Achilles & Patellar Tendons with Jarrod Antflick

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Okay, I'm sitting here with Jared Anflik PERSON. I actually, it's only been a few months since I've known of Jared PERSON. I met you, Daniel Bov with the Pelicans ORG, kind of told me about the things you were doing. Seems like you kind of stay hidden because I thought I had found mostly all of the tendon people, but here you are.

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So why don't you tell the people, I guess, who you are, how you got into attendance?

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So thanks for having me, by the way.

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I listened to a couple of your podcasts on some of your other guests, some really interesting discussions. So I am a sports physiotherapist. I have started with a Bachelor of Health Science, which was my first undergrad, then a second undergrad and a Bachelor of Applied Science,then a Masters of Sports and now PhD at Imperial College, London, in bioengineering. I have a couple, I have three supervisors, one's Peter Magnuson PERSON, who you probably know quite well, and to the other two are Professor Anthony Ball and Dr. Angela Kedgley PERSON. And really my PhD WORK_OF_ART is really looking at the structureand pain relationship, in tendons. How did I get involved in tendons? Probably 14 years, 13 years ago. I was working a lot in track and field, and obviously it's quite a prevalent disease in track and field, very performance limiting.And I just became extremely interested in it. I was living in the UK at the time and was introduced to managing some tendons with Dr. Lorenzo Maski PERSON, who worked and published some research with Hockhan Alfredson PERSON, so the Alfredson Ecentric Protocol. And I used to help Lorenzo PERSON do some of the early stage polydokinol injections and just got interested in doing some ultrasound imaging with him and sort of leaned over his shoulder quite a lot. And then I ended up working in track and field, as I said, and we had a lot of tendonproblems. And so myself, one of my great colleagues, Dr. Noel Pollock PERSON and another great colleague, Dr. Toby Smith PERSON, sorry, just Toby Smith, not Dr. Toby Smith. And we would sit down and talk about loading and tendonopathy and how are we going to get to the bottom of it. And so it's sort of stemmed from there. And my interest sort of piqued a little bit around trying to manage tenetopathy in the elite sprinter. So I used to work for British athletics up in Lee Valley in London and traveled with them, went to world champs in Russia GPE.I went to a couple of, well, went to quite a few diamond leagues and assisting some of our mostly sprints and jumps group. And that's sort of where it stemmed from. And then in 2013, I purchased the first UTC machine, which we'll probably get onto. And that sort of broadened my understanding, or at least open my eyes to the usefulness and the importance of structure in tendonopathy.And that's sort of where it sort of all kind of began.

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I've been told I need to go down the track and field, be more into track and field

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because they kind of are good with managing tendons.

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I mean, I'm in the basketball space and probably NFL ORG that I care about. But what did you see in track and field?

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What type of tendon issues and what kind of problems were they having? So I would say when people

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say I need to get into track and field, I mean, Olympic EVENT sports, particularly track and field is of the

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purest nature. And these are athletes that are very poorly funded, poorly paid the majority

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across the board. But yet it's about, you know, hundreds of a second and their training

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programs and, you know, the intensity of training has to be so, so high to win a medal to

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PB to represent your country. So it is for me, one of the purest sports,

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and I would encourage anyone that wants to understand,

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even just strength and conditioning or elite sports medicine,

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as track and field sort of is one of the pinnacles of sport. What kind of tenonopathy we would see? I mean, it was mostly Achilles tenonopathy and Patelotteninopathy. I was one of the contributors for the British Athletic Muscle Injury Classification paper, which was looking at hamstring injuries and return to play. But we would see a lot of Achilles and Patelotanopathy.And what we found was more than anything is that with a hamstring injury, you're out for a sprinter. You're essentially out. You can't perform, whereas a tendonopathy, you can kind of warm up. So we found that it was more performance limiting disease rather than abinary you're in, you're out kind of thing. So it was managing these elite tendons, you know, from 400 metre runners to sprinters to jumpers, to field event athletes, trying to manage themin season and get them ready for competitions because every competition is pivotal for a track and field athlete, whether it be coming into a world or an Olympic EVENT cycle. So it was really just trying to do the best we could. Now, we didn't have the sort of funding that some of the NBA and Premier League football and Premiership Rugby ORG had and has. So it was trying to be as innovative as we can and could be.So it was a very interesting, very close-knit medical team and really just trying to get to the bottom of it. But a lot of the things that we see, obviously, our sprinters and some of our jumpers are Afro-Caribbean NORP. So we would see, you know, anything from Plantarous related to parotentanopathies, and you're sort of thinking, why does race have anything to do with it? Because unfortunately, there are predispositions to tendonopathy, genetic predispositions of tendemopathy.So, you know, whether it be Patelottenatopathy or Achilles tendonopathy, we would see quite a lot of it. It's quite prevalent, as it is, for example, whether it be Patelottenatopathy or Achilles tendonopathy, we would see quite a lot of it. It's quite prevalent, as it is, for example, in the AFL. I'm Australian, as you can hear, our Aboriginal NORP population is prone, very highly prone to Patelotanelotapathy. And so just trying to provide an education to coaches to athletes, loading programs, structured loading programs, because they're not competing every weekend that we really could make quite a differencein their seasons. They can get, you know, three loading bouts into a week, whereas in the NBA, which is where I spend a lot of my time now, hitting three loading sessions in the week is extremely, extremely difficult. So it was a much easier environment in some regards because we had time, but in the other regards, it's a much more difficult, much more stressful environmentbecause if you have a raging Achilles tendonopathy, for example, it's going to be hard to do a training session. Every training session is really important. And we found that if you missed less than 85% of your training sessions leading into a world or Olympic EVENT cycle, you're probably not going to make the team or at least PR or make it to the final. So those stats are really important. You need to really be training 85% of the time.

Speaker 0423.54s - 432.1s

What are the genetic? What are those genetic things that those people get? Is it something with the collagen or what is it?

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Yeah, so it's the COL 501A polymorphism that Malcolm Collins PERSON in South Africa spent a lot of time researching and we know that when you have that expression, it doesn't necessarily mean that you will have tenetopathy, but your likelihood increases. And so there are sort of Nigerian backgrounds, some Caribbean NORP backgrounds that will are more prone to tenonopathy. And I've had sprinters that are mixed Nigerian or Caribbean NORP and they, you know, have ruptured their Achilles or have penanopathy, their brothers or their sisters have tendonopathy. And so, you know, not that we screen for it because I thinkit's, I think it's not ethical to do that, but it's interesting to note that some backgrounds do have this polymorphism expressed. And so they are more prone to tenetopathy.

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Polygon 5, what exactly, if you can answer that at the structure level, what is it, what is it doing?

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I mean, that's not, that's, I'm not a, I'm not a microbiologist.

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There are people that are in a better suited position.

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Hazel Screen PERSON, for example, is a, you know, a tendon researcher.

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And she's, that's the kind of question that she's more, more, um, O'Fay to be able to answer

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rather than me. Yeah.

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Yeah. I've seen, I've seen images of like what's going on with the type one or the type three. And then there's the type five.

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I think Michael Care had a video talking about the, for me, it was just the, the very little bit

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that I, but yeah. I'm a lowly, I'm a lowly

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physiotherapist, you know, these kinds of things are, you know, for, for the cell biologists and

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those sorts of people like Michael, Michael's group, who I'm loosely associated with Peter

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Maglinson. I was, I was aware of tendon ruptures in, it was some presentation, I think, on African Americans NORP having more likelihood.

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And I think it was in rugby having a crazy, more high likelihood of tendon ruptures.

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Maybe is that the same thing going on as like the tendonopathy and the tendon ruptures are more likely because of this genetic thing?

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Yeah, I mean, it's part.

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It might be part of it it part of it is also training

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load uh trying to quantify training load for example in basketball is extremely difficult obviously

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you know we don't do in game monitoring so it can be a bit more of a challenge um but i don't think

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you can't just nail it down to one thing you can have that polymorphism expressed and yet still never,

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ever have symptoms. Vice versa, you don't necessarily have to have that expression, that gene expression and you will still get to the end. You can still rupture. So I think it's more than, it's usually more than just one factor, although there seems to be this association with this polymorphism that Malcolm Collins PERSON has looked into and written some interesting papers on.

