Tendon & Cartilage with Jess Ellis

Okay. I'm sitting here with Jess Ellis and we met in Vegas a few years ago. No, and oh, yeah, yeah. We Vegas for the elite basketball conference and we spoke this past year at um, what is it? I have lectures. Elevate? Elevate? Yes. Yeah. Was it? Yeah. So you gave your, I gave talk on ten and you gave talk on the cartilage stuff and we had some pretty good conversations outside of that. And then some of your, we had some patella femoral conversation that was, I was like, we need to do a show because you're saying a lot of things that I'm not seeing in the research and I guess we'll get into that today. But you got a, this is a tango and cash show. You're a guy that knows a lot of movies. I've never, do I need to watch the movie? Yeah, you do. It's a great 90s flick, Stallone and Kurt Russell. Kurt Russell, Longhaired, copped, kind of wild and then you got tango, Stallone, glasses, button up and they, they work as a team. So you got tendon and cartilage and yeah, it's a good movie. You need to see it. You got to be drunk, though, or have some inhibition of your brain to watch it. I, I've always loved Kurt Russell. Deathproof was a, I like that movie a lot. I didn't like how the, the female was one. The bad guy lost. It was not good, but the, you got to tell people who you are. Yeah, my name is, Jess Ellis. I'm a physio by trade. I've been practicing for 16 years. You're from Minnesota. I'm from North Dakota. So very close to you as a neighbor. In the last decade, I've been leadership roles within the New York Knicks and the Portland Trailblazers and then also at XO, so I was director of PT. Prior to that, I did concier work with tennis and prior to that, I was wearing triple pleated khakis and seeing 30 patients a day and hating my life. So that's kind of the evolution of me for my career. I did my PhD on the wearable, the ethics behind wearable technology and the NBA. So to see data rights and how data is being used for and against players. The ethics. So what do you mean? It's a qualitative study asking a lot of questions about, I mean, anytime that you have data on someone, there's a change in power dynamics and there's a conflict of interest. So it's an ethical question at that point. So we put so much emphasis on how valid or reliable are these wearable tech, but there's no studies or anything talking to the tested the athlete and their beliefs behind the use of the data. So it was a qualitative study, 15 players interviewed and kind of looked at the other side. What did you find? If you're not utilizing the data in day to day and having them as an active participant, there's a lot of mistrust that happens. They don't like sleep data used. It's going to do it. It should be an independent thing on their behalf, not through the team. There are a few different types of athletes that either like technology or not. So the Ivan Drago's are the ones that want the 1% better. They're the ones that want to get better and use that tech. They're going to be much more engaged and they're the adopters. The second group are the resistors. That's the big brother group. I don't want anything on me. And then the third group is the optimizers, which is they're compliant with the direction, but it has to be it does not take away from their day to day activity. And how do you make that as seamless as possible? So it's not disruptive. And that's with those three types, you kind of have to do different strategies on how to approach tech in the NBA. Well, how did you make it out? Well, I'm actually from Wisconsin, but the biggest city is Minneapolis. So like Minneapolis, I was in Minneapolis because no walkies further away Green Bay. Green Bay is not a big city, but there's just further from me than Minneapolis. So many opposites. I was in the big place. I go, how did you break out of North Dakota to end up in the NBA and end up in these roles at you? I hate country music and I don't drive a pick-up truck. So those things I left and I went down to Phoenix knowing that that was the highest chance for me to get into pro sports with all the different opportunities. So I married my wife and we moved down there. And now you're back. Yeah, we're in Scottsdale. I have a private space, a lab where I work with athletes. I have an education company called rehab code, which thank you for sharing some of my material, but that's where a lot of what I talk about when it comes to clinical side. And then yeah, that's kind of my two headed beast at this point. Okay, I want to talk on Patel Femreau, but we were talking a bit about tendons before and even at the the elevate, you said some really interesting stuff on tendons. The Achilles Island, what do you mean? The Achilles Island. So I talk about this because it is the one joint that takes on ground reaction forces immediately. And that's the issue is it takes longer for an Achilles synopathy to recover and to get past that acute phase because it cannot hide. So it's it's an island of itself. Now Patel are tendin, it can be dummy proof like it doesn't have to be great rehab or it doesn't have to be great as long as you're loading it to get past that acuity phase and just to get it to respond to certain loads and thresholds. A lot of times they go off and they kind of respond on their own, but they're also hiding between two joints, the glute and the the soleus slash ankle. But that's the difference is you cannot hide from the forces being administered to the calf complex, which makes that even more problematic. And likely one of the reasons why you see more ruptures to that tendon verse a quad or Patel or tendon. Yeah, okay, that makes me think because I have dealing with a little bit of Achilles myself and then Patelor is yeah, I can just I can still play a basketball and do everything that would load my or Patelor without doing it because I just land with stiff knees or I just just shield away from knees bend at my hips. The Achilles is they're not a strategy to avoid. Like you can't people can't do more heel striking or they can't just skip over that foot. You're thinking like you can't you have to you're going to be loading the Achilles if you're going back to. I mean, yeah, there are there are some strategies and some of this is you know anecdotal, but I look at the rear foot is the rudder of the foot. So how does that calcanius look on when it takes on ground reaction forces? And a lot of times what I've noticed is an everted calcaniol position. So there's more loading on the medial side. It's not great for the Achilles complex. There's more traction and loading on that medial side and it's similarly kind of unwinds the sub tendon twist that it naturally happens. So sometimes when I train the Achilles, I will twist it from a medial to lateral orientation either by taping or manual and have them trained to make sure that I have good vector pull happening on the medial gastroc because we know the medial gastroc is likely the most inhibited portion of the calf. I'm trying to get and twist the tissue to then align better and I use that strategy a lot with Achilles repairs when you're really fighting a you know an altered pulley system that doesn't work the same anymore. The collagen fibers are all over the fricking place and it doesn't have that natural pull like it once was and that's why you can't really pull up in the end range planar flexion very well. It's sometimes it might be a strength issue but more importantly the tendon complex is completely different at this point. So they're more they're getting more medial stress are they their foot is looking like more everted pez pez planis yep so more flat footed more of a everted position and more loading. So if you can get more of an elevation to the medial side which will then will put more load on the lateral side of the calcaneus will have a better orientation to the Achilles. Yeah and then even like playing around with the stiffer sole which means that pushes the center of mass or the mechanical advantage of the foot further out can help with improving the mechanics of the calf complex. You said something at that at that conference this this whole fall step thing fall step people are typically where they're rupturing it in the NBA. Is there a research you're saying this that there's when you get older there's more fall steps. Well there's more fall steps I think because it's a strategy to beat the defender at one point in space and if you a are older or b if you are not athletically built to have that same ability to produce power, you're going to find strategies to create distance and win the strategy. So I find that it is sometimes a strategy used more for individuals that are not as elastic, because they're not able to generate the same amount of pop with a more highly toned or stiffer complex. So it's more about the game and how you change if you A start to get older and you're having to find ways to accelerate or if you're just naturally not as athletic. This is seven years in the NBA looking at a lot of games sitting court side watching stuff, but there are some studies that talk about the mechanism. I'm just talking more from the performance side and why somebody would inherit that type of strategy. You got good memory, dude. Oh, I'm certain things. I'm sure we've talked about a lot of things that just forgot, but when you say one thing, it's usually something I think about every day and I'm like, I did, I never, I was like, I wonder if there was a study on that that you were talking about, but it just made me think about it that it's like, it's more about a study not on the mechanism. I mean, it does talk about the mechanism, but it's more about the prevalence of most Achilles ruptures happen at that type of movement. There is some dialogue that talks about, like you see these individuals that have like a previous calf strain and then they that leads to an Achilles tear and the thing that I've noticed or what I've been reading is there's a combination of a delayed neural firing to the gastroc and it's the combination of it not firing as quick as it needs to and then there's a drop in the calcaneus into more dorsiflexion and then there's that delayed firing. It will fire then, but it's at the moment when it's dropping into that eccentric loads to the tendon. So it could be a combination of the tendon itself, not being able to take that force or the inhibition of the gastroc and firing at a delayed as it's moving down into a calcaneal drop. Yeah, I think I think Colin Griffin, I had him on a long time ago. I think he was he was getting at that that your that the calcaneus is dropping