Today’s episode features Dr. Keith Baar, professor at UC Davis and renowned tendon training researcher and expert. Professor Keith Baar received his PhD from the University of Illinois where he discovered the molecular signal that causes load-induced muscle hypertrophy. Keith is currently the head of the Functional Molecular Biology Laboratory (FMBLab) at the University of California Davis.
Over the last 15 years, Keith has worked with elite athletes, as the scientific advisor to Chelsea Football Club, USA Track and Field, Paris Saint-Germain Football Club, British Cycling, The English Institute of Sport, Leicester Tigers Rugby, and the Denver Broncos. He also spent time as an assistant strength coach with the University of Michigan football team where he was an undergraduate. Keith’s current work is focused on how loading and nutrition alter tendon/ligament/ECM health and performance.
Tendon training is a vital aspect of athletics, and we’ve had several previous podcasts covering this topic, such as with Dr. Ebonie Rio that were tremendously successful. Tendon training is one of the most important emerging topics in the athletic performance field. To that end, Dr. Keith Baar is a leading researcher on tendon training, and his methods are getting athletes serious results. Whether you are looking at rehabbing injured tendons, determining the best course of training for avoiding muscle strains, or getting better elastic performance in healthy athletes, this is an incredible and information dense podcast. Topics span all ends of the spectrum on tendon action in isometric training, tendon rebuilding, nutrition and modes of loading.
Today’s episode is brought to you by SimpliFaster, supplier of high-end athletic development tools, such as the Freelap timing system, kBox, Sprint 1080, and more.
Podcast: Play in new window | Download (Duration: 1:12:26 — 58.0MB) | Embed
Subscribe: Apple Podcasts | Spotify | Amazon Music | Android | Pandora | iHeartRadio | JioSaavn | Podchaser | Gaana | Email | Deezer | Anghami | RSS
Dr. Keith Baar’s Key Points
- What got Dr. Baar interested in tendon health and performance research
- New ideas in tendon health and regeneration
- The dynamics of muscles and tendons in isometric training exercises
- Tendon stiffness and compliance, and how training impacts those factors
- Fast versus slow exercise and effects on tendon tissue
- How to balance fast and slow training for a total effect on the tendon
- How maximal overcoming isometric exercises work from a muscle-tendon perspective
- Fundamental differences between static stretching and long isometric holds
- Why and how loading is critical for tendon health and rehab
- The role of nutrition in tendon health and performance
- The drawbacks of a vegetarian or vegan diet on tendon health and performance
Dr. Keith Baar Quotes
“If you load (muscle-tendon tissue) faster or slower, you are going to get different mechanics”
“Tendon remodeling is actually extremely fast…. there are dramatic changes that can happen in these tissues in a very short period of time”
“(The tendon) is like a tree, the first few years you are building the inner rings. The other rings you are adding on, you make the tree bigger and stronger as it ages, that tissue is more dynamic. The center, core part of it isn’t as dynamic unless you have an injury”
“As you have more crosslinks, you have more stiff collagen”
“The cross-link component is something that we change dramatically with our activity, what we eat, and how much enzyme activity we have”
“The more lysyl oxidase you have, the more cross-links you have, the stiffer the tissue… what we do when we exercise, any type of exercise we do, we are going to increase the amount of lysyl oxidase we have, that is going to add in cross-links”
“When we are doing activities, we have the capacity to break down our crosslinks. When we pull on a tendon fast, it’s stiffer, and when we pull on it less fast, it’s less stiff. If I load my tendon quickly, all the collagen in my tendon works as a sheet, and it pulls with the muscle… it’s working as one unified grouping.”
“When we do really fast exercise, we don’t break cross-links, we are adding more cross links, we are getting stiffer”
“As the tendon is relaxing we are getting sliding, things aren’t sliding equally (the tendon) becomes longer over time. We’ve broken cross-links. We have broken more than we have resynthesized. By doing a slow movement, we’ve made it less stiff, in the collagen in the tendon”
“In the tendon if we load fast, we get a stiffer tendon, and if we load slowly, we get a less stiff tendon”
“If you are doing (a long isometric contraction), if your tendon is continuing to lengthen, then your muscle needs to continue to shorten, so it is not really an isometric in that way”
“A true isometric contraction (with no tendon creep) is not very metabolically costly since you can do it when you are dead”
“If I have a super fast athlete who has a lot of non-contact muscle pulls, then I know that they are having an issue with stiffness, and I am going to load them more slow than fast, I am almost going to do no fast movement at all, because they are going to be fast when they are doing their sport and their training. So I can just do protective movements that are designed to keep them from getting those non-contact muscle pulls”
“(Using slow movements) we’ve made our tendon a little less stiff, it’s going to be more protective of the muscle”
“The faster a person is, the more muscle pulls they get”
“Women get 85% fewer hamstring pulls and groin pulls than men do… estrogen directly inhibits the enzyme lysyl oxidase, which is the cross-linking enzyme. So women’s tendons are less stiff, power based performance is lower as a result, but they get less muscle pulls.”
“A tighter joint means fewer (ligament) injuries… for ligaments, I want the joint to be as tight as possible.”
“If I want to increase stiffness I want to have a fast movement”
“0-30% of your 1RM, as fast as you can move it, that’s where we have the biggest effect (on tendon stiffness)”
“When I am talking an isometric for a health based movement, I’m talking a 30 second hold”
“In (overcoming isometrics) the muscle is shortening as quickly as it possibly can”
“There is a beautiful meta-analysis that shows if you do static stretching it has no effect on injury rate. There is research that shows if you do heavy strength training it reduces injuries by 2/3. In the heavy strength training, velocity is low you are getting the low-slow movements (for tendon health)”
“What you are doing with the static stretch is you are over-riding the muscle spindles and the golgi tendon organs, you are not getting the shear force from a contraction (when you hold the contraction you are going to get more sliding because the muscle is contracting) and when the muscle is contracting we are going to get different signals from the muscle spindles and the golgi tendon organs. So what that means is when we use a muscle contraction to get this kind of stretch on the tendon, we are going to get an overall different system effect than if we use a passive stretch on the system”
“We can heal any tendon bit, while all the stress goes around it… the problem is if you don’t load it, the cells don’t know which direction to make collagen”
“What you have to do for the collagen to re-orient, you have to get load through that tissue so the cells know, we are supposed to synthesize collagen in this direction, and that’s where the creep is very important”
“Slow concentric and eccentric aren’t giving you as much (tendon) creep, because there is movement”
“The reason Vitamin C is essential is it is a mandatory co-factor in this prolyl hydroxylase reaction where we are making collagen”
“If I am going to do a protective session that’s only for my tendons, ligaments, and my connective tissues, it is going to be a short session, and I am going to do it an hour (after) I have the gelatin and hydrolyzed collagen”
“We are just trying to provide a loading stimulus together with the amino acids needed to provide new collagen”
About Keith Baar
Professor Keith Baar received his Bachelor’s in Kinesiology from the University of Michigan where he also served as an Assistant Strength and Conditioning Coach
with the University of Michigan Football team. He then received a Master’s from the University of California, Berkeley and his PhD from the University of Illinois where he discovered the molecular signal that causes load-induced muscle hypertrophy.