Speaker 0607.76s - 622.54s

Okay, so you said your PhD WORK_OF_ART is going to be on structure and pain relationship because there was that maybe kind of echoed for a long time that structure doesn't matter. But tell me, does it matter?

Speaker 2623.44s - 825.98s

Well, I think it's a really interesting question. And in answer to that question, yes, it does matter. And then I will sort of elaborate. I think some of it has come around from imaging other parts of the human body. And for example, if we look at the lumbus spine, you know, if you're over the age of 40, the statistics suggest that you are likely to have awful imaging and you might not have pain.And my retort to that would be along the lines of the load magnitudes are very different. It's a different structure. There are faster joints. There are, you know, many tissues that attenuate force before you get to the lumbus spine. Whereas at the Achilles, other than the FHL and maybe a little bit of TIPPOS, there is nothing that can attenuate force other than the Achilles tendon.So, you know, I think structure does matter. And if, you know, if you're an elite functioning athlete, track and field NFL ORG basketball, when we believe, and Sean McCullough's PERSON work was very clear looking at hyper-echogenicity in Achilles tendons, had a relative risk of 7.4, that you are likely to experiencetendonopathy, pain, discomfort or worse, if you do have areas of hyper-ecogenicity within the tendon. Conversely, if you are a sedentary, I'm not going to label anybody, but if you just sit at a desk most of the time and you very rarely have a need other than to walk to the shops or walk from your car to somewhere and you don't sprint and you don't jump and you don't run regularly, then the need to have a normal tendon is not entirely necessary, although obviously we all strive for perfection in some regard and human physical perfection, but you don't necessarily need to have a perfect tendon. And I think where I think that the argument falls down where structure is not important is that if you just apply the rationale, well, lumbus spine imaging, you know, some people don't have, you know, have lots of, you know, whether it would be faster,drawn hypertrophy or degeneration, arthritic changes, or lumbus spine bulges, and they're pain-free, well, that's fine. You don't necessarily, the load, the load, the load going through those joints are a hell of a lot less than the Achilles. You don't necessarily need to have a perfect lumbus spine because the load magnitudes are a lot less and the loading rates are a lot less.But in the Achilles, you know, when you look at some of Karen Sibbonagles and Baxter's work, which is the same lab, you have 56 body weights a second when you're sprinting. The lumbus spine doesn't get anywhere near that. And so the need for normal structure is really important when you are at a high function, when you are a high functioning athlete. So that's sort of my long summary on where the structure is important. I genuinely believe that it is quite important.And having scanned and reviewed tens of thousands of Achilles tendons, when structure is changing or when there is altered structure, you can, you know, you wouldn't bet your life nor your house on it, but you can pretty much near guarantee that if there are a high functioning athlete at some point, they will develop symptoms. Yeah.

Speaker 0827.7s - 847.08s

So when it comes to looking at the structure, like the health of the tendon, you have those like MRIs, ultrasounds, whatever. How do people go about it? How do you go about looking at tracking tendon health or tracking the tendon structure?

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So in terms of tracking, I mean, I use a UTC machine, ultrasound tissue characterization. I've used one now for over 10 years in its many different incarnations. That's how I track tendon health. So we go to the NBA and the NFL and the Premier League ORG and we scan Achilles and Patelotendons. And then we do that in the NBA every six weeks and then we just monitor them. I have some code that helps me graph and present or visualize the data in a more digestiblemanner and we track changes over an NBA ORG season. The same cannot be said for other modalities, unfortunately. I mean, if my PhD, some of my PhD is done using a 70 MRI running T2-Star PRODUCT mapping UTE, which is an hour and a bit per Achilles tendon. And that doesn't include, that's just the scanning. That doesn't include the analysis.So in terms of speed and ease, you couldn't really use MRI and say that that's easy to track because I can't see 17 players times two Achilles tendons, you know, sitting in a 7T or even a 3 PRODUCTT MRI and then trying to extrapolate all the data from that. You've then got shear wave elastography and I should think shear wave is very useful looking at stiffness. I think there is some usefulness in it. I think there's probably only a couple really, really good machines out there that are useful for it. There's the supersonic machine that comes out of France GPE. I think is probably the best, but it's a big unit. It's enormous and it's extremely dear and it's notportable. Deer meaning expensive and it's not portable. So I think shear wave has potentially has its place probably more in a research setting. There is some new versions of shear wave that's coming up with infrared that are coming out with infrared and laser. That might be useful.I can't speak of it. I don't use shear wave. And then gray scale ultrasound and obviously the issue with gray scale ultrasound is it's shades of black and white being gray. And so it's difficult to track tendons using gray scale ultrasound. And color Doppler we know is not particularly sensitive to change. What sensitive to change is not sensitive to improvements.Unfortunately, and you can have an athlete that has no color Doppler PRODUCT one day and has been for a 10K run and now all of a sudden has Color Doppler PRODUCT. So Color Doppler PRODUCT is interesting. It's also part of my PhD looking at Color Doppler in the region of interest in our activities tendons. But unfortunately, it's very hard to quantify and reliably quantify.

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So every six weeks, how did you arrive, like, kind of at that wanting to look at things every six weeks?

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Because can you get significant, let's say you just have a healthy tendon and you overload,

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like you significantly overloaded.

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You could see changes like the next day, right?

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Yeah, so Sam Rosengarten showed that in his, that was one of the earliest UTC papers in sports.

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And he found that at day two, there was an increase in type two.

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And the interesting thing about that is that that was one of the very early UTC machines that probe sensitivity was quite low. And so I suspect that if he readed that paper with some of the newer, I've got a 16 megahertz probe, that you would find that that would be profound. You would, there would be quite a noticeable change in structure.So yeah, we do know that tendons change.

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They try and adapt to their load stimulus as best they can. So why the six weeks? I think that's a really interesting question.

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I think I have scanned players every two weeks to monitor there in improvements or lack thereof.

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Six weeks, I think, comes down to scheduling for the NBA ORG. I think anything more than that would be quite difficult. It's getting player buy-in. It's, you know, their travel schedule. It's a whole bunch of different factors. But I also think, excuse me, I also think, you know,you can get meaningful change in attendance in six weeks rather than, you know, three days or a week or two. And then I, conversely, I think you can't reliably, I don't think you can reliably say after a three-month period that you can really track a tendon. I think a lot changes in three months.

Speaker 01128.88s - 1142.24s

So there's been this this idea with the with the structure that a healthy tendon won't rupture i think that's been even carried over to a healthy tendon won't get get pain won't have tendonopathy um yeah where do you stand with that

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you agree with that statement i do agree with, but there are two caveats to it.

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One is fluoroquinolone-induced tendonopathy.