and then that delayed contract. So it's like the tendons getting pulled at both ends when it's vulnerable because the heel, whereas it should have been pulling a bit earlier. And I mean, it's kind of like if you're rock climbing and you got a spot, I'm never rock climbing. But if you had a spotter that like started to like nod off and that person dropped and then they woke up and pulled the rope to like save the person, that's that that dropping of the person and then the the quick pull from the guy up top spotting is when it snaps. With this whole like so that that presentation with the foot like that medial or that more, I guess flat footed that proper if I said that. Yeah, flat footed presentation. I was thinking of this talking to a killy's guy the other day, maybe it was yesterday. Yeah, killy's guy yesterday college basketball guy. I was thinking of the sub tendons and I'm like, I wonder if there is a certain presentation, if there's a presentation like that, would you have more, you kind of talked about it, right? You have medial gastroc is probably more like weaker than so would you have certain sections of the Achilles tendon that are weaker than other sections and you'd want to bring them up? I mean, possibly that's, you know, we can talk about stress shielding, we can talk about the neural aspect of firing. If you look up at the knee, that's the same thing that happens with, you know, AMI or just a weak quad is the vast slatter Alice will fire at a quicker rate and what happens is that firing then changes the way that the patella is sustained in the groove of the of the trochlia. So it's very similar like these decondition or previously injured structures, there can be segmental changes of firing. So yeah, it could change that and maybe you alter the way that you put your foot so that you can load the medial head more. But that's going into more of the, you know, back in the 2000s, when I first I graduated in 2009 and we were drooling over the ability to fire specific exercises for the VMO and there's never been research to show that there's specifically things that can fire just the teardrop. So a bunch of nerdy PT's were very, very upset about the inability to find that. Do you think there is any truth to that? Like certain exercises to people will say, bias, they'll quote, bias, you know, we're going to bias. I don't, I don't, you know, I'm not sure. I mean, clearly when you start playing with length tension changes, you can play where you can generate more force. But at that point, if I feel like it's something that's maybe more compartmentalized, then I just really, and it's a compartmentalized and an inhibited area, then I want to put a some form of a elected stem to wake that up quicker. That okay, that vastes that are Alice because I've, I had it when I quit college, I went to California and I was like, COVID so I was, I was lifting heavy, but really no basketball. A lot of the hoops were taken off and they were boarded up in California. I did find some so I'd dunk, but I was just like lifting heavy, dunking just really, I guess heavy explosive training. That was about it. And my, I got Patel O'Femeral pain. And then my vastest lateralus, like just sleeping, or maybe as well, I see that I'm just sleeping at night or doing anything. I felt this, this tone, this really big tone in the basketball. It was just annoying. And then I think that's contributing to the Patel O'Femeral pain. Maybe if it was pulling the kneecap a little differently. Yeah. Is there any truth to something like that? You're, you're an of one, right? You've just felt it yourself. But that is something I look at. I look at tone. If you're a client of mine or a patient, I would likely do some compartmentalized manual therapy to that area, either in, you know, heavens forbid that I touched the IT band because it's so strong that why would you ever form roll it? There's still neural input to that tissue. And there's still that interaction or interface between that vastest lateralus and the IT band. So I do put some merit either dry needle in or soft tissue, lengthening massage to that area to help that little bit of if it's one or two millimeters at change because what we find in the Patel O'Femeral joints specifically at 10 to 30 degrees. That's not a great range. And the reason is is it is a high stress low, sorry, a low surface area high concentration of stress to the distal patella. And also it's not sitting in the cup of the trochlia very well. So it can have a tendency to tilt in that range. So you're telling me that there's a there's a not a great location to just put localized stress. And then it can be it, you know, maneuvered a bit laterally that can piss it off. And I've looked at enough MRIs with MBA players and their trochlia doesn't look great. But the lateral portion of the trochlia is the thing that shows more wear, which tells me that lateral side is just dropping into more compression. And that is a combination of hip adduction and internal rotation, which causes more pressure to the lateral facet of the patella. And also in baseball, we call the tears in necessity, which is basically I'm going to throw 98 miles an hour. I need to get my shoulder this far to throw it. And there's going to be changes to the labrum. There will be tears in the labrum. And if you put them in MRI, it's not going to look great, but they're still able to accomplish the task in basketball. I call it the wears of necessity, which is with time the trochlia will wear the patella cartilage will wear. It's not a bad thing. It's just the outcome of thousands and thousands and thousands of jump shots and deceleration points within basketball. The wears of necessity. Okay. So tendon pain, we don't need to get into maybe well pain is complex, but tendon pain maybe quits, maybe more talks about more simple with patella femoral pain. I've never I've never found a good everyone's the because we go to a structure and that'd be like, oh, he's kind of a patella is irrelevant because everyone gets kind of a patella with age patella femoral pain. We don't know the structural problem. Let's just rehab it. Based, I'm probably someone off there, but that's kind of my understanding. What's what's going on with patella femoral pain? What does happen? It's a physics problem. And that is you got this bone, it's a sesmoid bone, it's a floating bone in a groove. And what is its value? It's one of the most important bones of your body because it creates a change in your moment arm for your quad. And it's stronger. And it can generate more force through a longer arc of movement. So as much as it can produce force through that bone, when it's injured or with time of degradation, it also leads to pain. So it's as much as it's a proponent of function, it's also can be dropped into more of a dysfunctional pattern or a dysfunctional issue. So knowing that, you got to look at it from it is a it's a dynamic pulley system because it moves within the groove. Now, another hinge joint that we talk about is the tricep. This is the fallcrumb, but it does not move. It is a fixed pulley. The knee is special because it glides with arc of movement, which means that joint is engaged through the whole range of motion. You can't hide. Just like the Achilles on Achilles Island, you cannot hide load through the patella femoral joint. You can with the tendons in some ways, but the engagement and the compression that happens to that bone is always on. So that's where you get the problem. Now, your job is to find where there is improved tolerance to joint angles that can produce force and then respect the areas that they can. And again, I kind of talk about this stress concentration. So when you're in shallower ranges and when doctors say don't do the knee extension through, you know, it's going to kill your patella femoral joint. From 30 to 0, it is a very hot spot. So think of a stiletto stilettos, like a very pin point pressure to the inferior pole and the inferior part of the patella. As you go into mid range, so 40 to 60, it's going to get better congruency and it's going to drop in the trochlea and the cartilage behind the kneecaps going to be better to take on force. And then so think of more of a snowshoe. So you're spreading that force through a longer period of time. And then as you get back to 90, you have a really nice positioning of the patella, but the problem is is there's so much force at that point in that range of motion. So if I'm looking at angles, that can be problematic to the specific cartilage or the trochlea, it's likely deeper positions at 90 and up and also early stages or early shallower ranges. Is that okay? So I talked to Claire Robertson maybe many years ago and it, I, it sounded like the leg extension, like it was that zero to 30 is like the, the, the lot of pressure patella femoral is it, is that the right term patella femoral pressure? And then when you get like the 40 to 60 is pretty good. When your feet are on the ground, is it like the same or is it kind of opposite or what's going on? Like in a squat in a squat. Yeah. I mean, that's just, yeah, the mechanics may change a bit. I know for a fact with people that have patella femoral pain, if you do a TKE from 30 to zero, they respond pretty well. So, but I also know people with patella femoral pain don't do well in a split stance position with the leg being in the back position. And that's because you're at about that 30 degrees of flexion, but the thing is it's the relation of the hip. Now you have the hip in either neutral or an extension and now the length pension ratio of that quad is tighter and now there's going to lead to more compression behind the kneecap. So a lot of times I have to modify that position into more bulk area and with more knee flexion to do different exercises, but the split stance position will be tough. So, you know, for me, it's more about probably deeper ranges in close kinetic chains. So 60 to 90 and kind of plain shallower with close kinetic. Okay. When you get to 90, like so this idea of the pressure is the pressure is really distributed well behind the patella femoral pressure is really well, but the problem then becomes there's a lot of force that you can. It's the absolute pressure. It's the absolute total amount versus so it's built to take it on in that that orientation and how all those facets kind of fit nicely in the trochlea, but it's the totality of force at that point. What is the force coming from the quads compression compression from the quad and the patella tendon? Okay, compression, it's like it's it's like it's pushing the kneecap