He did his postdoctoral studies on the molecular mechanism underlying the muscular adaptation to endurance exercise under the direction of Dr. John O. Holloszy at Washington University in St. Louis. From there, Prof. Baar founded his first laboratory in the School of Life Sciences at the University of Dundee in Scotland. Keith is currently the head of the Functional Molecular Biology Laboratory (FMBLab) at the University of California Davis.
Over the last 15 years, Keith has worked with elite athletes, as the scientific advisor to Chelsea Football Club, USA Track and Field, Paris Saint-Germain Football Club, British Cycling, The English Institute of Sport, Leicester Tigers Rugby, and the Denver Broncos, to maximize the effects of training for both endurance and strength while minimizing injury. His research is focused on determining the molecular mechanisms underlying the physiological and functional adaptations of the musculoskeletal system to nutrition and exercise. The result of this research is almost 100 peer-reviewed articles in journals from the Journal of Applied Physiology to Nature. His current work is focused on how loading and nutrition alter tendon/ligament/ECM health and performance.
Transcripts:
Keith Baar: A lot of what we do when we work with athletes is we’re looking at their injury history. If I have a super fast athlete who has got lots of muscle pulls, non-contact muscle pulls, then I know that they’re having an issue with stiffness, and I’m going to load them more slow than fast. I’m almost going to do no fast movements at all because they’re going to get fast movement when they’re doing their sport, when they’re doing their training. So I can just do protective movements that are designed to keep them from getting those non-contact muscle pulls. If I’ve got somebody who’s never had a non-contact muscle pull who’s maybe not quite as fast, now I can do a combination of lots of fast movements to try and improve their stiffness and improve their speed. Not necessarily top end speed, but improve their stiffness, and then just enough slow movements to keep them healthy enough.
Joel Smith: That was UC Davis professor and connective tissue expert Dr. Keith Baar, speaking on muscle stiffness, resistance training speeds, and athletic performance. You’re listening to the Just Fly Performance Podcast.
Joel Smith: Today’s episode is brought to you by SimpliFaster. SimpliFaster is an online athletic performance technology shop, distributing items such as the Freelap Timing System, GymAware, kBox, 1080 Sprint, and the SpeedMat. I’ve gotten many of these items from SimpliFaster and can confidently say that they make today’s best training technology available to everybody. The Freelap Timing System has revolutionized both my practices and my athlete assessments, allowing me to look at the 10 meter fly capability of dozens of athletes in a matter of seconds. It is wireless, compact, portable, and incredibly versatile. The kBox and 1080 Sprint are fantastic tools for any coach looking to build speed, agility, and implement training scenarios that go beyond the traditional weight room. The 1080 Sprint is being used by great coaches, training some of the fastest sprinters in the world, and it truly represents high-performance speed training.
Joel Smith: I can personally attest that SimpliFaster’s customer service is second to none. Christopher at SimpliFaster responds quickly to queries, and anyone who makes a purchase from SimpliFaster is in good hands. If you want to acquire some of the best high-tech training equipment available, stop by at SimpliFaster.com. That’s Simpli with an I, Faster.com. They are the future of coaching technology.
Joel Smith: Welcome to episode 156 of the Just Fly Performance Podcast. I’m your host, Joel Smith. Thank you for being here today. On the show, we have Dr. Keith Baar, professor at UC Davis and renowned tendon training researcher and expert. This is another gem in the line of tendon and connective tissue training shows that we’ve had so far, the most recent of which was Dr. Ebonie Rio. I know that this is something that you guys are really interested in. I’m really interested in it. Who out there, as a coach or a coach of athletes, hasn’t dealt with tendon and connective tissue injuries and issues and knees and Achilles and all these things? I think this is stuff that’s really important, not to mention, too … and I’ve said this at seminars, this thought that we tend to think of things from just a muscle perspective, but you hear the term, “Sprinting is electric,” and you see the research. The connective tissue is absolutely critical in being fast and explosive. It’s what makes us athletes in many ways, and we can’t have it without muscle, but the tendons are critical.
Joel Smith: To that end, I’m really excited to have Dr. Keith Baar on this show. He received his PhD from the University of Illinois, and he is currently the head of the Functional Molecular Biology Laboratory at UC Davis, where he leads a team of researchers doing some of the best and leading research in the world on tendons and connective tissue. Over the last 15 years, Keith has worked with elite athletes of many different sports, track and field, football, soccer, cycling. He has spent time as an assistant strength coach at his alma mater, University of Michigan football team, where he spent time as an undergraduate. Keith is a guy who is incredibly smart in the world of research, but also has experience in the trenches, and he really applies it and ports it over to things that are usable by everyday strength coaches, sports performance specialists, track and field coaches, the people who just want to jump higher and have healthier tendons. Dr. Baar does such an awesome job in this show and in his work of creating ideas that are very usable by us to get better output and health from our athletes.
Joel Smith: I know that these shows have been really popular before on connective tissue. This is an amazing follow up. It is incredibly information dense. I would definitely recommend probably listening to it two or three times. I know, for me, I listened to it twice, one in recording it, one in going through it, and in going through it, there were so many quotes I wrote down that also really helped me capture some of the information that Dr. Baar was putting out. So if you’re listening in your car or something, I would definitely take a look at some of the quotes from the show. I think you’d really get a lot out of it, on Just-Fly-Sports.com, on the actual webpage and show notes.