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Okay, so people that have had fluoroquinolones like syphyloxysin, which is used for UTIs or prostateitis, it's an antibiotic, they are very unpredictable, understanding whether or not those tendons will become tennopathic or not, or rupture. We don't know.We do see a lot of fluoroquinone-induced ruptures. I see a lot of fluoroquinone-induced tendonopathy and ruptures. I've seen a patient that had came into me who was post-op bilateral Achilles repair that ruptured his Achilles tendon at the time, jumping for a football when his previous workload was just cycling. And a year before, he'd had a bout of stomach problem when he was in Asia and was given IV high-dose fluoroquinolones.And a year later, he ruptured both his Achilles tendons. Coming back to the second point, plantarous related tenonopathy. One could argue and say that might not be tenonopathy purely just from the tendon or tendon overload. It's an interaction between a vestigial tendon and lynx,which was a paper that was published some couple of years or quite a few years ago, now maybe 10 years ago, demonstrated that the stiffness qualities of the plantarous is much higher than the Achilles. And my analogy is more akin to a garot, which is sort of that martial arts weapon, which is a wire when you bring it up against somebody's throat and you come up behind them. And essentially, the planteraurus robs and causes irritation along the medial, medial Achilles. Now, some people present with irritationof that fat layer between the two tendons and yet may not have a huge amount of changes within the Achilles tendon. And, you know, some recent work in the US with some basketball players has demonstrated that the understanding of Plantiris in the United States GPE is probably not as well understoodas it is in Europe. We've done a lot of work. Hock and Alfredson PERSON has done a lot of work on Plantiris related to inopathy. We started doing some work. We started a paper looking at a percutaneous release of Plantaris PRODUCT and we did, we got to about five or six of them and we just sort of stopped doing it for no other reason. Then it's a difficult process doing an ICT. We also started a paper looking at the use of hyluronic acid or Austenol, Synvisk, Durulane PRODUCT, I think, you guys might call it,between Achilles and Plantaris PRODUCT. And essentially, it's sort of a hydrodissection like a lubricant, and HA occurs naturally within the IFM, which is part of the IFM, interphysicular matrix. So we, you know, we inject that between the two tendons. So in answer to your question, does a normal tendon experience tendonopathy or rupture?No, a normal tendon shouldn't, but there are caveats to that. Fluoroquine, excuse me, fluoroquinolone-intuced or plantarous related, those sort of tendons. And then obviously, if you have a blunt force trauma to a tendon from being kicked or whatnot, then chances are you might become somewhat symptomatic. But on the whole, normal tendons should not become tendonopathic. Normal tendons should not rupture.

Speaker 01357.6s - 1362.38s

How common are both of those two things, Floricorinolones and Plantaurus?

Speaker 21364.22s - 1485.52s

So maybe it's because I do a lot of clinical work in tenanopathy. I do see fluoricinolone-induced tenopathy. We probably see, I know this might not seem a lot. We probably see a half dozen a year. Plantaris related, we see a lot. So every clinic we will probably see out of maybe 10 patients,we'll probably see three, maybe four plantaris related, if they're just Achilles problems. So we see quite a lot. And plantaris occurs 85% occurs in 85% of the population. Mainly, we thought it only occurred in 15% of the population, but a Dutch study, a population study found that it occurs in 85%.So we know that it's there. It's anatomy is very different in different people. We published a paper probably two, three years ago, looking at the different attachment sites of plantaris, depending on where it attaches. If it attaches, obviously, it's a tendon that runs immediately, crosses the knee joint and travels underneath gastrochs over the top of Salaris, depending on where it attaches. If it attaches, obviously, it's a tendon that runs immediately,crosses the knee joint and travels underneath gastrochs over the top of Salaus, that, you know, when it does attach, if it attaches the medial facet, you may not have symptoms. If it attaches, you know, on the posterior facet behind the Achilles, essentially wraps around it, then you probably will have symptoms. And that was an MRI study that we did with a bit of ultrasound as well some years ago.So Plantaris-related mid-portion Achilles synomopathy is very common. You know, it's probably more common than we would have thought previously. And I was in, I had to go in a theatre yesterday to look at a patelotendon with one of the surgeons I work with, and I just stopped by one of the clinics, and one of the surgeons I work with said, you know, it's interesting. Our imaging techniques really have opened my eyes to understanding that plantarous-related tendamopathy is a lot more prevalent than it ever was,and we probably missed a lot of them in years gone past. So, interesting. And the thing is, it just kind of like gets stuck. more prevalent than it ever was and we probably missed a lot of them in years gone past so interesting

Speaker 11485.52s - 1492.72s

and the thing is it just kind of like gets it gets stuck on the achilles the medial achilles or what's

Speaker 01492.72s - 1498.8s

causing some reaction yeah so it can it can it can it can invaginate so it can actually insert into

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the achilles it can insert under the parotene on it can just sit next to it. And as you go from knee flex to knee extend dorsaflex to or planar flex to dorsiflex,

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it goes nice and tight and it can just flick past.

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But as I said, the anatomy can be varied.

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It can actually have a retinaculum that goes around the Achilles and the plantaris

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and keeps it nice and collared quite close to. And we see all manner of variations of them. I've seen some some of them half rupture in some elite sprinters going around the bend where they partially rupture their plantaris. It feels like they've ruptured their Achilles, but their Achilles is entirely normal. So, yeah, the morphology of it is very varied and the anatomy of it is very varied.

Speaker 11545.32s - 1553s

Big thick ones, I remember, I measured one that was, that was nine millimeters in diameter.

Speaker 21553.86s - 1559.16s

That's a big old antarous tendon. That can get like an hypertrophy. So, yeah.

Speaker 01559.74s - 1568.98s

Yeah, and then the things you were, you were talking about, is that only one method is like the injection to try to get them separate? Is there like other things to do?

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I mean, that's one method.

Speaker 01570.44s - 1574.64s

You can try and load around it, avoid end range dorsiflection with a straight knee.

Speaker 21576.88s - 1603.48s

We were doing a percutaneous release. So sort of like an injection, but we would actually rupture the plantarous tendon. And we had really good results with it, although the cohort size was only five or six. And then plantaricectomy. So we remove them, and our surgeons will make a very small incision around the Achilles, find it, strip it out, and it sort of comes out just along the distal to the medial,head of medial gastrox, and you take it out, it looks like a piece of spaghetti. Yeah.

Speaker 01604.16s - 1611.46s

So that's one way of dealing with it. Recalcitrant. Achilles synomopathy as a result of plantaris.

Speaker 21612.26s - 1673.78s

It doesn't matter how many injections sometimes. Sometimes you just have to take it out. And I've seen, you know, my most vivid memory is a lovely, lovely gentleman who was his father played for Inter Milan ORG. He was on the junior squad for Inter Milan ORG and his career was ended because he had Achilles problems, was put in a wheelchair, etc., etc.And 30-some-odd years later, we reviewed him because he wanted to, he was stopped playing football and was into triathlons and he just couldn't get enough running volume in and when we scanned him he had the I mean this enormous bontaris tendon we tried to manage it conservatively couldn't so one of the surgeons took it out and you know I got an email from him about eight months later saying you know I'm running pain free it's the first time in 30 years I mean for some people it's very emotional.And he was very emotional. He clearly he came to see us. He was crying that I could have been a professional football player. I mean, could have would a hide scientist 2020.

Speaker 01674.2s - 1680.54s

But, you know, that he'd had something so simple that just wasn't seen and wasn't managed.

Speaker 21680.72s - 1692.3s

But 30 years ago, we didn't have any of the imaging techniques or the understanding that we do have now so yeah yeah um and the the conservative management for like a like a regular

Speaker 01692.3s - 1697.32s

old achilles tendonopathy i think most people probably are familiar with that how does that change

Speaker 11697.32s - 1704.44s

if it's the plantaris you kind of said don't do the dorsi flexion with an extended knee

Speaker 21704.44s - 1822.02s

yeah i mean i think some people um have a very very pronated foot and You kind of said don't do the dorsi flexion with an extended knee. Yeah, I mean, I think some people have a very, very pronated foot. And so putting a medial post in and just to help normalize, because if you're very, very pronated, you're probably going to load the medial aspect of the Achilles. And so, you know, using a medial post is very useful. Potentially a hill raise, just to unload the Achilles a little bit.You know, loading is really important. You might need to give them some non-steroid land inflammatorys if you're a physician or if you are in the habit of prescribing those sorts of things, just in the acute place to get it to settle down. But then loading, you know, I think one of the reasons why people's tenetopathy continues on and on and on, and we know that, you know, in the elite cohorts, Patelottenamoply, for example, people keep it for 32 months is because potentially we take away the load stimulus too aggressively.And I've had these conversations with Professor Magnuson on numerous occasions where we think that because people get tendonopathy, we all of a sudden take away their load. And maybe that we know that can be catabolic for the tendon. And, you know, maybe we need to still keep a load stimulus in, but just modify things a little bit. And so I, when I see patients clinically, I would say how much running you're doing at the moment and can you manage what you're doing. And if they say, no, I can't manage it at all, then, you know, it's very clear we need to sort of chop out a bit of their running volume. But if they can runand they just have minimal soreness, I might say, look, keep the running in, but look, here's a loading strategy that we need to implement or we might go for an injection if we can't manage it conservatively. So it depends where each patient's up to in in their in their phases if it's just a recent presentation then my desire would be to not take out too much training or running volume or playing volume and just manage it

Speaker 01822.02s - 1838.08s

conservatively that way so this this idea getting the tendons healthier and you have that UTC scan, what have you found, what is the way to get the tendon healthier?