down into the into the groove or yeah, pushing it into the groove. Yep. Okay, so it's like you have when you get that idea, you talked about the snowshoe. So like 40 to 60 is like really the snowshoe a lot of distribution of pressure and that stays from like the 40 to 60 going to 90 going even deeper. Does that that pressure stays like a snowshoe? I mean it starts to narrow a bit again as you go deeper, but instead of it being hit kind of in the distal part of the patella, it's putting more load on the superior or the proximal part. So if you go into more flexion, you're going to be loading the upper portion of the patella and the quad tendon, which is why why you see the quad and patella tendon ratios change with movement. With the with the patella femoral, I guess, where you typically see it, you said you see it more, where do you see the pathology more on the underside of the patella lateral side, medium side, where is it? It varies. It varies, but central lateral to the patella and lateral portion of the trochlia is common. The cartilage has about six millimeters of cartilage. It has the most cartilage out of any part of your body. So there's a really good bed of cartilage behind the patella and the trochlia is a very thin layer. So only about two millimeters. So there's a variation and difference between those two. But when you look at a lot of MRIs from NBA players, you're going to see that central to lateral and then I would say inferior portion of the patella. Okay, so it's more it's more inferior. So you think if it is more inferior, if you were squatting deep, you wouldn't be hitting that inferior. You'd be hitting more than the superior. Yes. Yeah. And is that so where where you find the if you look at the MRI and you see where this pathology what do you term them as lesions or what do you call it? Yeah, osteocondrom defects is or a cartilage lesion would be terms that you could use. And there's studies that show that you can use cartilage mapping technology on MRIs to see where there's excessive wear or maybe more tendency to load within the knee and it looks at the water the water movement and also the proteoglycan inner interchange of load. And what they find is there's some hot spots that you can start to map on the knee saying this is an area that is getting more pressure. But the research shows that once it degrades down to a three or four lesion, which is mean it's getting into a thing called the tide mark, which is a mark on the cartilage where you've basically the last line of defense cartilage and now you're in the sub-control bone interface. So when you are looking at MRIs and you see that it's progressed past the tide mark, now we're talking about early signs of OA. But anyway, the T2 signaling and the mapping are more effective early on like stage one or two. It's a better technology to use as more of a preventative mindset than actually when it's gone past. What is why when it's gone past? Because you can't like play anything. The signaling just gets worse. It's just not as accurate. Okay. So wherever this lesion is for when you're looking at these with the MBA guys and you see it has it's on the certain spot. That lines up. Does it line up with where you're thinking the pressures will be highest when they're moving? And then that's where they get the most pain and then you try to stay out of them? Yeah, I mean, I talk about it in like when you saw my talk, it's let let the sleeping be sleep, which is the control defect. How do we make sure that it stays like this is aware of a necessity? It has changed and altered the joints. So the rules have changed. But how can we make sure that it doesn't wake up? And that's in itself is really focused in on workload. How much spike acuity wise? Are they taking on to that knee? That could wake it up. And also there are times where you probably would never be able to return an athlete to sport if you asked it to do in isolation things that will it just would take too long for it to look good or they may never look good. And by doing that, you're basically honoring kinematics at that point and not kinetics. And honoring that dysfunction is there and they will find, through this constraints of movements, there will find a way to kind of be successful. So I think we can kind of put our hat on and say, we want to make this perfect return to place scenario with proper KPIs. But when you're dealing with something notably like a cartilage lesion, those rules are different. And sometimes it's just graded exposure on the court. And if they're still responding well, they may never look good with a pure isolated knee extension isometric or a isokinetic test. It may take two years for it to actually generate enough force that would make them cleared. So how do you, how are you then in? I think you talked about it in your talk or maybe it was when we were speaking. Was it like a lateral lunge exercise where a lot of people, yeah, if you could give that example. I mean, again, with a lateral more frontal plane movement, and if you have a central lateral lesion or sensitivity, you're not going to do well with a lateral lunge, they likely will inherit more of kind of a stiff knee and it just kind of like a hitch where it just doesn't look like clean knee flexion. And that's one movement that I do if I just have about 20 minutes of time to screen how you look. I'm going to have you do a lateral lunge body weight and then I'll have you hold weight and do the same thing. I'm looking at quality of movement, but more importantly, I'm looking at how much trunk flexion are they dropping into to avoid knee flexion. And is this like you said, you got to obey the kinematics. If they're not like looking good or they can't like hit this without pain, you're just kind of leaving it alone or is this something we need to, I'm writing stuff down. I'm making observations. I'm talking to the S and C coaches that will be working with them. I'm getting them on the humac norm to look at their isokinetic and their torque curves and to know that this is a management scenario and we need to get that curve to climb up. But I'm not sitting looking at somebody saying that I'm going to sit you because you're not generating enough force. Because if it's not reactive and showing effusion and they're actually able to hoop and play basketball, I've seen Hall of Fame Hall of Famers with knees that would make you cringe. And they're still putting up 20 points a night. They can't do very, very basic things in the weight room. So it's just one of those things that if you haven't been in the trenches of pro sports and looking at how true athleticism is and how they find success. And I think out of any athlete, the NBA athlete finds compensation the easiest because most of what they do is they jump from their ankles, not their knees. So you're thinking that's how they get people like with this bad patella femoral defects, lesions can still succeed is just they're just finding ways not to load that certain area of the patella femoral joint. And then in season, you manage it by loading it. You are micro dosing, you're finding ways to slowly climb that sensitivity or at least drop the sensitivity to actually load it because what you're doing is the cartilage doesn't have any nerve, nerves at all. What they feel pain is the bone itself. And with time, there will be continual micro cracks or there could be almost like an osteocyte that kind of gets embedded in between the cartilage and the bone. And it's, you know, that's really a way to strategize and manage fluid. And with time, those micro cracks will stimulate localized healing and fibroblasts will come in and say, well, we're going to do something about this. They create a callus, which is type one collagen, which is your tendons. And they fill the space. And it fills with time. Now you can go and go to a dock and have them put a drill in and drill through the bone and create this huge bleeding. And then what happens is it's this, this steroid of healing, basically this huge signal. And now it accelerates or you can do it in a more chronic nature with the body naturally doing it. But the problem is is highly cartilage. I've mentioned in my talks, it's the supermodel of all human tissue, which is it's beautiful. It cannot be recreated, but it's dumb. And it doesn't know what it's doing. And when you have a change in high-linked cartilage, 80% of it is water. 20% is proteoglycans and condrecites. And when you put in fibrocarilage, that water to cellular activity or cellular component is much different. So it does not work as well with the interchange of fluid. And that fluid interchange is called Darcy's Law. So it's, yeah, I'm in the tendon world. It's like the, I think Keith Barr is talking about that. But the, well, maybe you get it more at the wrap around regions, the enthesis, enthesis, have you say it? Yeah. More of that. Yeah, you get more of the cartilage. And the proteoglycans are more fluid to get to be good with the compression or to handle compression. But when you go to like the cartilage, that's all it is for is compression, right? Well, the cartilage has two roles. It has compression to take out ground reaction forces and gravity and to create the most frictionless environment to between two joint surfaces. The one is shearing and one is basically taking on load and it's an internal pressurization system of hydrostatic pressure. And we can talk about kind of the temporal nature of the visco-lasticity of cartilage, which is if you have high force or high strain, there's going to be just the, it's a rate dependent issue where now the water content can't get squeezed. It's squeezed out from the sponge so it takes all that pressure from the internal structure of the matrix and absorbs force. And if it's a slower application, so it's very similar to a tendon, a slower application of load, it uses e-flux or a removal of fluid through the matrix. It pushes out into the joint and then that spikes hydrostatic pressure. So a lot of the load is being taken on from this really stiff water balloon of fluid and not so much the interfaces of the cartilage itself. Because when we think of fluid in the knee, we need to go into Newton's law of fluid dynamics and synomial fluid is a different type of fluid because it has viscosity and it changes with stress. And that's why it's a non-Newtonian fluid, which it does not abide by Isaac Newton's laws of fluid. It is just like paint. If I take a paintbrush and it's thick, that viscosity is high, the moment I start to spread it with speed on the wall, it thins. And that's what happens with that