Joel Smith: But for the show today … and a couple things as well. You’ve heard Sheldon Dunlap, who was a previous guest on the show, who really has an innovative version of Triphasic Training for athletic performance, mention Dr. Baar’s impact on him. Jake Tuura, who’s a strength coach at Youngstown State, who will be an upcoming guest, is actually the most recent guy who got me interested again in what Dr. Baar was doing, because he’s had some amazing results from Dr. Baar’s methods. Today’s show is all about tendon training. It’s all about tendon health and regeneration, the dynamics of the collagen networks and the fast and slow exercise isometrics, how that impacts the tendon, tendon stiffness versus length, basically training tendons for health versus performance, which, if you’re training athletes, is a critical distinction, and it’s what Dr. Baar was mentioning in the teaser.
Joel Smith: We’re also going to talk about how maximal overcoming isometric exercises work, as well as extreme isometrics, or long-hold isometrics, and really how all these little tools in the isometric realm have an impact on tendons and muscles and how that adds up in athletic performance. We’re going to talk a little bit as well about nutrition and tendon health and ideas there on optimizing what we’re getting out of that type of training. Again, this is just a fantastic show, super information dense, but Dr. Baar lays it all out just very eloquently in a way we all can understand, and I know you guys are going to get a lot out of this show. With that being said, let’s get on to episode 156 with Dr. Keith Baar.
Joel Smith: Keith, what stoked your interest in tendons and connective tissue and that whole area of the sports performance and physiology spectrum? Because I think it’s a little bit different. Muscles are one thing, but tendons are another. What lit your interest in that part of the field?
Keith Baar: Yeah. There’s two things, really, that started me working in this area. The first one was that, at the time, we were funded by the military to produce a motor, and the best type of motor that could not run out of energy is a muscle-based motor. We were actually engineering muscles with the design of having a muscle that could power devices on a spaceship that was going to do a long-term flight, or it was designed for these really ambitious goals that you needed to have a motor that had the potential to regenerate itself, and it wouldn’t run out of energy if it was given the right supply, so all of those types of things.
Keith Baar: Every time, what we would do is we’d take these beautiful, little engineered muscles that we’d make and we’d put them onto a machine, and they would always fail at the interface between the muscle and the machine. That made it quite obvious that that’s not the way it happens in the body, and you actually have an interface between the muscle and the machine, which is our skeleton. We tried to then start understanding how this tissue, the tendon, was actually working and what was really interesting about it, because if you talk to any engineer, if you do what a tendon does, which is take a very compliant tissue in a muscle and attach it to a very stiff tissue in a bone, that’s always going to be the point where there’s the greatest, what we call, strain concentrations or stress concentrations, and so that’s where there’s going to be the most chance for an injury.
Keith Baar: We did a number of different studies that were designed to understand how a healthy tendon works, and a lot of those studies, what we would do is we’d go into a rodent. We would take out a bone on one side, and we’d take out the muscle on the other. We’d isolate the tendon, and we did this with a tendon that goes along the front of your shin called the tibialis anterior tendon. The reason we picked it is because it’s nice and long, and what we could do is we could draw little lines on it. That was really important because what we wanted to do is we wanted to not only pull on it and see how much load it took to stretch it, just measuring the distance between the two grips, but we actually wanted to look to see is it the same at every point? If I pull on it, if I look close to the tendon … or I should say close to the bone or close to the muscle, do I see differences in the stretchiness?
Keith Baar: Sure enough, what we found was that we looked close to the muscle, you had this really very compliant region at the tendon, and if you looked close to the bone, you had an extraordinarily stiff part of the tendon. Really, what we found was that the tendon was this graded mechanical tissue. From that, we realized, “Okay. This is why our muscles are pulling off the machine, because we don’t have this graded interface between the muscle, which is compliant, and the bone that’s stiff,” and our bodies have created [inaudible 00:09:59]. We’ve evolved these systems where we have one tissue that’s compliant on one end and stiff on the other, and that was really important for our understanding of basically what these tissues were doing.
Joel Smith: Yeah. I think that’s really interesting. That’s actually the first question I was going to ask you, is this whole compliance and stiffness spectrum, because I remember in grad school, my first research class I took … which I didn’t end up going there. I finished with my master’s, but my first class there was like a basic research compilation project, and it was on tendon compliance and stiffness. I got an A on it, but in hindsight, I actually completely misdirected the research. I didn’t do a very good job of … I actually contacted one of the … It was Kubo … one of the study authors later on and asked them about the stiffness and compliance and training thing, and he said, “Basically, the conclusions you made, you can’t make those.” But I still got an A, which was cool.
Keith Baar: Yeah. No, that’s very good. There’s a really big difference between the beautiful work that Kubo has done and the work that we did in the rodents, and that’s that when we do it in a rodent, what we’re doing is we’re taking out the tissue, we’re holding onto the muscle on one end, the bone on the other end, and we’re pulling directly on the tendon. Whenever we do these things in a human, we can’t obviously do that, so what we have to do is we have to use something else to generate the force, because here, what we’re doing is we’re pulling on it. Every time we pull on it, we pull on it with the exact same load and the exact same velocity. That’s super, super important for understanding the mechanics of the tissue, because if you load it faster or slower, you’re going to get different mechanics.
Keith Baar: When we do these studies in humans, what we’re doing is we’re using muscle contraction as a way to load the tendon, and that’s great because you can get a measure. The problem is that that assumes that nothing has changed within the muscle. As I load my tendon, if I load my tendon today and then I train for eight weeks, and I load my tendon in eight weeks, the trained muscle has also changed. What’s really important to realize is that trained muscle has a matrix within it, and that matrix within it is made up of collagen, and that matrix also is changing dramatically as you change the muscle’s functionality.
Keith Baar: There’s a beautiful study that just came out a few months ago that shows that if we look in a muscle, we actually see that there’s the muscle cells that are producing the force, and then there’s the little satellite cells on the outside, which are the stem cells, which help us fix any injuries that we have, and there’s also another population of cells. There were seven in total, but one of the new ones that they discovered was a population of cells that are actually cells that are tendon cells. They’re actually in the muscle, outside of the muscle fibers, and they’re probably the cells that are producing the matrix within that muscle.