Speaker 21839.52s - 1921.64s

I mean, I think, you know, first and foremost, it's mechanotransduction. So it's really a load stimulus and we know that if you, you know, first and foremost, it's mechanical transduction. So it's really a load stimulus. And we know that if you, from all, whether it be the Aaron Patsas PERSON papers, whether it be from Mads-Cons ORG guard's work, that loading is key to changing tendons, whether it be mechanical properties, whether it be actually changing the tendon. And regular, consistent loading,trying to get to a heavier, higher strain rates upwards of 6% is really, really, really important. And so, you know, in an answer to that question, it really is, there are systemic causes of tendonopathy, as we know. You know, diabetics, people with doubt, people with cholesterol, high cholesterol, postmenopause of women, they're my more challenging patients to manage. And if you can keep all of those sorts of things under control,keeping your alcohol down because alcohol has quite a profound effect on tendons and inflammation. But keeping a tendon healthy is all about regular loading and keeping the training volume and intensities progressively increasing, obviously, but, you know, sharp spikes is why people would come and see us in the clinic or just, you know, not being able

Speaker 11921.64s - 1922.12s

to adapt.

Speaker 21922.12s - 1935.72s

And I think what is quite difficult to understand is that not everyone adapts the same way. And I had a fascinating conversation many years ago. I did a paper with the Royal Veterinary College of London ORG in equine tendons.

Speaker 11936.14s - 1938.38s

And he was a very well-known racehorse trainer.

Speaker 21939s - 2075.22s

And I said to him, you know, how do you track your tendons? Because the SDF, superficial digital flexor tendon, are prone to very large central core lesions. They call them bullseye lesions. And it basically just, it's a let go. Essentially, just the central tendon just denatureizes and pops.And they get these bowing of the tendons. And one of those, you know, really interesting questions was, you know, how do you keep an eye on these racehorses? And some of them are worth a lot of money. And he said, oh, well, we kind of don't. We just all race them and they've got a certain amount of volume to do.And if they don't, if they can't do the volume, then that's out. They're out. What does out mean? Well, we either breed them or we make stuff out of their bodies. I said, but, you know, have you ever thought about monitoring them? And he said, what do you mean?And I said, well, not every racehorse, not every human needs the same level of adaptation, needs the same stimulus. And he sort of thought for a minute and he said, so what are you saying? And I said, well, X horse might not need as much running volume as Y horse. He didn't like that. I think he thought that was probably more work than he wanted to put into the horses. But, you know, I've presented some years ago at RVC, I'm sorry, at Biva, British Equine Vetry Association ORG meeting. And there were a lot ofhead scratching after that when, you know, we talk about load monitoring in elite athletes, human athletes, versus the lack of elite monitoring and equine athletes. And simple things like speed guns and knowing the volume, they know the volume because they can, they know how far they're running, but they just don't know the speeds. And the speeds are really important because obviously the faster you go the higher the the the impact on a tendon is so fascinating conversations and you know then you start talking about using GPS for race horses or speed guns and yeah absolutely but to keep the tendon healthy it's consistent loading progressive loading progressive overloading with,you know, a load stimulus that is, you know, without peaks and troughs. Probably is an answer

Speaker 02075.22s - 2105.08s

to that. So that the changes, you can actually, you'll actually see like the tendon get healthier with implementing that by keeping people within within their sports um doing things that they i guess doing the sports that they want to do uh you're also doing like heavy isometrics heavy slow strength do you think that is having an effect on the on the health of the tendon or is it just without a doubt okay no without a doubt

Speaker 22105.08s - 2108.68s

I mean the isometrics that I I think

Speaker 12108.68s - 2112.34s

have some really good evidence for is the high strain

Speaker 22112.34s - 2191.38s

isometrics for three to five seconds I mean it's the Aaron Patsas PERSON work is three seconds I think anything beyond that is opinion and hearsay unfortunately I think if you want to do isometrics to get your athlete warmed up, okay, fine.But I don't think it's the panacea that everyone thinks it is or thought it is. I think isometrics have its place, but I think we talked about this last week. I have a healthy relationship with strength conditioning coaches because the programs that I build are around strength and conditioning principles. And so heavy slow resistance is absolutely crucial for not only tendon health, but also that muscular tendon disjunction and the other side of the tender, which is the muscle. So I think it's really important that athletes maintain a regular healthy load stimulus,whether it be on field, followed by the, I call it the medicine for the tendon, which is a load stimulus. And that usually looks like a heavy slow resistance, bent knee, straight knee,maybe a heavy ISO on the leg press. And then for Patelotend, it's just a lot of quad loading, unfortunately. Yeah. Repeated, high volume, repeated, repeated, repeated.

Speaker 02191.68s - 2193.72s

So some people really struggle with that.

Speaker 22193.72s - 2199.32s

When you say high volume, you're getting like a number of sets, also like frequency

Speaker 02199.32s - 2201.44s

throughout many days or what exactly?

Speaker 22202.64s - 2330.9s

Yeah, I mean, it's a modification of the Konsgaard PERSON program and I present it back to the group in Copenhagen about, I thought that the Konsgaard PERSON program had too much volume. It was all double leg and it was five different exercises. And so I presented a modified Konskard program, which was essentially knee extension, single leg knee extension, single leg, leg press, and then a squat variation, whether it be front, back, goblet, split, however you like, but all three exercises done in the one setting can be separated by a differentexercise. But starting with volume, and we know that the mechanism of that from the Konskard paper is this, you know, elevated college and turnover rate. And that is the reason for the volume. And then you have to, you have to whittle that down to something that represents a more strength and conditioning program, which is maybe five sets of eight reps or six sets of five, that kind of thing where you're really trying to push strength. But all of it is important. And the analogy I gave or the example I gave to last time was an elite tennis player who, when I said, you know, your goal was to hit 1.5 times body weight.And she was a strong, you know, top three British athlete, British tennis player, very, very strong. And within three weeks, she'd hit 1.5 times single leg body weight, ISO strength. And but she still had Patelotentanopathy. And I I said that's great and the team that's fantastic she's hit that but the program is is biased to a volume to start with because we want this college and turnover rate to change and so unfortunately I said this to a patient yesterday in clinic I said you know if you show my program to a goodstraight conditioning coach that have a chuckle, why is the physio doing programs like this? Ha, ha, ha, ha. And I said the rationale is very sound, is that it's not, doesn't fit perfectly along strength of conditioning principles,but the goal is to condition the muscle, the muscular tendon's junction and the tendon, but also to change this collagen turnover rate. I think that's really important. And you need, so you need like a

Speaker 02330.9s - 2339.52s

significant volume to get the collagen synthesis up. Yeah. Correct. Yeah. Four sets of, four sets of six

Speaker 22339.52s - 2348.44s

or three sets of eight is just not enough. It just, you just won't get your desired effect. And I see a lot of rugby players and a lot of rugby

Speaker 02348.44s - 2351.12s

SNC coaches.

Speaker 22351.32s - 2353.26s

They're all about power similar to NFL ORG.

Speaker 02353.58s - 2357.26s

And it's no fault of this because they have a goal in mind.

Speaker 22357.26s - 2371.3s

But, you know, when you're trying to manage tendonopathy, there's a couple of ways to skin a cat. But unfortunately, if you're trying to manage tenonopathy, there's a couple of ways to skin a cat. But unfortunately, if you're trying to change a tendon, three sets of eight of one exercise is not going to tip the scales.