interchange of fluid within the knee. When you sit for a long time, it becomes very cushion and thick. And that requires you to get the knee moving and create heat and shearing, which then will thin it out and it spreads between the two interfaces of the joint. So what does this viscosity mean when from like a, I think we had talked earlier, you were telling me about some things you do for someone with the Patel Femmeeral Pain with like speeds of movement with holds because when it comes to a tendon, it's like, okay, the viscosity is just like, if you move fast, it's an elastic stiffens up, it's elastic. When you move slow, you get this like fluid movement to come out of the tendon, you get things kind of shuffle around in the tendon, more of like a health effect. What's going on with the Patel Femmeeral joint with speeds of movement? So again, we have two roles of cartilage, compression and this exchange of micronutrients with loading and unloading. And then we have shearing and how these two have frictionless environment. So when I want to create more reduction of shearing, this is when we start to talk about something that I've been talking for the last year, which is a principle by Bernoulli, who was a physicist from the 1700s, who wrote a book called Hydrodynamica. And if you, you, me, ever want to start a cover band like a Metallica cover band, I think it should be called Hydrodynamica because that's just an odd name. But what he found was there is an inverse relationship of pressure and velocity. So if you have a higher amount of pressure, you have less velocity of, for the fluid to glide through the joint. And vice versa, if the pressure drops, there's more fluid. So if you go and ask somebody to just start doing isometrics, either overcoming or yielding without good preparation, you're asking it to do a high pressurization movement. When knowing that you have a pathology of the knee, it needs to have additional work to coat and get it prepared to do it, to create that frictionless environment. So what I talk about is the Bernoulli Prep, which is doing velocity-based movements first, to get that sheer thinning fluid to kind of coat the whole complex. And then with graded exposure, you start with high velocity low pressure. And every stage, you get more pressure to the knee. So you start out either on the bike, or if you do knee extensions with very low weight and just speed and just kind of get this fluid to kind of move through the knee, maybe some banded TKs for speed with light load, that's your first stage. Then the second stage is I like to share the load between the glute and the knee itself. So I find almost a coupling sharing movement, maybe even more glute dominant, but you're starting to sneak in some loading through the knee. So that'd be like a high step up on a box, where it's more of a glute derived movement. Or maybe I have them do some form of a goblet squat, or a front leg elevated split stance, where it's glute and knee working together, but it's a little bit more glute specific. And then I transition into pressurization, which is I'm going to do some form of isometric loading, whatever feels appropriate for that person. And then after the isometric loading, I go into some form of iscentric loading, and then I end it with plyometrics to basically prepare that joint to take on rate. And when you do that, if you do it enough, knowing that you have a management scenario with this knee, if you see them one day and they're able to go through with no issues, and then you see them in two days and they can't get past the second stage without it being sore, you already know that the knee is starting to respond in a way that you don't want it to. And that's the problem with some of these knees is that they become so chronic, it's like chronic pain, they've lived with it for so long, they're not very good at being a historian of how to manage the knee, and they can be their own worst enemies. So with creating kind of this graded exposure prep, prior to you having them do sport or do it like a training session, they start to understand how the knee is responding to load and you can make adjustments from there. - Okay, that first part doing the high velocity to coat the knee, 'cause when you have the Patel Femre Opane, is there less fluid or what is it? - Well, a lot of times when you have a cartilage problem, you have more fluid, you have kind of like resting residual effusion, and then when you have resting effusion, it increases the hydrostatic pressure of the knee, when you have more pressure, you have less velocity. So if you have an underlying swollen knee that constantly just doesn't, it's not a dry knee is what we call when there's no fluid, that's what we try to strive for. If there's residual fluid that already changes the pressure at the start point, so you're already dealing with increased pressure again, that means that fluid exchange is gonna be slower. - With the, okay, with the tendons, 'cause there's that work with Lauren Pringles on the pathological tendons having more, more of the protege glycans, glycosemetal glycans, fluid, and then you want to squeeze it out. And I've kind of looked at it. I think he's talked about this too recently, the pressure and, but he says pressure and perfusion. Is this a similar line of thought? So like the tendon is naturally like high pressure, so like you don't have much perfusion, maybe this is blood flow, you have lower perfusion, exchange of nutrients because the pressure is so high and tendon. But then when you get pathology, well actually, now this doesn't completely make sense to me, but anyways, for you, how are you looking at, is there a difference with tendons or are they the same as cartilage in terms of this pressure and fluid when there is like pathology in each of the structures? I think your, so yeah, when you have an engorged tendon, it's gonna be more painful and you wanna squeeze that fluid out. I think for the cartilage, it's the fluid outside of the matrix and if that is high, then you don't have a good, that good sponge. We call it cartilage breathing, which is, when you compress, it squeezes out and then when you unload, it draws back in and that's how the cartilage breathes and it creates micronutrient movement. But if you already have a high amount of fluid externally to the cartilage, that interchange of micronutrients is reduced. So your case, the hydrostatic pressure is higher in the tendon, the cartilage, it's probably more outside of the cartilage and it's not allowing that nice fluid exchange. Okay, yeah, yeah. So the cartilage is the thing that should have this fluid in it. Yeah, it's just, there's a backup of pressure because that, so it's critical to get the knee with no effusion and that's gonna allow that quad to fire better. It's gonna just, you're gonna be able to glide through with the patellar femoral joint with more efficiency and again, that fluid exchange is better. Okay, and the weights for the tendon 'cause the tendon takes on fluid is like, just do an isometric, like a heavy isometric and the fluid squeezes out. But with the patellar femoral, if you just go into the heavy isometric, you didn't, you could actually make it worse. You didn't take care of anything. That's where you're looking at the high velocity stuff. Yeah, yeah. And then even when introducing more of the pressure-specific work, when we're talking about that sub-control and bone interface, it's not a cartilage issue. It's something beneath that. It's a desensitization. It's a graded exposure and how much are you gonna dial and pull the levers to say, "I'm gonna load that" and at what magnitude? And I've talked about this with my talk and even on some of my social media, but the peppy lapue. And the peppy lapue is just like the cartoon. He's kissing the gal and he's doing small pecs. So it's, you know, high frequency, low intensity or low to moderate intensity and low duration. So your isometric load would be 30 to 50% your one rep max or tolerance and you're doing it for five to 10 seconds maximum and you're doing it frequently throughout the day. Within maybe a six-hour frame, you're hitting it multiple times in the day, but you're just trying to hit the calis. You're just trying to engage that area to desensitize it to create that interchange of fluid to get some of that cellular activity to start building again, that fibrocarital, it's not perfect, but it's something. And that's much different. You're gonna smoke a lot of your patients with patellar femoral pain by doing the opposite, which is the tendon is like you're making out with someone. Like it's high intensity, high duration and you don't do it very often. So that's the opposite. - Mm, yeah. Okay. This kind of, this was one thing I remember you saying, it was kind of conflicting with, well, I guess just advice from other people with in the patellar femoral space, which maybe can be, it's more like the, maybe more of the people that have a really flared up patellar femoral joint and you try some loading and it just pisses it off so they'll be like, okay, we'll load you every third day or every fourth day or every fifth day, maybe. But what you're getting at is like multiple times a day, this type of loading and it's trying to get this, this, and I kind of think of myself where I'm like, I've had patellar femoral pain many times in my life. And if I just do nothing, it does not get better. Like with the tendon, if I flare up the tendon, I can kind of rest and it will get better after day after day. And then I can go back to sports and sometimes be good. Now if it's a chronic tendon pain, it's like I gotta address all the deficits. But if it's just an acute flare up, goes away in a few days, I'm back to 100% in no time. With patellar femoral pain, it's never been, it's never necessarily been like that. I don't know if you could look a long term with people, if they just rest with patellar femoral pain and you're talking about this bone desensitization, is that not gonna happen? You're not gonna get this kind of like scarring over this, you need to get this scarring over this touching of the callus frequently. Yeah, yeah, I feel like for one thing, if with the peppy lapu, like I'm not going to do this strategy if this joint is hot and it's irritable, I'm just offloading. I'm getting them on a bike, I'm having them wear a compression. sleep. I'm just trying to clean out anything that's residualy. Or if there is bone marrow deema driving into the bone, like I want to get out of that, maybe some anti-inflammatories. And then as that subsides, then you can start to condition