Keith Baar: The big thing that happens when we train or when we change all these loadings, we’re not only changing what happens in the tendon. We’re changing the matrix in the muscle. We’re changing the muscle itself and its ability to transmit the force. All of these things are changing, and to the whole system together, we’re changing the mechanics of it. That’s really important because when I test it, I pull it using a machine, holding the bone, holding the muscle, and I’m loading the tendon. That takes out any changes that happen in the muscle, but when we do these experiments in human, we have to use the muscle as a way to load the tissue.
Joel Smith: Yeah, it makes it fairly complex. I know the last tendon podcast I did here with Dr. Ebonie Rio, and some of the work I was doing reading her work in preparation for that, it was like Achilles tendonitis, big, big issue, and doing calf raise or basically strengthening the plantar flexors seems to have a benefit, but it doesn’t … It has a benefit faster than the tendon can remodel, so where is this coming from? It’s a very dynamic system. It’s not just the tendon. You have to look at all things, but I imagine that makes it … Like you said, it can make it a lot harder to really pin down where these changes are coming from, and it’s a lot more layered system than just one plus one.
Keith Baar: Right. It goes back to things like you just said. Oh, it’s happening faster than the tendon can remodel. A lot of that’s actually from this feeling that we have or this information or maybe some of the older work where we know that, oh, well, tendon takes a long time to turnover. There’s this idea that a tendon is very slow in turning over. There’s beautiful work from [Kathia Henemier 00:14:42] who showed that the core of the Achilles tendon doesn’t change after you’re older than 17 years old. But there’s new work that’s coming out, and it hasn’t come out yet, but it’s coming out from [Luke Van Lune’s 00:14:54] laboratory in Holland, and he’s probably one of the top two or three people in the world about protein turnover.
Keith Baar: What he’s doing is he’s taking people who are getting total knee replacements and he’s giving them deuterated water so he can label all the proteins that they make in the two weeks before their total knee replacement. They then cut off the top and bottom of the knee. They take that out, and his research team is taking that out, and he’s looking at bone turnover, cartilage turnover, ligament turnover, and he’s comparing it to muscle. What he found is that the ACL ligament, the anterior cruciate ligament, its turnover is the same as the quadriceps muscle.
Joel Smith: Wow.
Keith Baar: The posterior cruciate ligament is actually at about 50% less turnover, so it’s not loaded as much, but it’s still turning over at a relatively fast rate. Even though we say, “Oh, these things are happening faster than a tendon can remodel,” tendon remodeling is actually extremely fast. We’ve had some success with things where people were getting MRIs six weeks apart, and they’re looking and they’re saying, “Oh my god, what have you been doing? Because there has been these dramatic changes to your tendons.” We know that if you go out and you overdo it today, you’re going to have a tendonitis. There are dramatic changes that can occur within these tissues in a very short period of time.
Joel Smith: Yeah, that’s interesting to know. Actually, shoot, I’m going to have to hit you up and email you after we’re done with this to hopefully get some of those studies to put in the show notes, because it’s just amazing to me how fast the research can change and evolve. It’s like a new study comes out, like with the Achilles. If you know that … Before, it’s like, “Well, maybe the calf is taking part of the load, more of the load. The muscle is taking more of the load, and that’s why this is happening.” It’s just you don’t know what you don’t know.
Joel Smith: Actually, I’m really glad you mentioned that study with Henemier because I was actually just even … I mean, again, sometimes we make assumptions, but this idea … and I’ve heard it before. If you’re going to be an athlete, you really need to train your fascial system as a first priority because, like you said, at 17, that’s the max thickness. It’s kind of like if you spent too much of your time doing weight training and other stuff before age 17 as opposed to your elastic and speed and sprinting and jumping, your sport, now you can’t make up for it.
Keith Baar: Yeah, but we know now that that’s not entirely true. Kathia’s work is wonderful. What we think is potentially happening is the core isn’t changing too much. It might remodel. It might reshape. It might have reorientation, but then what you’re doing is you’re changing things around the core. You can make the tendon bigger or smaller. You can change all of those types of things. For that purpose, we did a really nice case study on a professional basketball player. What we did is when the basketball player came into the NBA, went into the NBA combine, they do MRIs on both legs, on both knees. He was found to have a hole in the middle of his patellar tendon on one of his knees. Then we developed, together with his training team, and mostly driven by his training team, developed a program for them to really try and target that one area to try and fix it.
Keith Baar: What we found is that just by doing our loading and nutrition program that over the 12 months following that first MRI, it completely went away. The central core of the patellar tendon, which had a hole in it, which was filled with water, and you could see it on the MRI as a white hole, that was completely filled in over the period of 12 months. We have people who’ve done that significantly shorter. What you also saw was that the size of the tendon close to the patellar actually went down because the patellar had been inflamed. When you got out the core problem and you fixed it, the actual core of the tendon, or the tendon close to the patellar where the injury was, was actually smaller. But if you looked at the midsubstance, if you went halfway down the patellar tendon, it had actually gotten thicker.
Keith Baar: Over the 12 months … and he played 50 NBA games, as well as the training we were doing … we had already changed his patellar tendon diameter quite significantly, decreasing it at the top, increasing it where you would hope to have a bigger, stronger tendon. We know that we can do these things. We know that these things happen … That period of time, the 12 months, was simply because you don’t want to put somebody into an MRI all the time, but we have people who I’ve worked with who basically, within six weeks, they’ve already seen that kind of a change. These transitions are happening really quickly, and you’re getting to the point where you can actually reshape these tissues relatively robustly.
Joel Smith: That’s interesting to me. Based off that, then what would you say is the relevance of Henemier’s research in light of that? You had said basically the shape is set, or it’s somewhat set at 17.
Keith Baar: It’s like a tree. The first few years, those are the internal rings, and the outside of the rings, the other rings that you’re adding on as you make that tree bigger and stronger as it ages, those are the things that are more dynamic. That part of the tissue is more dynamic. The center, core part of it maybe isn’t as dynamic unless you have an injury. These were all relatively sedentary people. They were … Well, no. For Americans, they were massively active because they were from Denmark. They were always active. They were going around on their bikes. They were doing all these things. The interesting thing about the study is that there were a few people who weren’t on the line at all. They were really, really low.
Keith Baar: What’s entirely possible is those people had a serious Achilles tendon injury, and they actually had to go through regeneration, and you didn’t see the same pattern with those people. If you’re going through normal life, you’re not competing at a very high level, you never are getting damage to the area, there’s no reason for us to turn that over because the collagen is still functional. But if you’re loading, if you’ve got lots of good nutrition that’s supporting this system, you’re going to have higher rates of turnover, and the rates of turnover are going to be high enough so that you’re going to actually see dynamics to the size and the functionality of the tendons.