Speaker 02373.18s - 2377.88s

And then if you're doing that, like, pretty high volume, it's just going to, is it going to be

Speaker 22377.88s - 2379.76s

a less frequent per week?

Speaker 02380.02s - 2381.74s

Yeah, so it's two, three times a week.

Speaker 22381.96s - 2402.74s

Okay. You know, and if you're an elite athlete and you're still playing, it's one to two times a week. And I think some of the, obviously, research has done in a vacuum, so to speak, elite sport is not that way. You know, I would wish that I had the time to do three times a week loading with an NBA ORG player,

Speaker 02402.84s - 2413.86s

but realistically, that's not possible. We know because of scheduling three or four games a week loading with an NBA ORG player, but realistically, that's not possible. We know because of scheduling three or four games a week plus travel is not impossible to get that many sessions in, but one to two is feasible.

Speaker 22414.74s - 2460.44s

And one to two with maybe two exercises, knee extension leg press or leg press and a squat, nice and slow, long durations. And we know from Ansefia Aguard's paper that duration is potentially one of the, that along with magnitude and frequency is probably one of the more important variables in building a program. If you do one second contraction, concentrically, one second contraction. Ecentrically, you may not get the desired effect.And obviously from the Aaron Patsas PERSON paper, when he looked at high and low frequency, the one second frequencies didn't really stick to scales, especially well as a three second frequency. So duration is really important, how long your tempos are really importantis when you're trying to load a tendon.

Speaker 12461.78s - 2467.64s

Yeah, I had had that thought years ago when I first got into tendons.

Speaker 02467.74s - 2483.22s

It was about, I was thinking, maybe it was on tendent stiffness. Like, they were like, you don't increase tendon stiffness when you do something like a plyometric and, but you will increase it with lifting. And I was like, that doesn't make any sense to me.

Speaker 12484.1s - 2485.84s

And, but the argument was for time under

Speaker 02485.84s - 2497.12s

tension said there wasn't enough time under tension with the plyometric than there was with lifting what is that all about is that is that accurate is that or what i mean you you can change

Speaker 22497.12s - 2578.68s

stiffness qualities doing plymetrics but are we talking healthy or are we talking non-healthy tendons and so we know that a non-healthy tendon loses its stiffness. So a tendonopathic tendon loses its stiffness. And so the goal is to regain that. How do we regain that? We have to put a load stimulus in.And unfortunately, some of the tenopathies I see the muscular side of the tendon has whittled away. They have a loss of mass and tone. And so putting a player that has Patelotanopathy that has no base strength, that has lost a lot of medial quad and then we see a lot of proximal quad atrophy,putting them through a plyometric program, you're probably going to end up back where you were before they had tendonopathy if you make gains with them. So I think there's an element of biometrics are really important. Rate of force development is really key.But on the other side of it is, you know, you need to have a foundation and you need to have a good basic strength to build on your rate of force developments and to improve tenant stiffness. But I think you can, you know, if we were talking normal healthies, yeah, I think you canget stiffness from both. Don't ask me for a number on, you know, which one is preferred.

Speaker 12578.86s - 2590.82s

But I know that, you know, there was a great paper by a Danish NORP group a couple of probably 10 years ago where they looked at and Peter Parkinson PERSON actually brought the centre to me and opened my eyes to it.

Speaker 22590.86s - 2653.6s

He said, I made some comment about, well, you know, you need to sort of progress to those biometric type loads to improve your rate of force development. He said, but do you? And I said, yes, with a question. So he sent me a paper and the paper was very simple. It was a strength training group doing knee extension, a control and a group doing rapid ball kicks, just aiming for speed, velocity. And in the end, the group that actually did the bestwas the group that did no ball kicking, the group that actually did the best was the group that did no ball kicking, the group that just did strength work, knee extension. So, you know, when I say best, it was improvements in rate of force development. So, you know, I think there's many ways to skin a cat. I think we have to understand whether or not it's a tendonopathic tendon or a healthy tendon. Because tentopathic tendons function differently that have other mechanical property deficits that need to be addressed before you could probably push them into fasterrate loading.

Speaker 12656.82s - 2659.4s

Yeah, a lot to think about for me.

Speaker 02660.68s - 2664.88s

The equine world, that's where the UTC started, right?

Speaker 12667.16s - 2713.72s

Yeah, because I was kind of under the impression I had read the some of the old horse tendon books and it seemed like they had some pretty barbaric practices like old school practices but I thought they had I kind of was under the impression they moved on because I was thinking UTCs had like kind of gained popularity but one of the one of the interesting things was, I was under the impression for like many years, maybe still kind of currently am of like if you have that very unhealthy tendon,the way to get it back for humans, heavy slow strength, like isometrics, the good regular loading within sport, whatever it is. But then you would get these holes with the horse tendons that just fill in and they're not doing the isometrics and the heavy lifting. Do you think it's just a product of time that things would just fill in with the loading for them, which would be like

Speaker 02713.72s - 2720.32s

walking, jogging, yes. Trotting. They call it trotting. Yeah. That's a really good question,

Speaker 22720.32s - 2725.76s

actually. The only thing I would say is those tendons don't completely normalize. So

Speaker 02725.76s - 2733.46s

those equine athletes that do get these huge bullseye lesions, they take a year, so they will

Speaker 22733.46s - 2817.08s

put them in the paddock for a year. And that's a long time. And I don't usually have a year to rehab a tennopathic tendon. Keep in mind, though, they do stand. So they sleep standing up. And they walk around a lot. They don't get to sit down like we do. So there's always a strain or a load stimulus going into their tendons. Do I think that if you left a tentopathic tendon long enough, it might repair? Yeah, it probably would. It probably would heal, depending on what the goal of that athlete was. If it was just to walk pain-free, then, yeah, I'm sure they would get better and they wouldbe able to walk pain-free. If they're a high-functioning athlete with multiple body weights going through that tendon, sprinting and cutting and jumping, I think if you could get a year off, I'm not sure that they would probably return to that sport. We know that in the equine population, those tendons that are very sick, that get this bowing, and they get really, really large with the SDF tendon, they don't, they don't go really backto entirely normal tendons, and they don't function entirely normally. So, you know, when you're buying a horse, if you see a bow tendon, it's buyer beware. They can be really troublesome. But they, like you said before, they did have some awful barbaric practices of firing and really terrible stuff.

Speaker 02821.92s - 2831.68s

Yeah, that's what pin firing. Pin firing. Yeah, they still, some places still do it, unfortunately. But yeah. Yeah. Okay, so you, those, Daniel Boe PERSON was telling me, like, the isometric,

Speaker 22831.84s - 2835.04s

you love those short, like, three to five second isometrics.

Speaker 02835.6s - 2841.3s

The idea behind that is that for, obviously, the effect of the muscle, muscle tendon unit,

Speaker 12842.42s - 2845.46s

is it to get strain on the tendon? Like more strain on the tendon?

Speaker 02845.82s - 2848.18s

And when you do like the longer duration,

Speaker 12848.66s - 2850.08s

you're kind of thinking you're not getting

Speaker 22850.08s - 2851.64s

that same level of strain.