the patellar femoral joint with loading. Maybe you start in angles that are more tolerable, and that's where we start. And again, you're kissing the lesion and you're off, but maybe it's in a where the contact pressure is more dispersed and not localized to the area. And as they respond to that, then you can kind of say, we're going to encroach and go into the spot that's more challenging. But again, it's always that low intensity hydration, sorry, low time and then frequently throughout the day to just stimulate it. But yeah, it has to get out of that anti-inflammatory phase. And the other thing is patellar femoral joint, it may take some time, but then we forget about it and then you just move on with your life and then you piss it off again. Because you do need it, see the knee extensions and you weren't really focused and it's now awake. And it may take two weeks, but that's the other issue about this whole thing is sometimes it's very easily forgotten because it just kind of gets better on its own. Why not a higher duration? Why not the higher duration hold? Why do you want to do this? Like 30, 30, 50 percent holds for a few seconds, just like, like, I guess, yeah, why not hold for a longer duration? I mean, the patients don't read our textbooks. That's number one. It's this king, like I can say something in absolute and you do something opposite and it's better. Like you need to take in to affect every patient is different. But if there's a principle or if there's something you need to explore initially, start there and if they respond well, then great. Load it for a longer period of time. I would say with a car ligage issue, probably start with more durational changes than magnitude and I think that would be different with tendons. So you're still changing the principles. So you may stay with the intensity of contraction but hold it longer. So that would be the first thing that I would start to adjust once the knee is responding well. But that last bit when you're producing high force high rate, that's again, when we talk about Darcy's law in the exchange of the temporal reaction to stress, that's where you're challenging more of the internal pressure of the matrix because it doesn't have enough time to exchange a fluid and prepare to have it more of a natural increase in hydrostatic pressure of the entire knee. So that's why magnitude and intensity is pushed a bit longer. And the other thing is time is much, I think you have to have a discussion with your client or patient that it's going to take longer than a tenetopathy. Why do you think it takes, they tend to take longer because we're dealing with the supermodel of tissues. We're not dealing with, you know, this is the, they're the divas or the divos. They're the ones that it takes longer and it's because there's so much stress and pressure that happens behind the patella femoral joint. And again, it is a dynamic pulley where it's engaged through full range. It cannot hide. Biking. What's your idea behind, behind heavens biking for some of this patella femoral prep? Biking's okay. It's just the amount of resistance. I, I look at biking as a functional range of motion and kind of this compression offloading through range to pump. It's more of a pumping mechanism. But for higher resistance, it's probably not great because you're in those deeper pressure points of the patella femoral point. Once, once you get into that 90 degrees, that's higher pressure. But generally, generally doing, as like a warm up lower, lower resistance. That's great. It's going to, yeah, it's going to help. What exactly in your head is it helping? I mean, it's, you know, it's internally warming up the tissue. It's warming up the synovial fluid. And, you know, old guys when their knee hurts, what do they do? They go grab a heat pack and they throw it on their knee. And miraculously, it starts feeling a little bit better. And we don't, you know, this could be another talk, but heat shock proteins with intendids and also the cartilage. They start to wake up at 102 to 106 degrees Fahrenheit. If you put it on for 20 minutes, 15, 20 minutes, it starts to wake up the cellular activity to kind of like clean up some of the debris and some of the kind of the metabolites that are just kind of stagnant. So heat is helpful. You just got to look at what your dad does. Okay. You, we kind of, you have this high, the kind of your sequence there, that high velocity thing. And then you kind of do something to pair the glutes and the knee, that next thing. And then some form of isometric loading. Then you go into some eccentric. What's your idea behind doing eccentric loading? I want, I want to get that joint to start to glide through the troplia. And when I say eccentric, I'm going, you know, sub maximal, like just, I want, I just don't want it just to be specifically a yielding or overcoming hold. I want through range to kind of get through that whole range of motion or sorry, that range of joint congruency through the whole knee. And I just prefer eccentric over concentric. Okay. And then like, your last one you said, you go into some plyometrics. What's what type of, you know, probably more extensive, extensive and absorption versus, you know, higher ground contact times, differ landings. Again, that's that Darcy's law that I'm trying to manage. So it's probably more absorbed, absorption in nature and acceptance of force. And this was something. So how did you come up? How many how many ex the sequence you have here? Yeah, how did you, how did you come up with this, is just trial and error? trial and error, dude. Like just seeing enough, NBA players with bad looking knees and they're still playing basketball. And how do we, how are you strategizing in the weight room that they're still loading the knee? Respectably. And the fact is having being the person that kind of brought ice kinetics, kinetics back into the league. Like I was in a phase when they were more used as a laundry coat hanger than anything. I actually purchased a brand new one and I kind of created the new way. And now there's a lot of teams that use it. And I chose to use it because I was using other ways to test knees and I couldn't, they were, you know, using hip strategies or doing things that were kind of not allowing me to make a better clinical decision to front office to say this guy is good to sign or not. Because I had all the MRIs in the world to look at, but I didn't have a good functional benchmark. So getting ice kinetics now, I started to marry force production or torque curve related to pathology and seeing how it responded. And by getting that information, then we started to adjust what the guys did in the weight room to try to address some of these issues, even though that they were pain free. Was there? They were, they weren't pain free. They were just hiding the way that they played basketball. Were there things on the courts that were really pissing off the telepharmal joints? I mean, the acceleration loads. So if you look at the Excel D cell ratio, if you have a low ratio, that means there's a higher amount of D cells. That's one of the first things I look at players that have a high risk or they may start to show some reactive effusion. That's one of the metrics I look at and mechanical intensity as well. When it's, so you're, you kind of have this iso kinetics. What's what is this? I don't know what you're talking about. What is this thing you speak of? Yeah. So iso kinetics is basically equal speed. That's what that word means, which means I'm setting a specific speed that you have to push through a bar, basically in the extension machine. And I'm not allowing you to push any faster than I've asked it. So many times we test at 60 degrees per second. It's a nice profile of how much force that you can produce, but you can also it's better than doing a nice metric test because you actually see the torque curve of how strong they are. And with again, the patella creating a longer arc of movement for the moment arm, your strongest at about 50 to 70 degrees. And you want to see how high that peak is, but then also are there any areas within the curve where there's torque decay. And if there's torque decay, that means it's not accepting load through one part of movement. And if you can find that, then you can start to load it in the weight. room or you can get on the humac or whatever isokinetic company use and you can train it. But basically it allows you to see a full expression of force through an arc of movement and it's isolated to the extensor mechanism. Okay. And when you have that, an area of decay or an area that they just can't, this is what you're thinking is this is the delusion that communicating to the nervous system and then shutting off the quads. It's an inhibition. Yep. That's just saying I can't produce force. It's harmful and then it finds way to produce force later or earlier in the curve. So in the research, like Patelr attendance, the thing is like a stiff, the, the stiff knee strategy, stiff landing strategy with Patelr ephemeral. I don't think I saw that. I think I saw more like what is the, what was the commonality in the research with someone with Patelr ephemeral pain? It was like their knees cave in. Yeah. Or they just don't. Yeah. I don't, I don't know on that. I do know that like if you're looking at the curve, there'll probably be a drop in force around that 30 degrees. Again, that's a mechanical disadvantage to the quad. It's not very strong in that position, but it'll likely be kind of a low hill from about 30 to 60 and then likely build up after 60. I think I remember in your talk an injection, injections, yeah, what are these for the Patelr ephemeral joint? So when you're looking at the hydrostatic pressure and the fluid, when you're having a struggling knee, the body senses that it's struggling. So what, what fluids in the knee is called synovial fluid and the main ingredient to synovial fluid is hyaluronic acid. So H a and that is the mechanism or ingredient that helps with thiccotrophy, which is a changing of thickness of the fluid to do its coding. But the issue is as you start to have a failing interface or intersurface of the joint, the body knows that and it'll start to dump more interstitial fluid to help. But the issue is it doesn't have hyaluronic acid. So you're deluding the concentration of H a. So you're just putting more fluid in its increasing pressure, but it doesn't have any of the good stuff that helps with coding. So the example I say is in high school, I drink, I'm no angel and I stole alcohol from my parents. They'd take a bottle of