the stimulus, the positive stimulus to the connective tissues with the same stimulus for the rest. So most of us aren't gonna run three hours. Maybe most of your listeners do, but even if you're doing say an hour, if you split that into two 30 minute runs, if you can do that, that's actually gonna be more beneficial to you across the whole system, your muscles, heart and your connective tissues, than just doing one 60 minute. With about an eight hour gap. With about an eight hour gap if you do it. Yeah, so basically what you do is something in the morning, something in the evening, you go to work during the day, like the rest of us. And that's a perfect way to do, and so a lot of us end up doing that, especially amateur runners, because they wanna have more volume, they can only do so much before work, they can only do so much after work, so what they do is they do a little bit before and after. And that's actually really, really beneficial to the whole system, because now I've given two stimuli to my connective tissue. I've given the same stimulus to my skeletal muscle in my heart. And now what I've got is I've got an optimal loading for those, the whole system. That's been excellent. Um, I could chat with you for another hour and I keep learning every single minute. I think I can't think of the last time I've been so informed on a chat with someone. Um, the amount that you've covered has been amazing. And the amount of insights that you are having, like stuff that I've tried to keep my pulse on for ages and I just haven't been learning this stuff. And so, um, thank you very much for all this cutting edge research, all this insights has been very practical for someone who wants to rehab their tendons or, um, reduce their risk of tendon injuries. Um, so thank you for all the work that you and your team do. If someone wants to learn more, are you active on social media or is there a website or anything? social media links that I can include in the show notes. Yeah, so I use, now we use Blue Sky because it's a little bit more friendly and more scientific environment. So I'm muss If you just look up Musselscience, you'll actually find it there. And so that's one way that we get our message out. I just posted today, because they're... the medical school came down and did a video and a little article. So you can see kind of a little bit of what we're talking about when we talk about these isometrics just in the video there. So that's probably the easiest way to stay up to date with what we're doing. And it's always a pleasure to come on. And I know that it's very difficult to communicate science and it's very difficult when you're working full time trying to help people to actually be able to figure out where the science you need to know is. And so that's why I try and come on to these types of podcasts to try and help to disseminate a lot of stuff that's been going on. I've been doing research for over 20 years. This is probably the time in my career when I've had the most exciting, most actionable data that's coming in. That's totally cool. So that's great. making sure that we can get the word out and we can share it with as many people as we can. Well, I'll share that the muscle science links and everything in the show notes for people to learn more. Thank you very much for your time. Thank you very much for all the work that you're doing and thanks for coming onto the podcast. Absolutely. It's my pleasure. If you are looking for more resources to run smarter, or you'd like to jump on a free 20-minute injury chat with me, then click on the resources link in the show notes. There, you'll find a link plus free resources like my very popular injury prevention five day course. You'll also find the Run Smarter book and ways you can access my ever growing treasure trove of running research papers. Thanks once again for joining me and well done on prioritising your running wisdom.