Speaker 12853.22s - 2854.24s

Correct. I mean, the argument,

Speaker 22854.38s - 2855.8s

I was working with the Premier League ORG football,

Speaker 12855.8s - 2859.5s

I literally just arrived home half an hour before this zoom,

Speaker 22860.1s - 2948s

where, you know, giving him a different load stimulus, but actually giving him a very high, high force isometric. So if you read the Aaron Patsas paper, it's 90% NBC ORG. And that's the goal of those short durations. If you were to say to do that 45 seconds,and he asked me exactly that question, why am I, why I'm not doing 45 seconds? And my response would be, do you think you could hold that for 45 seconds? He was like, absolutely not. So the response would be, do you think you could hold that for 45 seconds? He was like, absolutely not. So the argument would be what are you trying to, what's your target stimulus by doing a 45 second hold?And we talked about this last week. Some of the analgesic loading came from fibromyalgia by a paper bicosic in 80 something around 84, 86, whatever it was. Teninopathy is not fibromyalgia. And so, you know, the analgesic loading or the 45 second holds, I don't think, and, you know,Seth O'Neill PERSON published a follow-up paper to some of the, from the Rio GPE paper, showed that there wasn't any benefit, and there's been a subsequent paper since then. So, you know, I think when I, when I explained why I want to do the heavy isometrics to Daniel PERSON at the PELs was, you know, the load stimulus needs to be high.And the argument would be 45 seconds means it probably wouldn't be 90% NBC. And why are we trying to do 90% NBC? Because this is with the effect that it has on the stiffness strain rates and elastic modules of the tendon. But yeah. Yeah.

Speaker 02948.44s - 2987.76s

Yeah. Okay. So let's, I, I've, I've had, like many people, total tendon and the 30, 45 would provoke pain symptoms. And I was thinking just like, why would this be the case? Because like an isometric should be kind of tolerated well. And I was like maybe it's too much strain.I don't know. Is it too much load on the tendon? Have you seen? And then I'm even thinking with a three to five second, like the load would be so much higher, the strain would be so much higher.Would that be more likely to set off a tendon? Is that something you found?

Speaker 22988.88s - 2994.22s

Yeah, I mean, it definitely could do. I think with the patella tendon, one has to really ask the

Speaker 02994.22s - 3000.24s

question, you know, what's the morphology at the knee? And so Patella PRODUCT alter, players that have

Speaker 23000.24s - 3130.54s

Pateatella alter where their patella sits a little bit high, those players don't tolerate knee extension particularly well because their patella sits a little bit high, those players don't tolerate knee extension particularly well because their Patella PRODUCT is not going down into the Troclar early enough. It sits quite high. And so they don't love knee extension, if that's your loading apparatus. If you have retro-Petella changes, so cartilage changes on the back of the knee,they're not going to love the extension because we know the compressive forces are much higher. Knee extension is a great exercise. Please don't, please don't, you know, so don't quote me saying that I think it's a bad exercise, but all exercises are good exercise and all exercises are bad exercises. Just, I think it's content specific, so, or context specific, sorry. But the morphology is important you know some peoplepresent with proctalopatelitis but it might not be that it might be heartledge issue it might be a plic or a pleaker as people call them it could be fat pad impingement which is similar to a pleaker or a plika however you want to pronounce it so i think understanding what the what the pathology is why they've got the pathology is really important. But, you know, I think the extension is a really good exercise. The coming back to your question around the isometrics,I don't do long-hold isometrics because I'm not convinced that it provides enough usefulness to the athlete, to the tendon. And I would much prefer to get buy in doing another exercise, a different exercise, where I know that I'm really getting to the nuts and bolts of it. Because, listen, athletes are a rare breed. If you look at the percentage of people that get into the Premier League ORG or get into the NBAor get into the NFL ORG, it's really low. And so these guys are unique specimens and they need to get better quickly. And so would I prefer to have, you know, three tools that work and two that might or just use the three tools that work or three loading strategies that work. And that's sort of where I come from. I want to get complete buy-in from an athlete.I want to really get to the nuts and bolts of what works. And that might not be doing long-hold isometrics

Speaker 03130.54s - 3144.08s

because I don't think the stimulus is high enough. Yeah. And my own experience and probably the experience of many thousands of others, it's like to get the analgesic, they could just warm up, right?

Speaker 23148.26s - 3155.02s

Exactly. Get on a bike, have a a cuddle do a couple of squats get on a leg press do 10 reps of something moderately heavy and they're probably warmed up

Speaker 03155.02s - 3164.64s

so yeah i i would agree but but i'm not saying don't do it i'm saying use it sparingly and

Speaker 23164.64s - 3180.38s

it not be the only thing that you do. Because chances are people with long history of telogenopathy have, you know, quad atrophy. They have things that they need to work on. And that's probably your target.

Speaker 13181.1s - 3181.78s

Yeah.

Speaker 03182.16s - 3182.7s

Yeah.

Speaker 23182.7s - 3188.94s

I mean, I look at after actually conversation with you and a few others is like,

Speaker 03189.44s - 3216.22s

I'm thinking that just getting good load through the quads, I guess with that, um, is probably a beneficial thing for like the, maybe it's doing something to the inhibition that you're getting from the brain. Um, I'm curious on when you do those like three to five, like 90% to get the, um 90% to get the, try to get the tendon strain. If you have a muscle that is so weak, that will not allow for the level of tendon strain, right?Potentially not.

Speaker 23216.64s - 3279.6s

And so I don't normally start with that level of intensity with someone that might be in a lot of pain because they probably wouldn't be able to do it due to pain anyway. So I just start with, you know, moderate load. I like the use of BFR. I think there's some really good evidence for BFR and tendons,Patella Antichilles. So I think that's a very useful tool, very useful adjunct. We know that there's in Patellofemoral research for BFR occlusion training, that there's some analgesic effects from doing that.I think it's really useful. So I would do an isotonic to start with it might be that you need to limit their range if they have a very beat inferior patella pole if they've got a calcification at the inferior patello pole uh you might need to modify the loading range the depth I think that can be quite important getting someone with you know a beat inferior peteleapole where you get this camming effect in deep knee flexion they're not I think that can be quite important. Getting someone with, you know, a beat inferior patelopole,where you get this camming effect in deep knee flexion, they're not going to love it. You can get them there eventually. But to start with, I think, get them into a range. They're comfortable so that can actually do some work, do some loading.

Speaker 03282.08s - 3308.84s

I had a call yesterday with this girl bilateral.good and it's she was a physician so she had kind of knew what she was doing but I couldn't offer any insight I felt like like differences Pateller Oz or at least distal Patelotellor Tenopathy I guess not Osgood. Have you seen that the the distal patelatellopathy? And are there any differences for getting those people back?

Speaker 23309.64s - 3326.24s

I mean, it's a distal insertion tenonopathy. It just happens to have an evulsion sometimes. It doesn't always have to, but it's a distal insertion tenonopathy. And so I treat them very much the same as I would proximal. They just need to load consistently, long durations be be really patient with it but it's

Speaker 13326.24s - 3336.56s

it's a it's an insertional tenonopathy without a doubt yeah um okay i cover a lot of these

Speaker 23336.56s - 3342.96s

you have me thinking of too many questions but uh that's fine the so you kind of actually

Speaker 03342.96s - 3345.66s

address some of these anatomical variations with the Patelottenopathy,

Speaker 13345.86s - 3352.22s

like the Patelah Alta changes on the backside Patela. What exists for Achilles tendon?

Speaker 03352.9s - 3358.64s

Are there any of that exists for Achilles? Yeah, I mean, you can have a Hagelin's deformity, which is a bit of a bony bump.

Speaker 23359.18s - 3383.78s

The diagnostic criteria for that is a little bit loose, but that exists. Whether you have an enormous plantarous tendon in close approximation, that would change your loading strategy, as we talked about before. You know, we do see very rarely accessory salacious tendons or very, very low salius tendons. How that changes your loading strategy, I'm not sure it particularly does, but some of these athletes get compartment-like symptoms.

Speaker 13386.44s - 3398.66s

So, yeah, I mean, you know, the usefulness of some of the imaging techniques might change your learning strategy and the range in which you work based on what you're seeing in your imaging.

Speaker 23400.82s - 3409.18s

When we talk about that, so we talk about the isometrics, 35 seconds, when it goes to the heavy slow resistance,

Speaker 03409.72s - 3412.46s

I say heavy slow strength, but I guess heavy slow resist, HSR.

Speaker 23413.5s - 3415.56s

How heavy do you need to go?

Speaker 03415.8s - 3417.84s

How heavy are you going to try to get those tendon changes?

Speaker 13418.9s - 3420.98s

I mean, initially it's a volume-based program.