vodka. I'd make a mark where the vodka was. I'd pour it in my coke bottle and then I'd put the bottle underneath the faucet. I'd fill it back up to the to the line. I'd put it back in the cabinet. Now you have diluted vodka. You have diluted H a. So now when you get the injection like a monovisc, which is a huge, it's a large amount of H a. It helps with lubrication. You're trying to improve the concentration gradient of that fluid that's in the knee, which then will help with coding between the surfaces. So if somebody has a cartilage issue, ideally getting them on two to three times a year without H a injection might be good for them. Because your body can't do it itself. Yeah, it's just not sending the right stuff. And really, again, what we talked about, they're dropping more fluid. It's creating more pressure. And then with more pressure, shit happens. It can't find a way to manage the effusion. So what happens is your fat pad likely gets engorged with fluid and then you start to get recesses or what we call a baker cyst in the back of the knee. And it's a one way valve and you start to get fluid pushed in the back of the knee and it can't come back out. And now you have this fluid filled cysts in the back of the back of the knee. Okay. Yeah. When I go to the, I have that sponge bob analogy for the tendons, you know, they swell up, but it's like hard to see. It's hard to see. It's the inverse. Hard to see. Okay. I was going to say, but I was going to say to the naked eye because like someone has a tendon that's, and I'm like, I don't think you can see it to the naked eye with the knee, though, the hotel femoral joint, you can actually see this effusion. Yeah. I mean, you need to track it. That's one thing I teach my patients. Like every morning, your, your audits are, you look at if you have any bogginess or any kind of puffiness in the knee. That's one check. One check is you do range of motion. So if you have full extension and if you have a baker's cyst, it's not going to like that because it puts, pushes fluid in the back of the knee. So you'll start to feel stiff with extension or vice versa. If you put them in and range flexion, they're going to put more pressure on the super patella pouch, which is the pouch just above the patella. And then they'll feel stiff there. So that's a morning audit check of, does it look puffy? And what's your range? Does it feel stiff? If I get that information and they come in, then I know that the knee might be waking up because a lot of times pain is not the first thing that comes. It's the effusion. The beast is waking up. Yes. Yep. Okay. I did a show with Matt Watson. He talks about the fixatropi, whatever. I've actually never heard of that term. What's, yeah, can you explain that a bit more? I mean, fixatropi is related to a French physicist named Hagen Pooswa. You don't need to try to spell that. And it's just the relationship of what I talked about with the viscosity of fluid and how it changes with force. And it starts to thin as you apply more rate or force to it. It starts to thin, just like paint or just like if you had honey and you would start to stir honey with speed, it would start to loosen up. Yeah. Okay. There are things in the Patello-Femero pain world. One of them is the taping. And like some people get results from taping. Is this something you've used? What are you thinking is happening when you? I think like the diamond taping, the caudal taping. Yeah. I mean, if you're going to do taping, I probably would try to offload the lateral facet, pulling it more central because we know again, 30 degrees is not great. And that's also a position, almost a loose pack position where the kneecap can shift. And again, if you have fluid behind the knee, that can shift even more. So gliding it more medial to get it more centralized is good. And then, if you've seen individuals with tennis elbow and they wear those show part straps, right? So what happens is, how that hurts, I'm going to put a strap here as forces come through the forearm, it hits the strap first, dissipates force, and then it doesn't hit as much on the origin side of the common extensor. Now you flip that to the knee, right? If you put pre-wrap and roll it up to the inferior pole, as force comes up to tendon, it hits that pressure point first and then hopefully it dissipates force away from the irritable tendon. So that is another strategy of taping is supporting the patellar tendon. It probably wouldn't be more for patellar femoral joint. It likely for patellar tendonopathy, but I would at least explore if that helped. Okay, I had a bunch of YouTube videos on patellar tendon. One of them was on getting the quad strong, getting the knee stronger, but then like loading the knee. And then I was like, but there are strategies to offload the knee if you get better ankles, calves, if you get better hips, glutes. When you're looking at people with patellar femoral pain, I think in the research, they were like calf training can help hip training can help. Do you think not getting at like root cause type things of like, does someone present with a strategy that just overloads the knees? But more like a thorough rehab plan, do you think there's actually, you said D cells, like the big one for patellar femoral pain, but you can't, how do you hide, can you offload a D cell? I guess if you bet more at the trunk. Yeah, you can't, you can't, it just requires the impulse. If you have a longer impulse, you have a longer time to accomplish the strategy. But when you cut that strategy time and half, you can't, you can't inherit that. So you either injure yourself, you fall over or you take four more steps. Yeah. Yeah. So it's one of those. But here's the thing, like the world that, you know, I'm getting old, I've been in the, in the profession long enough, now I'm going to start talking about other shit that's not as relevant. But like back in the early 2000s, like we talked a lot about the hip for knee pain and making sure glute meat and the lateral hip musculature is important. And we like we always do in our profession, we just blinders on that. and we just do that. So a bunch of patients had knee pain that just started to get hip strength and they still left PT with a shitty quad because it wasn't a dress, but they had a great clue. Now as we transition, now we've gone into the other world of like isolation, isolation, let's get handheld, dinonometry, let's get our force profile, let's get the quad stronger. And it's like, well, how about the knee or the patellar femal joint is failed because they're not using strategies to use their hip or their ankle. And that's the causation of their crappy kinematics. So again, now we gotta get the pendulum to the other side and respect the kinetic chain. It is very cringe-worthy to say that because we've used that term way too much in very ambiguous ways with no real methodology, but I do think, yeah, you gotta look at the glute strength, you gotta look at solias. If you have a deconditioned solias, it is the airbag to the knee. It takes on force first. And if you can dissipate enough force from the ankle, then the knee's like, you know, they're doing great. They got a roommate that's pain rent on time. They're not that shitty, I'm gonna get you in two months and now the knee is paying for rent because the solias isn't doing the job. I've never heard of a soul, there's a study on the fat pad being the airbag of the knee. I've never heard of the solias as the airbag of the knee. The fat pad is the barometer of the knee. So there's been a longitudinal 96-month study to show that if the fat pad shows hyperocorque or hypode, so at least some fibiotic changes or some excessive inflammation to that area that there will be cartilage pathology in your future. So I call it the barometer because it tells you how healthy your knee is because stuff gets dumped into that area. What is the point of us having that, I mean, we have fat pads all over, but the big infertileer. The fat pad is a way that you manage friction, manage friction behind the tendon. It is a way to buffer forces. That's why you have fat pads. They're like brake pads. And when we look at the patella tendon, most of the damage is on the posterior band of the patella because not only is it dealing with tensile forces, it's dealing with compressive forces as well. So now you have this bony interface that starts to create damage because it's the weakest link of the tendon. And now you're going this ultra stiff anterior band of the patella tendon and this degeneration to the patella, sorry, the posterior band. And it's the combination of compression and tensile. - So you say these changes on the fat pad, this patella femoral problems are probably coming about. If I did a couple shows with Jill Cook years ago on the difference with patella tendon and patella femoral, when you're looking at these MRIs of these lesions of patella femoral joints, if they have these fat pad changes, do they also have tendon changes? Are these all going on at the same time or? - Yeah, I mean. It is a joint that's losing the battle. So you're likely having tendonopathic changes. You're likely having high signaling to the fat pad. The research shows that there's not a lot of hypocococytid findings where it's more of like a fibiotic or stiff fat pad. Most of the studies show it's more of this engorged inflamed fat pad where there's more fluid. So yeah, I mean, they're neighbors. Like it's just, it's gonna happen. - What's the soleus? You said if it's deconditioned, you're gonna get this more of this knee stress. How are you determining that? - How do I test it or how do I determine the mechanism? - Both. - Yeah, I mean, if you're decelerating and if you're not decelerating with a more planterflex position, let's say you're landing more midfoot, you've just changed the moment arm of the ankle. You're asking it now to stop the same rate at half the distance. So that's the issue. Deceleration needs to have torso back, foot and planter flexion, giving it enough time to plant and then let it to be a transition forward. The moment you start landing midfoot, that airbag can't respond as well. And if anybody doesn't know what I'm saying, I'm from North Dakota and it's airbag. - That was the big thing when I moved to Ohio. I said, I said sandbag and everyone's like, what did you just say? And I'm like, yeah. - Sandbag. - So yeah, the foot position is important because it's gonna really challenge the ankle if it's a mid-stance room, it hits that midfoot too early because then it just doesn't have enough time. So it could be just positional or