Joel Smith: I see. In a way … and please correct me if I’m wrong … it has an impact on it, so the function up until then does have an impact, but it’s not the determining factor. It’s like a part of it. It’s a big influence, but it’s not going to … You can obviously still have plastic changes outside of that.
Keith Baar: Exactly. I think part of the reason that you might have been thinking of that is it is really hard to change speed, top end speed, as you get past 13, 14 years of age. Is that potentially because we’ve already set tendons, and so our stiffness is set? We know that that’s not true at all. One of the ways that we know that is that I get the opportunity as part of some of the work that I’ve done with the USA Track and Field Team, is that I’ve had the opportunity to talk to a number of incredible coaches. One of them, John Smith, who’s a world-class sprint coach, he told me this great story that he can always tell just by listening whenever his female athletes have gone out and wore high heels to a special event because just three, four hours walking around in the high heels is enough so that when he hears them contact the track, he can actually hear a difference in how quickly they’re contacting the track.
Keith Baar: These things are extremely dynamic, as far as the stiffness, as far as we can play with that quite dynamically. We can change that within a period of days, really.
Joel Smith: Yeah. I think it’s awesome how that neural imprint can carry over based off of the footwear, and then you get out of that and you’re on the track, but you still can hear it, even in different shoes. It’s really cool how the nervous system can port over.
Keith Baar: Well, in there, it wouldn’t necessarily be the neural component because if I shorten your tendon, I can make it so that with the same neural input, we can change the stiffness of the system, just because until you’ve done enough, I can change the cross-links within the collagen, and that’ll stiffen it up into that position a little bit. If you put yourself into a cast for a few days, and you get yourself out of the cast, it’s really stiff and sore. If we wake up in the morning, we’re feeling like, “Oh my god,” really stiff. After a few steps, you’re going to break down what you’ve done in the time when you’ve been sleeping.
Keith Baar: But if you’re constricting your muscle and tendon into a shorter position for a while, and you’re walking around, you’re using it normally, you’re actually going to develop cross-links. You’re going to develop changes within the tissue that then you need to mitigate in some way, or you’re going to see consequences of that. Some of the consequences are good, like you’re going to be maybe a step faster, a little half-step faster, quarter-step faster. Some of them are potentially bad. There’s a potential for a greater risk of injury.
Joel Smith: You’re listening to the Just Fly Performance Podcast, brought to you by SimpliFaster.
Joel Smith: Yeah, thanks for clarifying that, Keith. Basically, you’re saying that the effect to the heels is more like the mechanical compression of the foot more than the nervous system being in a mode by being in the toe, kind of like a cast, if you will, that ports over for the next thing.
Keith Baar: Yeah. It’s just that you’ve got this … It’s not a compression, really. It’s just a shortening of the Achilles.
Joel Smith: Oh, yeah, that too. Obviously, yeah, that too.
Keith Baar: Yeah. It’s just a shortening of the Achilles, that the Achilles is now shortened. At the same muscle tension, you’ve got a shorter Achilles. If you do that long enough, that’s going to change the mechanics of the muscle-tendon unit.
Joel Smith: Got you.
Keith Baar: Then when you go back and you have to go through a full range of motion, it’s not going to have the same compliance and stiffness that you would be used to from everything else you’ve done.
Joel Smith: Cool. Perfect. Yeah, that makes perfect sense now. Speaking of that, the tissue lengths and all these things, the first that we’ve alluded to, or you’ve alluded to as you’ve talked already, but I think there’s this big thing between tendon stiffness and compliance. You were already talking about how closer to the bone, it can be one type of thing, and closer to the muscle, it’s another. But is there really a general setting, like this tendon will generally get stiff or generally get more compliant by this type of training, and we’ll shake that out for health or performance? How does that matter in the context of training and performance and what changes we can make?
Keith Baar: Yeah. That’s a great question. It goes to the basis of what is … The biggest question there is, how do you change the stiffness of a tissue? Stiffness in these tissues is determined by the collagen content and orientation, so how much collagen is there and how it’s oriented. That’s a really, really important component because if I have more collagen, I have the potential to have more stiffness, but I don’t always get more stiffness, because that’s only one component of it. I’ve got my collagen content on one side, and then what you have is you have the collagen molecules. They’re these beautiful, spiraled molecules that are brought together in a really regular pattern. They’re a regular pattern. There’s overlap between the fibrils, and then those fibrils are cross-linked. That means that they’re connected together by an enzyme, which connects to amino acids between the two collagen molecules, and that just provides the attachment between them.
Keith Baar: Then they’re organized into these structures, and as you get up to the fibers, you get fascicles, and then the fascicles actually can slide relative to each other as well, and those are linked together by cross-links and by other things that we’re just starting to begin to understand. What we know is that as you have more cross-links, you get more stiff collagen. You can have the same amount of collagen protein. If I cross-link it more, I have just made it stiffer. Now we’ve got two ways that we can control this. The Henemier study only looked at the collagen content. It’s only looking at collagen. Is the collagen there the same collagen that used to be there months or years or decades ago? What you’re not seeing is you’re not seeing the cross-link component, and the cross-link component is something that we change dramatically with our activity and also by what we eat and how much enzyme activity that we have.
Keith Baar: Okay. The main enzyme for cross-linking the collagen is an enzyme called lysyl oxidase. That enzyme is really, really important. It’s a copper-containing enzyme, and it uses … Well, and that’s one of the first components of it. There’s a second enzyme that’s really important called prolyl hydroxylase. That one’s really important, and that one is the one that we need vitamin C for, because that one is important not for cross-linking the collagen. It does cross-link a little bit, but what it’s most important for is actually making collagen. If you don’t have prolyl hydroxylase and vitamin C, you don’t make and export collagen. Okay, so that’s where that comes in. That’s making collagen, and then what you have is you have this enzyme lysyl oxidase, which cross-links it together. The more lysyl oxidase you have, the more cross-links you get, the stiffer the tissue you have.