Speaker 03421.22s - 3427.36s

So, you know, I've asked people to rate their difficulty. And so I would say

Speaker 23427.36s - 3470.24s

anywhere between six or seven out of ten difficulty at the end of a set. If they're finding it particularly easy, then they need to put more weight on. And that progressively changes. So the magnitude goes up, the volume goes down. So, you know, initially, why don't do one-RM testing? I don't think many people do anymore. I think it's usually three-r-rm testing. But I think, you know, initially, why don't do one-r-r-m testing? I don't think many people do anymore. I think it's usually three-RM testing. But I think, you know, you want them to feel like they're working,that they're actually doing something productive. And so around that perceived exertion, I think it's quite a, I think a lot of people can relate to perceived exertion. So how hard do you find that? Is that easier? Is that hard?People can sort of, they're pretty accurate with it. So I sort of use that as a metric for them to gauge their

Speaker 03470.24s - 3482.5s

intensity of workload. And you said volume based early on. So like you're doing, is it just more, well, higher number of sets, higher number of reps, and you're working down to higher intensities?

Speaker 23483.34s - 3545.98s

Yeah. So with, with heavy slow resistance program, it's four sets of 15 of each exercise separated by an adjunct, whether it be hamstring, calf raiser, if we're talking to teletendom, in between each of those different exercises. Same kind of thing with the Achilles PRODUCT. But then if you want to do BFR, I would sort of, I do my BFR in a more cruel, cruel way. I essentially would try and do them to failure.Most people would probably follow some of the published research, which is 30, 20, 15, 15. Yeah, I'd like to train athletes to failure if they can tolerate it as long as it's safe. And, you know, we're not going to do any long-term damage i think there is some there is some really good some of the nielsen which was one of the earlier bfr papers demonstrated that you can sort of train them with very high reps to almost failure and you get some good you get some really good muscle tendon or that was a musclepaper but you get some really good muscular effects yeah i was

Speaker 03545.98s - 3553.06s

i'm kind of aware recently people talk about bfr for for tendon adaptations and um i i'm trying

Speaker 13553.06s - 3564.9s

to figure out necessarily why because it's like the the load is so light so it seems contrary to when we had that isometric talk you have to lift very heavy you know yeah i mean

Speaker 23564.9s - 3637.3s

from what i gather i believe it's the increase in lactate. The lactate stimulates this fibril production or collagen production. So I think there's a lot more work coming out. The Danish group, Michael Keir and Peter Magnuson's PERSON group are going to publish some really interesting work on it. They do some biopsy work up there, which is really impressive. And they will have probably a few more answers for us in regards to why but interestingly i used to present on the use of bfr and i would always say great for muscle and then thisyou know big red line across but not useful for tendons and now that red lines come has been deleted and you know some really good published research on on the usefulness of BFR four tendons. So, yeah, it's, it's, I think there is a place for it. I have it in all my programs. It's just obviously people going to a gym can be hard enough, elite athletes aside, but your generic, you know, you're sorry, not your generic, your average population, generalpopulation, they struggle enough to go to the gym, let alone, you know, purchase a occlusion cuff that's safe, that calibrates pressures. I think that's useful. They find it difficult enough. Yeah. So if it's having that fiber production, do you think

Speaker 03637.3s - 3642.08s

it's having this, it could have this heightened effect on college synthesis? Yeah, absolutely.

Speaker 23642.44s - 3653.64s

Yeah, absolutely. But we're going to know more in the next probably six months or so. One of Peter Magnusson's PhD WORK_OF_ART students is going to publish some really interesting stuff shortly.

Speaker 03654.08s - 3666.88s

Yeah. There's this talk on seated standing calf of the seated is just a worse gastroch exercise. Where do you stand with that? There's usefulness for both or what?

Speaker 23667.88s - 3744.02s

It is definitely usefulness for both. I mean, you know, C2D is generally has a greater bias to Salaes, the standing has a bit of both, but has a bias to gastrox. So, yeah, I mean, we published a paper some years ago looking at the loading positions for Achilles' standing or straight leg. And we found that the dorsal flexion range is really important, but it's the moment arms.So if you were going to load someone and you wanted high strain rates, they have to go to end range dorsal flexion range is really important, but it's the moment arms. So if you are going to load someone and you wanted high strain rates, they have to go to end range dorsal flexion, but also with a long lever. And so it would be a standing calf raise. And that was Marvin Yeh's PhD in 20, gosh, when was it, 20, 22, I think, 2021, 2021, something like that. That was an imperial paper looking, using inverse dynamics. Really interesting paper.But you do get, you do what limits your load on the tendon in a ceded position is how much dorsal flexing you can get into. So the more dorsal flexing you get into, the higher the loading rate is.

Speaker 03745.34s - 3782.54s

And that's like across Patela Achilles. If you get into deeper, you change the joint position to get to like a deeper level, like more knee bend, more dorsiflection. You're going to have higher, you start off with a higher tendon strain, like a higher elongation. And then the next part is coming from how much the muscle can pull.Exactly. I asked this to Karen PERSON, and I was like, there was this idea. I think it was put forward by Greg Lehman PERSON of stretching for tendon adaptation. And he was kind of speculating like, why don't we just, couldn't we just do a static stretch and get tendon strain? Where do you stand with that?

Speaker 23785.14s - 3817.52s

I think you need to have a higher load stimulus than probably what you're going to do stretching, but also the isotonic nature of the contraction, even though the tendon doesn't know whether it's doing a concentric and eccentric contraction. The load duration, as we talked about, is really important, but the magnitude, and I'm not sure just stretching, you're going to get enough, probably going to get enough stimulus for the tendon.And you're also not going to change the muscle by just doing stretching. So. Yeah. Yeah.

Speaker 03817.72s - 3841.94s

Yeah. You got time for a few more? I do. I do have to take my son to swimming shortly. Okay. Like in what, you got eight minutes? Yes.Okay, perfect. Okay, so this, we talked a bit about tendonopathy, tendon rupture. Do you think they fall kind of, do you think they're similar? Because I was, yeah, go ahead.

Speaker 23842.84s - 3938.88s

No, I mean, I know where you're going to go with that. Karen PERSON would say they're not the same and they're definitely not the same. But tendonopathic tendons can rupture. The tennopathic tendons, they increase their cross-section area when you see them nice and thick. And that's because they're trying to, or the tendon itself has this influx of, you know, agricans, product of glycans fluid because it's trying to increase its cross-sectional area.But it can still fail. And so this whole thing where I've heard in the past, you know, terminopathic tendons don't rupture. Yeah, but they do. They definitely do. If you have enough disorganized structure, then you may rupture.But also those that rupture without thickening, increasing in the cross-sectional area and this sort of fusiform looking tendon, those that rupture, I think they're a unique group. They do have structural changes. So if you ask any surgeon that does these Achilles repairs, they would say, I'm a ruptured tendon.Yeah, well, that's extremely tenetopathic tendon. And I had a young elite squash player come in last week who said, I've never had tendon symptoms. You know, all I'd done was I'd had to take three months off because I had this very bad chest infection. And I always then got back to playing three times a week and I ruptured two weeks later. It's this rapid accumulation of load with no adaptation on the tendon there's obviouslysomething going on at a several level where they're just not all of a sudden tendon knows it's too much load and not thickening which is what you really want to see I think what you're what

Speaker 13938.88s - 3943.72s

you're experiencing with these tendons is this rapid accumulation with that no adaptation

Speaker 23943.72s - 3995.36s

and I've seen these I've seen these tendons that, you know, they asymptomatic. And because I scan, serially scan a lot of NBA ORG teams, I have seen and unfortunately seen a couple that have ruptured and their pre-scans were very teninopathic. The surgeon would say, I've repaired it. It's extremely tenepathic tendon. So, you know, we know that's extremely tenepathic tendon.So, you know, we know that normal tendons don't rupture, fluoroquinoline induced aside, normal tendons don't rupture. There's always a reason for these tendons rupturing, and whether it be, you know, a rapid increase in their training volume or intensity, there's a tipping point at which the tendon just won't adapt. And so, you know, but that being said, ruptures are not, if not all ruptures

Speaker 13995.36s - 4001.64s

have tendonopathy. Yeah. I know Karen PERSON probably said something similar to that because I've had

Speaker 24001.64s - 4005.32s

lots of conversations with her about that. Yeah. Yeah.