reactionary, that's an issue. And again, if you're dealing with an Achilles issue, let's say an Achilles or an Achilles repair, it does not like in a range planterflexion. That's why you see a lot of control lateral or if you have someone that has an Achilles repair, sometimes they tear their ACL or vice versa. The ACL, they don't have a strong enough quad, they overuse their calf and they tear their Achilles. The, there's such a good relationship between the two, but if you are not having that negative torso angle with a planterflex and now knowing that the Achilles repair isn't strong in that position, it's gonna transition quicker out of that range. And now the quad has to do more because the ankle didn't do it the first, you know, through their planterflexers. And Eric, my friend Eric Merritt talks about, you know, a decondition knee, the soleus becomes the predominant the sellerator. It becomes the body's knee extensor and it's influencing the extension through the ankle. The big patella, when I've had patella femoral, I had it, one time had it real bad. I was dunking every day, but I worked at a gym in Minneapolis and we did band-resisted sprints, you know? So I had to hold the band behind a guy while he's sprinting. And then, you know, when he finishes, I have the decelerate. I have to decel and it takes me like 20 steps to decel 'cause it hurts so bad. But this feeding into, there was this study, I think, Baxter and then Car, I don't know his first name, Josh Schrinny, Car and Silvernago, loading index. They had study on loading index of patella tendon and patella femoral joint. One that stood out to me was the Spanish squat. It was like a ton of patella femoral joint. And I've had people try spandas squats with patella femoral and usually kind of, well, it depends, but a few people, it's really blown it up. What do you make of a study like that? So for like patella tendon, they had their own mathematical way of, with like the impulse and the rate and other things. With the tendon, it was kind of useful for me 'cause I'm like, this does kind of line up with what I think someone's gonna get in more pain as you increase the speed, as you increase demand on the quads, but with patella femoral joint, I was like, I don't know if you could just go down this list of like walking as low and then all these things and then do you think there's a way to like, would that be useful, I guess, after this whole talk of what the complexity of the patella femoral joint, could you have a loading index scale similar to a tendon or is it like, what are you thinking? I mean, again, it matters on the synovitis or the, you know, the congeollision or at least the area that is overly sensitized is likely related to the joint angle and how that relationship of surface area of pressure behind the kneecap. So like we said at 90, there's a huge spike in absolute compressive forces at that point, though you have the best position for the facettes of the patella to sit in the cup of the trochlia, it's still the highest position for that joint. So I think your index, 'cause I know the index is really, you know, the decline single leg squat is the worst. Like, so that was a great study. I just think for patella femoral joint, it's more, it's very unique you don't almost have to look at like joint specific positions to get a better under. standing. You said in your talk about seed been seed been might be right 90 degrees. Uh, what was that what you were saying or what was it? I don't I don't remember. I'm not sure on that one. I thought you was talking about seed been and you were talking about the patella femoral joint and uh, because okay, because he was like, he's not he's not past 90. Yeah, deeper than 90. Not no good. I thought you had some something you were talking on that. No. Uh, I jokingly said it because it was, you know, he's the anti parallel man. So in this case, that might be work. That's partial arc of movement away from the highest pressurization of the knee behind the knee cap. And even the condyls like the further you go down into flexion for a condual lesion, the more you're going to engage the posterior portion of it. So this thing, um, I think back when I first got my patella tendon pain, uh, which was just I guess, but they, they were watching my knee cap and they're like, Oh, it's it, um, is track is maltracking tracking laterally, uh, what I've been and I need to work the VMO whatever, whatever idea they had. Um, yeah, what's is there any stock to put into patella tracking? I mean, there is there's a few biomechanical things that can change the weight sits in the groove. One is trochlear dysplasia or a shallow angle of the trochlear. If it doesn't have a nice uh, depth to it, you're more likely to dislocate your knee and you're not going to load it very well through the trochlear. Uh, number two is the, um, patella, ulta. Patella, ulta is a tall patella, which means it sits tall, which means it doesn't fit great early in zero to 30. And something we looked at for our NBA guys was, yeah, we at least put a some level of concern if they had patella ulta, because there's likely they probably might have some issues with patella, femoral joint issues in the future. And when we talk about uh, OCD lesions and what's the worst of the worst, um, trochlear lesions that don't respond well to load are the worst ones to deal with and the surgical outcomes are the worst as well versus more of a weight bearing lesion on the medial femurcondyle or lateral femurcondyle. So looking prognostically at maybe a headache, we looked at patella ulta, how high does it sit? So, yeah, and then that lateral tilt, it sometimes can sit more on that lateral side. So, yeah, they probably were trying to address getting you to offload the lateral facet. But if you have the shallow groove, what do you, what do you do about it? Think call your mom and dad and ask why? Females are more victim to this. And yeah, there's a one sec have the classic dislocation, history or subluxation. And then patella ulta, the only thing is that there's that surgery to bring it down, right? If it's bad enough, yeah. Yeah. Yeah. Um, I mean, the other thing is we call it a q angle, but if there's a ear tibia is externally rotated too much, if then puts more of a vector pull on the lateral side, which again would address that lateral facet. Is that, uh, okay, that tibia rotation? I had a, this was a few months ago, I just do phone consult and a guy patella femoral pain. It's supposed to not my Instagram about, about tips for patella femoral pain. They've probably got like 50, 50 good replies. A few of them though were on that tibial, but the tibia being quote unquote stuck here in the external rotation, uh, is that something that that you see someone with patella femoral pain, presenting more? Yeah, I mean, I mean, you just have to train the knee. We only look at it as a hinge joint, but it's a modified hinge joint, which means it has transverse movement capabilities. And if you can get the knee to just rotate one millimeter more medially, that can help clean up some of the tracking issues or some of the, you know, compression issues that you're dealing with. So it's for sure, you got one of two planes to deal with, and we just focus on sagittal plane, flexion extension. And yeah, you, you need to address rotatory movement. Even frontal plane, I'd look at that. How much can it glide medially or laterally, but that's a little bit more when it comes to weight bearing lesions on the condyls. How do you get that to be a to rotate? P and F, um, getting them to having your hands and having them learn how to rotate into internal rotation. And then when you have them, you can have them do like a long, not a long sit, but you know, basically sitting and have them go into extension, but then bias into external rotation at the end, which is basically working on terminal knee extension and the, um, basically the screw home mechanism to lock it. And then to unlock it, you're going to do poplidious. So you're going to bring the ankle inward and go into flexion and work that range the whole time with the foot in an internal angle. And then you're going to go back up into extension. You're going to try to press out into external and then go back into flexion with internal. So you're getting that again, the sagittal movement, but you're doing some combined rotatory and you're trying to clean up the joint to see if the knee can do that transverse movement qualities. This, um, this research, I don't know if it's any research, the bio, well, end of king, I didn't show it end of king on patellar tendons. And I asked him about the biopsychosocial element and he was thinking that it's probably more, or the the psychosocial is probably more of a thing in the patellar femoral cases. Yes. Yeah. What are your, why is, why do you think this is the case? Because it's likely chronic. It's likely frustrating because they've slowly with time their function has regressed in a way that they can't, um, they're not dealing well with it. The pain patterning is a little bit more odd. It's more diffuse. Um, so yeah, I just think it's, it's more influential. You're going to start to influence your day to day life. And sometimes when you try to get back into the functional thing after time and it just continues to wake up and you're just not able to respond that, that's not great mentally. You start to lose confidence, you start to gain more fear, voice behavior. Now you say I can't, you know, I'm 40. I can't chase my kids anymore because my knee blows up. You know, the thing is it, it behaves in a way that it reacts and there's a fusion and that's not a great feeling either that you wake up one morning and what you thought was not much. Now you got a swollen knee. With, so with a lot of my, um, my phone calls I do, I ask if they got imaging for their tendons or for their patelle femoral. Um, just because, uh, and then if it's chronic, maybe it's like, maybe you need to get some, you can see what's going on in there. Is this something you like to see with patelle femoral is, is an MRI to know what's going on or yeah. Yeah. I mean, back in the day, I would never want to look at MRIs because I was so much a functionalist and now I'm talking to you for a while now on structure. So I think we've tipped the hat that structure is everything. Um, it changed us the way that the body will, you know, choose strategies. Um, I look at you have, I hate this term, the bridge between rehab and performance, right? It's just too much. We've said it too many times. But if we traverse through the gap of rehab to