Keith Baar: All right. What we do when we exercise, any type of exercise we do, we’re going to increase the amount of lysyl oxidase that we have. That’s the enzyme that’s going to add in cross-links. Okay. If we’re just doing exercise and we’re doing regular exercise, you have this potential to increase lysyl oxidase and accumulate more and more cross-links. The other side of it, though, is that when we’re doing our activities, we have the capacity to break down our cross-links. The way that it works is that as our muscles contract, as we talked about earlier, when I said that if we pull on a tendon fast, it’s stiffer, and when we pull on a tendon less fast, it’s less stiff. If I load my tendon quickly, all the collagen in my tendon works as a sheet, and it just pulls with the muscle. There’s no sheer forces. There’s nothing else really going. It’s just working as one unified grouping.
Keith Baar: When that happens, we don’t break down any cross-links. We’ve done exercise. Lysyl oxidase has gone up, so we’re adding cross-links in. When we do really fast exercise, we don’t break cross-links. We’re adding more cross-links. We’re getting stiffer. If instead I do the exact same exercise but I do it slower, or I do it in an isometric way, now what I get is I get the collagen within my tendon, the fascicles of the collagen molecules start sliding relative to each other, because as anybody who’s done a wall sit where you sit on a wall and you put your knees at 90-degree angle and your hips at 90-degree angle, it starts to burn after a while. The reason it starts to burn is because the tendon is starting to relax. As the tendon is relaxing, what we’re getting is we’re getting sliding. Things aren’t sliding equally. The muscle is pulling really hard. The tendon is sliding, and you’re getting this property of viscoelasticity called creep, which it creeps down slowly, and it becomes longer over time.
Keith Baar: When that happens, we get these sliding. The sliding breaks cross-links, and so now what we’ve done is we’ve broken cross-links, and then we’re going to get lysyl oxidase to add some back, but if we’ve done it right and this is our goal, what we’ve done is we’ve broken more than we’ve resynthesized, and the result is that we’ve decreased cross-links. Remember, cross-links cause the collagen to be stiffer, so by doing a slow movement, we’ve made it less stiff in the collagen in the tendon, and in a fast movement, we haven’t broken cross-links. We’ve increased cross-links, so we’ve made it stiffer. In the tendon, if we load fast, we get a stiffer tendon, and if we load slowly, we get a less stiff tendon.
Joel Smith: Okay. I got you. Actually, I have a good follow up off that for you, but before I get to that, actually I had a question with the wall sit, because I had never heard this before, that the burning came from the tendon action. I think it-
Keith Baar: It doesn’t come from the tendon. It comes from the muscle contracting-
Joel Smith: Oh, okay. I got you.
Keith Baar: … as the tendon continues to relax. The muscle has to keep working and working and working.
Joel Smith: I got you.
Keith Baar: As the tendon’s relaxing, it has to work more and more and more.
Joel Smith: Yeah, because I was like, “Yeah. It’s just the pH of the muscle.” I was like, “Is there something I’m missing here?”
Keith Baar: No. No, it’s not the pH of the muscle, either. It’s just that it’s having to continuously work, and you’re generating a bunch of byproducts. pH is one of them, one of many different things that are being generated. So all of those different things are going into this feeling, this burning feeling there. But the reason it’s burning is because if you were just sitting there doing an isometric contraction, you can hold it for a long time, but as you’re doing the isometric contraction, if your tendon is continuing to lengthen, your muscle has to continue to shorten, so it’s not really isometric in that way. You’re still having to shorten, you’re still having to have all of these cross-bridges moving, and so you’re not actually just holding it isometrically.
Joel Smith: Cool. Yeah, that makes good sense, too. Yeah, because if your muscle was just locked out and wasn’t doing anything, it wouldn’t get as tired. It’s just hanging out there.
Keith Baar: Nope, because we can do that when you’re dead. That’s rigor mortis. Isometric contraction’s not very metabolically costly if you can do it when you’re dead. Again, but it’s not a true isometric-
Joel Smith: Yeah. That’s-
Keith Baar: … because then the muscle is continuing to shorten as the tendon lengthens.
Joel Smith: That’s why some isometrics have actually been labeled extreme slows, because the muscle is extremely slowly lengthening to deal with … or contracting to deal with the lengthening.
Keith Baar: Exactly, and that’s what we say. We just said the fast movements cause it to be stiffer. Slow movements cause it to be less stiff. The slowest movement is an isometric. Still a movement because you’re still getting the shortening. That’s why that tends to have the greatest positive effect for the health of the tendon.
Joel Smith: Cool. Yeah, and that makes sense. I’ve heard so many anecdotes on that, iso lunge, iso wall sit, and I like to get more into protocols here as we go throughout this. One question I have based off that, is it kind of like a … I mean, I think of it like training. Maybe you started a program with long isometric holds, and then you go later on to some depth jumps or loading. With that, is there a counteracting effect, or because you’re breaking cross-links and creating this longer system, is that create more potential later on for when you do load more quickly and create the sheet? Slow set up for long, basically, is my question.
Keith Baar: Yeah. That’s a good question. Basically, what you’re looking at when you do these types of things is you’re looking at … A lot of what we do when we work with athletes is we’re looking at their injury history. If I have a super fast athlete who has got lots of muscle pulls, non-contact muscle pulls, then I know that they’re having an issue with stiffness, and I’m going to load them more slow than fast. I’m almost going to do no fast movements at all because they’re going to get fast movement when they’re doing their sport, when they’re doing their training. So I can just do protective movements that are designed to keep them from getting those non-contact muscle pulls. If I’ve got somebody who’s never had a non-contact muscle pull who’s maybe not quite as fast, now I can do a combination of lots of fast movements to try and improve their stiffness and improve their speed. Not necessarily top end speed, but improve their stiffness, and then just enough slow movements to keep them healthy enough.
Keith Baar: Remember, we’ve only really talked about the tendons so far. If I’m doing a plyometric load or an isometric load or any of these loads, I’m not only affecting the tendon, I’m also affecting the muscle. There’s beautiful work, early work, from Allurent where they showed that, “Look. One of the things that happens in a muscle when I give it a really big load is I get a huge increase in collagen, and I’m getting an increase in collagen synthesis, and I’m decreasing collagen degradation. So the matrix around the muscle is actually becoming more collagen rich. That matrix is now going to be stiffer and stronger here. Even if I’m doing an isometric in my tendon, I’m loading my muscle, and my muscle still has to prevent the sheer forces that we want in the tendon.