Speaker 04005.86s - 4011.94s

Yeah. Last time we talked, you were, it was actually a few weeks after I had looked at that carbon

Speaker 24011.94s - 4018.2s

14 data, but that rupture study about how they saw the elevated turnover prior to rupture. And then there was a tendonopathy study.

Speaker 14018.28s - 4029.8s

They saw the elevated turnover prior to tendonopathy. Exactly. And I was like thinking of that iceberg thing. But you were telling me that that early stuff might have been on just people that were

Speaker 04029.8s - 4033.14s

like non-athletes. Yes.

Speaker 14033.38s - 4044.4s

It painted in my head where I'm like, if the tendon is static after 17, it's probably going to be static if you're a non-athlet. But if you're an athlete, of course, the turnover would be higher. At least that was a speculation.

Speaker 24044.6s - 4123.74s

But yeah, go ahead. Yeah, no, exactly. I i mean i think from the rupture stuff we know that um some of these some of these patients that they're the c14 there was a there was the tendon was very metabolically active within the tendon prior to rupture but what we were talking about is the kachia henemae paper looking at c-14 and the central core of the tendon not changing. And my question to Kartier PERSON was, you know, do we think that that's, do we think that that holds true with tendons, you know, tendons that we're tryingto change? And I guess it depends on your cohort. If your, if your sample of tendons that they used for that study were non-athletic, non-exercising tendons, then maybe the core won't change. But I think in essence, the core of a tendon can change. And we have seen them change where, you know, how does a, Seth PERSON, for example, just put something up on Twitter ORG showing a partially ruptured tendon, and then six months later,no sign of the tendon rupture. So if we think that tendons don't change, then why are we seeing tendons normalize and go back to normal function? I've seen that in my league and basketball, and if you give them a high enoughand a regular enough load stimulus, the core of the tendon will change.

Speaker 04125.02s - 4135.08s

Yeah, that, I remember Peter Magnuson PERSON had a presentation I was watching where I guess back in the day they thought it was like rings of a tree, the tendon. Yeah, but that was like, I mean,

Speaker 14135.08s - 4160.26s

this was before my time even, but he was like, that's not the case. Like the whole thing has the ability to change throughout. I guess the last one before you have to go here is the tendonopathy continuum. I was telling you about this whole thing, reactive, normal reactive, disrepair, degenerative, and you were kind of saying that you don't use that. So how are you thinking about the process?

Speaker 24161.28s - 4286.38s

Yeah, I mean, it's a really good question. I think there are acute tendonopathies. So, you know, one day I'm relatively pain-free and the next day I've got a really sore tendon. And I think there is an acute nature to it. I think I don't go down the continuum that was that was put forward mainly because it's a theory. It's not entirely proven. And I think also the anatomy of a tendon, particularly, for example, the Achilles, you know, they might have paratinopathy. They might have plantarous related. They might have some other pathologies around it that probably doesn't fit into the continuum particularly well. I do believe that there is an acute nature. I do believe in a chronic nature of tendonopathy people that just have recurrent tendipathies. And I think, you know, I definitely do believe in that.But I don't necessarily follow a fixed continuum because I think it's an opinion of some tendon experts. I just not sure I think it holds particularly true in all cases. But I think the anatomy and thepathology of the tendon is really important. Are we dealing with a plantaris? Are we dealing with a linear tear?Are we dealing with a paroteneopathy? Are we dealing with eventual surface tear? What exactlyis the pathology? Because when you see enough imaging, you will see that potentially you kind of forget the continuum and you look at actually what's in front of you, which is during COVID when players were at home and then playing Premier League, we were seeing, I saw 10 in a row linear tears that went from along, the latricide all the way through to the MTJ and crossed immediately.Where does that sit in the continuum? I don't know. I couldn't answer that question. So it's a theory. It might work for some. And if it does, fantastic. If you're getting your patients better that have tenopathy, fantastic. That's all you could ask. I just not sure. I don't really, I don't think about it on a daily basis when I'm

Speaker 04286.38s - 4295.44s

looking at a tendon. Yeah. For the, for the average Joe PERSON's, because this is really in-depth,

Speaker 24295.44s - 4299.42s

the average Joe PERSON's that want to keep their tendons healthy and they compete in sport, what is,

Speaker 04299.46s - 4307.46s

what's your advice? For Achilles, seated calf rays, staining calf rays, two, three times a week,

Speaker 24308.08s - 4315.86s

Patela PERSON, regular quad loading, you know, leg press, knee extension, squat, heavy, you know,

Speaker 04315.86s - 4316.94s

just condition yourself.

Speaker 24317.54s - 4388.48s

You know, to be an explosive and robust athlete, you need a big engine. And those that engine comes from being nice and strong. There has never been a time where I've ever said to an athlete, oh, you need a big engine. And those of that engine comes from being nice and strong. There is never been a time where I've ever said to an athlete, oh, you have a kidney sent an op because you're too strong. Never. And I would question anybody, any clinician that's ever said that to a patient that you'vegot, oh, you've have a kidney synopathy because your calf is too strong. So I think, you know, the average Joe PERSON that would, that wants to play sport once or twice a week, just keep nice and strong. That's the key. You know, we know from some of the Delphi studies and, and there's systematic reviews that some of the things that, unfortunately, we are non-modifiable, that we can't change, age, previous injury history, things that we can change is strength, alcohol intake, BMI, those things we can change and those make a big difference to whetheryou experience Achilles on Patal tendon, keeping your body mass down, you know, those athletes that have Achilles tendonopathy or that have ruptured their Achilles, keeping their body mass down, it makes the goal of getting to a, you know, a multiple of body weight to return to play much easier.

Speaker 14389.4s - 4394.36s

If you're eating and putting on body mass, you just, that's like the carrot in front of a donkey,

Speaker 04394.36s - 4405.04s

you just have to keep on, you just keep on trying to get stronger and stronger, but you just keep on getting bigger and bigger. So those things are really important, but strength is really important. And obviously then training load load don't take three

Speaker 24405.04s - 4444.74s

weeks off and play three times a week if you take three weeks off go back to once a week twice a week but again it's age specific if you're a 17 year old athlete i call 17 year old athletes you know rubber bands because they're just so springy and bouncy they can kind of get away with it when you get to the ripe old age of me at 45 and a half this year, you don't have that, you don't have, unfortunately, that liberty to takewhen you don't train enough, you travel too much, you can't just, you know, go on the football pitch or play on the basketball court and rip it up. I don't ever rip it up,let's be honest, but I like to think I did. Yeah.

Speaker 04445.62s - 4459.58s

Well, some people try, and then they, they message me that they ruptured their particular attendant and I'm like, well, there you go. Rare. I don't want to, yeah. But, all right, Jared PERSON, tell everyone where to find you if you want to be found.

Speaker 24459.58s - 4462.16s

If I want to be found, I'm on Twitter ORG.

Speaker 14462.5s - 4465.52s

I'm trying to think it's at Jared Anflik, I think, or at JLA ORG.

Speaker 24467.02s - 4502.02s

I mostly only kind of use Twitter. I do have Instagram ORG. It's, I think it's JLA 8888. I don't know. It could be. I'm not sure.Maybe it's JLA underscore triple eight. But yeah, mostly on Twitter ORG. Yeah, I mean, I'm not sure maybe it's JLA underscore triple eight um but yeah mostly mostly on twitter um yeah i mean i'm around i am looking i just don't have time i have a lot of time these days to input into twitter conversations and battles but i am i am watching and listening yeah all right man

Speaker 04502.02s - 4506.4s

thank you for coming on thanks joe pleasure thank you for having me i really appreciate it