performance, the thing that lies in the middle that makes all the rules is pathomocanics and pathology. That is the bridge. Because if you're healthy, you don't have to deal with it, performance and everything is nice. But when structure changes, the rules change. And I think that's the number one piece about this whole thing is that's why patelle femoral joint issues are so complicated and frustrating and have again psychosocial tied into it is the rules have completely changed. And now you have to behave differently and it takes longer than you would expect. And you have to do low intensity, low durational hold frequently thrown about the day and it takes time and you have to do strategies to get the knee warmed up before you go do things and people don't want to inherit those strategies. They just want to go do their sport or do their hobby. How do you think these are being mismanaged out there? What are the, what are the things? I think cookie cutter loading strategies and protocols that just don't match. Not honoring the irritability and severity of the knee to kind of push through pain to get through it. That's I think it's sloppy. Not looking at the whole body and the responsiveness to getting more glute and hamstring and calf and exploring the whole thing. Changing the rules saying that isometric loading is not great. How do we do other things to load it and kind of getting off that stubborn clinical view of we have to do this. We have to do 30 second holds or 20 second holds from an overcoming isometric and train it that way. I think it's more of the subjectivity of each person's pain experience and how do you adjust to it? What is the end of zone we talk about the structural problems. I guess we look at a tendon although you do get really bad looking tendons. What the end of it I guess would be going to rupture. These pathologies get bad enough with Patel if I'm real joints. What is what's the end of it? Is it I mean. It's surgery. Microfracture is kind of starting to be not as much of a surgical strategy at this point, especially for athletes. For a patella femoral issue you're likely looking at some kind of implants, a condricite implant. There's a procedure called the macy procedure that's common for this type of joint. I think when you're having the macy's you got to have the conversation that if you truly want to be working and doing something in sports or requiring you to do some cutting and multi-directional activity, it's going to take a year and a half to two years with this surgery. When you're starting to see this with the lawns of balls of the world, there should not really be a timeline put on any of these players. It's really how long does it take for this need to start to accept low. That implant is basically they look at where the lesion is, they harvest this tissue, these condricites, they look at it and they literally cut it out to what fits that scaffolding and they put it into that area. But again, patella femoral is the hardest to get to come back from. I think I was at that Vegas seminar where we met. I talked to Rich Willie a bit afterwards. I don't think I saw his talk. But I think he was bringing up Penny Hardaway. Didn't Penny Hardaway have bad knees and I did this micro fracture thing? He had a micro fracture. Some of the grates had micro fractures. It was very a common. It wasn't like the menacectomy, but it was pretty damn common for guys to get it because it was the new strategy and most of them had in their career after that. Greg Odom, Penny Hardaway, I think Jason Kidd had it. There's just a lot of players that got under the knife to get this thing fixed and it just didn't respond. Was it worse back then and it works better now or what? They're not choosing micro fracture anymore. They're looking at cartilage preservation, harvesting their similar structure and then trying to implant that into their knee versus taking a drill and just asking the body to do its own healing. What's it what's it wouldn't do because it's not going to grow back to that cartilage? It's going to be an inferior tissue. Yeah. Yeah. Oh. Okay. Well, it helps that they got to learn that their own way. Penny Hardaway was my favorite back in the day. Way back in the day. Eddie Jones was mine. Eddie Jones like Miami Heat. Eddie Jones? Yeah. Yeah. The guy that got traded for Kobe to play more. Oh. Okay. Maybe that's why I like underdogs. How good was he Eddie Jones? He was great. Was there Eddie House too? One of my favorites as well. ESU, Long Sox, Instant Offense, No Defense. Oh. Okay. You got to clear this up a little bit more actually. You said earlier, the Iowa's, I have that meme of that, that Mojette guy putting the, he's clearly special. He's putting the square block into the round hole. He's trying to and he's drooling and I say tendons are dumb. Carthelage is more dumb. What exactly? I don't know if you've said it already. Go go more into it. How is cartilage more dumb? Cartilage is more dumb because it doesn't have any nerve endings. It's an inert tissue. It doesn't respond. It just is a sponge. Your true sponge Bob mean is cartilage. It is the loading and unloading and the only way it can move. Drone nutrients is through that mechanism. The cartilage breathes through the loading, unloading sequence. And when you sit for too long and we call it the movie theater sign, you sit for two hours and you get up and you start walking like an old man, it's because there's not been a good transfer of fluid through your cartilage and it starts to get engorged and it's not. It wasn't able to kind of like do it cycling like it normally does. So that's why you start to limp is because of this static position that takes, it changes the fluid exchange. Similar to the tendon. The tendon just, I think, yeah, yeah, it just takes on, I think it just takes on water being in like a slightly strained state from sitting. Yeah. Yeah. Okay. I think this was a lot for the telephemeral, but a lot of things I have not heard and I know other people have not heard because I think I've listened to every telephemeral podcast I can find and it's always very similar things of a lot of we don't know and not that good of stuff. Yeah. Yeah. I mean, yeah, it's just more, if you don't have the research, you have to look at the, the structural lens of what cartilage does. And again, it takes on compression and it takes on shearing. And then I started working with athletes and started to find that velocity work first and then working pressure. Then I did my homework and I found a guy named Daniel Bernoulli and then I read into a fluid dynamics and then I fell into Hagen-Pouzool and then I found in fell into Rhinald's number which is the turbulence of fluid and how it changes with pressure and then I fell into Darcy's law. So that's kind of where I'm starting to get more of this theory and how do we apply it in the weight room. I've, I think when we first talked, I was, I had some telephemeral. Why did it come about? Maybe just time off, time off at basketball for many reasons, but yeah, it was, I've been running the stuff you told me, given it to a lot of people too and good, good results reported back. Great. And it helps too. I need to think of things, I need to conceptualize things, you know. I need to have like an idea of what's going on instead of just like pain or no pain. I need to know like what, what's going on inside there. Even if it's wrong, I just want to have a picture of it, you know, like sponge ball. I mean, I, I got a, yeah, like vodka bottles and hyaluronic acid or peppy lipue and like those type of analogies are kind of what sit. I literally got a phone call the other day from individual on an NFL team and he said, guy had a nasty OCD lesion and, you know, we did what you've kind of been preaching and what you do in your newsletters and he goes, knock on wood, this guy's had no issues. So it's good to hear you and some others that are in this high professional setting that it like these strategies actually work. Yeah. Okay. I wanted to do this podcast when you, I told you you need to create a resource for Patelio femoral for the knuckleheads out there. So hopefully that's hopefully that will be done soon in the works because I mean, I was, I was complaining the, I have the Patelio femoral or Patelio tendon resource and there's probably, I don't know. in a multiplication factor of how many people have patella femoral and they reach out to me and I don't have the I don't want to I don't want to spend the time to DM everyone and explain things. So when you get this resource available. Yeah. I'll have to link it in the show notes. If you ever get it done because you have too many things you're doing but I think there's enough practical takeaways here things you people can experiment for themselves. You know, I think again, there is some subjectivity with each case but there are strategies that individuals should start out with. I plan to create a program and you know whenever that is I'll tell you and yeah, if you ever have anybody that needs to just send them away and I can at least have a conversation with them. Okay, you're always you're always talking movies and music. So give me your top one very top my favorite your top movie and top album. So I am a I'm a I'm a very dark person. I seem very nice and happy and I'm from North Dakota but maybe that's steered me into more darkness but anything dark I like I like dark humor. My favorite movie of all time is Requiem for a dream. Which is a drug movie. Have you ever seen that's recent isn't it last 10 years or so. It's old it's it's getting up there now it's old it was. Probably 2010 so it's 15 years old now. Oh, I think I think I have. Jennifer Conley Jared let oh Marlon Wands they start selling drugs and they get hooked on it and their lives going to a spiral great soundtrack great acting great story line. But most of the time people say I only can watch that movie once because it's so depressing and ironically that's my favorite movie and album dude I am a huge Neil Young fan. Anything that Neil does I listen to I'm an old soul so harvest moon is my favorite album. So yeah, wow. Okay, I thought you would struggle more with that but you did it. Not at all. Okay, tell everyone where to find you online or online you can you can hit me on rehab code. So rehab underscore code that's kind of where I produce most of my content. I do mentorship programs I have a newsletter and a career codex if people are looking for jobs for professional sports and college settings and then. You can hit me on LinkedIn as well. Perfect. Alright, thanks for coming on. Yes.