Keith Baar: The way that it does it is it improves the connection between the fibers. One of the things that it does to do that is it increases collagen content, some of the other force-transfer proteins, and now what you’ve got is you’ve got a muscle that’s better able to deal with the loading, and you’ve got a tendon that’s now less stiff, a muscle that’s probably more stiff, and now the combination gives you maybe not a dramatic change in the overall stiffness of the system, but it’s got a very big effect on injury prevention, because now we’ve made our muscle a little bit tougher, essentially, and our tendon a little bit less stiff along the muscle end, so it’s more protective of the muscle. The result is that you’re going to see a significant decrease in non-contact muscle pulls.
Joel Smith: Cool. Back to that player you were saying who comes in and has a lot of muscle pulls, and they have a stiffness issue, and you were saying you’re giving them slow work. Does that mean their tendons are too stiff, and you’re trying to allow that tendon to break down and pull more, or elongate more?
Keith Baar: Yeah, essentially. Essentially. One of the biggest things that we see in tons and tons of athletes across different sports, the faster a person is, the more muscle pulls they get. One of the things that we also see is that women get 85% fewer hamstring pulls and groin pulls than men do. Again, one of the things that we know about women is that estrogen, we’ve shown in our laboratory using our engineered ligaments, estrogen directly inhibits the enzyme lysyl oxidase, which is the cross-linking enzyme. The women, what that means is that their tendons are less stiff. Performance is a little bit lower as a result, their power-based performance, but they get fewer muscle pulls, so that’s great. Problem is that it’s the same collagen that’s in their knee, and so now what they’ve got is they’ve got four-plus fold more ACL ruptures because the same enzyme that’s being inhibited in the tendon and protecting the muscle from pulling is the same enzyme that’s going to make the ligament less stiff and more lax, going to result in more ACL ruptures.
Keith Baar: We understand this information’s out there. It’s just a matter of making sure that people are putting it together in a way that you can now structure something that’s going to be a little bit more useful in how you would put something together for an athlete, because really what you’re trying to do for the men is you’re trying to decrease muscle pulls, but you know that the ligaments are going to be quite, and that knee is going to be quite, stiff. You’re not going to have too much laxity in the knee because, again, they don’t have the same hormonal situation. As a result, more cross-linking in the ligament. The more cross-linking, the better because a tighter joint means fewer injuries. If you have a 1.3 millimeter increase in laxity in the knee, you have a four-to-six-fold greater likelihood of an ACL rupture.
Keith Baar: For ligaments, I want them to be as tight as possible. For a muscle, if my tendon is stiffer than my muscle is strong, instead of the tendon stretching when I hit the ground, the muscle is going to have to stretch when I hit the ground, and that’s a high-force lengthening contraction, and that’s when we get these muscle pulls.
Joel Smith: Oh, I got you. Oh, that’s interesting. I hadn’t thought of it that way at all, but that makes perfect sense. I was going to say, too, with the women, I had never heard that before, but it’s like working in track, I should have known that. It actually caught me by surprise a little bit, but now that you say it, I’m like, “Wow.” You’re definitely right.
Keith Baar: Yeah.
Joel Smith: But in track, they’ll say, “We’ll strength train women deeper in the season than men,” because they need it. To me, it’s like almost they need it to keep the stiffness higher relative to men who don’t need that as much later, just from a pure performance stiffness standpoint. That would make sense, right?
Keith Baar: Absolutely.
Joel Smith: I was going to ask you, too, about … We’ve talked about isometrics and slow isometrics as used for creating a longer, more compliant tendon. To make a stiffer tendon, I mean, I’m assuming that’s just heavy weight lifting or rapid heavy weight lifting or plyometrics. Is there anything that’s kind of-
Keith Baar: We know from force velocity relationship that the heavier I go, the slower I go. What we talked about is that if I want to get faster, if I want to increase stiffness, I need to have a fast movement. There’s beautiful data out there that shows that, look, the biggest performance benefit is max power work, is better than plyometrics, is this 0% to 30% of your one-rep max as fast as you can move it. That’s where we see the biggest effect because, again, the velocity is the key thing. When I’m strength training and when I’m talking to strength coaches, I try and make them understand that normally what a strength coach does is they look at what they control. They control the volume. They control the load, and they control the frequency. Those are the things they’re doing. How many times a week? How much are lifting? Really, those are the … and then how many sets are you doing?
Keith Baar: When we’re looking at performance-based work, if you’re looking to increase stiffness or increase performance, what you want to do is you need to … We’re actually not programming any of those things. We’re using those things as a tool to actually control the thing that we’re most interested in, in programming, which is velocity. If I’m going to do a lift, I’m going to use a weight that is going to either make me go slowly, because it’s a heavy weight, and that’s going to protect my tendons and muscles from injury, or I’m going to use a low weight, and I’m going to move it as fast as I can, and the result is going to be that now what I’m going to do is I’m going to get this high-velocity movement. That high-velocity movement is now going to increase the stiffness, which is going to increase performance. It’s going to potentially put somebody at more of a risk for injury.
Keith Baar: What we’re really doing when we’re programming as a strength coach is we’re programming velocity. That’s the key component. When you’re programming velocity, you don’t do as many repetitions in a set, and you don’t do as many sets because you can’t maintain the velocity as well if you do lots and lots of repetitions.
Joel Smith: Yeah, that’s good stuff. It’s good to have that in the memory banks, and then as well, too, I wanted to ask you this, was a common exercise in track and field that’s becoming more common … and the original guy on this podcast, Alex Natera, who pioneered it, and then other colleagues of mine who are using it are getting the same results of improved top end speed in track and field athletes, and that’s a maximal isometric push where basically you’re in a Smith machine, the bar’s on your back, and your foot is on a block. Your toe is on it. Your heel’s free, and your leg is about at the angle that it would be as your foot passes under you in sprinting. It’s just a short push as hard as you can into the pin, so like an overcoming isometric.
Keith Baar: Right.
Joel Smith: Based off what we’ve said, I’m curious what effect that has. You’ve talked a little bit on the muscle-tendon interaction. I’m curious how that hits that stiffness paradigm.
Keith Baar: Yeah. The key thing with isometrics is that there’s the overcoming isometrics, there’s the holding isometrics, there’s the resisting isometrics. The key thing with isometrics is less so whether we’re developing, whether we’re holding, whether we’re resisting and much more so about how long we’re holding for. In the type of work that you’re talking about where you’re trying to develop speed, you’re just going to do an isometric, but it’s going to last really, really short, so the snap of a finger. You’re just going to push up as hard as you can, and you’re going to hold it for less than a second, and you’re going to come back down.
Keith Baar: When I talk on isometric for a health-based movement, I’m talking about a 30-second hold. Again, the reason is based on the mechanics of the tissue. What happens in what you’re talking about where you’re doing a very short push, it’s not an isometric in the sense that, yes, the length of the joint doesn’t change. Technically, it’s an isometric, but just like we talked about when you do a wall sit and the muscle is shortening even though you’re holding it for 30 seconds, in the accelerator, basically what you’re doing is you’re accelerating, and the muscle is taking up all the slack in the system. You’re pushing up as hard as you can, and then you’re letting go. That whole thing, the muscle and the tendon unit are shortening that whole time. The design there is to stiffen the muscle-tendon unit as a unit when you’re doing that.
Keith Baar: When I’m talking about for healthy movement for health or repair of an injured tendon, what we do is we use a very long isometric hold. The reason we do that is because of that property that we talked about earlier, which was that viscoelastic creep. Creep in a tendon means if I pull it and I hold it at a certain length, and I measure the tension between the two ends of the tendon, and I hold it there over time, what I’ll see is that the tension goes up really high when I pull it, and then it goes through this relaxation, and it’s an exponential relaxation. The relaxation kind of gets to the bottom where the tension is as low as possible, around 30 seconds. It’s about 45% of the tension within the tendon is released in the first 30 seconds.
Keith Baar: If I go out to 180 seconds, it only releases maybe 5% more of the tension. That’s why when you go and you … I’m sure none of your podcast listeners do it anymore, but you hold a long, static stretch. You go and you reach for your toe. You hold it for 20, 30 seconds, and then you reach again, and now you can go further. All you’ve done is you’ve done the creep, and then you’ve taken advantage of, “Oh, there’s less tension there, so now I’m going to pull on it again, and my muscle-tendon unit together can stretch further.” All you’ve done is relaxed the tendon, and you’ve gotten this creep. When we’re talking about a healthy move where we’re going to get sliding of the collagen molecules, we need to get into that zone where we’re getting creep. When you’re talking about a performance movement, technically isometric because the joint’s not moving, the muscle is certainly not isometric at that time. The muscle is shortening as quickly and as hard as it can, which is exactly what it does when you hit the ground when you’re running full speed. Your muscle contracts isometrically.
Keith Baar: Beautiful work from Tom Roberts has shown that when you’re running, the muscle contracts isometrically, the tendon stretches and recoils, at least the calf muscle, some of the other muscles as well. But that’s really what you’re modeling when you do the really quick Smith machine accelerated push. Yeah, it’s an isometric because the joint doesn’t move, but the muscle’s not isometric.
Joel Smith: You’re listening to the Just Fly Performance Podcast, brought to you by SimpliFaster.
Joel Smith: Got you. Yeah, that makes perfect sense. I imagine it’s almost like you have a rubber band, and the muscle is like your hand pulling the rubber band up when inside the body … You can’t see it, but when [inaudible 00:48:50]. Like you said, it’s the same thing that happens in running. You’re basically just using that mode to teach the system to create tension faster as a whole.
Keith Baar: You rapidly create the isometrics so you can store energy within your tendon. Yeah.
Joel Smith: Cool. Well, while we’re-
Keith Baar: [crosstalk 00:49:05]
Joel Smith: That’s awesome stuff, by the way. Thanks for putting that out there. You mentioned stretching too. I wanted to get into that a little bit with static stretching, because people do still talk about it, and I’ve heard it’s almost more of the tendon than it is the muscle, or like you said, it is more of the tendon than the muscle. Could you go into that a little bit? Then one of the things I have been curious about specifically is the Achilles. If you were to stretch the Achilles a lot, is the tendon and the creep going to have a long-term effect on feedback loops? I hope I didn’t convolute the question, but I’m just curious about stretching and performance and all that.
Keith Baar: No, sounds good. No, you hit a buch of things there. Basically, the idea behind the static stretch is that people say, if you ask them why they statically stretch, “Oh, to decrease injuries.” Well, there’s a beautiful meta-analysis that shows that if you do static stretching, it has no effect on injury rate. If you do heavy strength training, it decreases injury rate by two-thirds. The heavy strength training, again, velocity is low. You’re getting the low, slow movements that are going to be protected. The stretching isn’t doing that. Part of it is because of what you said at the end, this idea of feedback loops.
Keith Baar: I always use the example of NCAA gymnastics, because the women in NCAA gymnastics, probably some of the most flexible women in sports at the college level. If you look at these women, they do a lot of static stretching, a lot of static stretching on the calf. Last year, they had 17 women who ruptured their Achilles tendon.
Joel Smith: Yeah.
Keith Baar: If stretching is really going to be really beneficial for explosive performance, that’s the group that stretches more than anybody else, and yet here they are, rupturing the Achilles. What we think is happening is that when you’re stretching, in order to get into that position, it’s not that the tendon and muscle are actually changing too much. The mechanics of the tendon-muscle interface don’t seem to change. What seems to happen is there seems to be override between the brain and the spinal reflex that is normally designed through the Golgi tendon organs and the muscle spindles where you can rapidly respond to changes in the muscle and tendon length.
Keith Baar: When we stretch, what we’re doing is we’re overriding the reflex to say, “Oh, no. This is normal,” and so we’re getting less of the reflex arc. We’re getting less energy through the reflex arc so that when we hit the ground following an explosive movement, we don’t turn on the reflexes as quickly, and the result is that we don’t protect the tendon the way that it needs to be protected by co-contracture of these muscles that are going to stabilize the joint, and that’s going to stabilize the joint and protect from injury. Well, if you have this chronic override on these reflexes, what seems to happen is you become more prone to getting those injuries because you’re not getting the co-contractions to stabilize the joint at the exact moment that you need to because the reflex is not as quick.
Keith Baar: We don’t tend to use the static-type stretching simply because what you’re doing with a static stretch is you’re overriding the muscle spindles and the Golgi tendon organs. You’re not getting the sheer force that we get from a contraction. When we hold a contraction, you’re going to get more sliding because the muscle is contracting, and when the muscle’s contracting, we’re going to get different signals from the muscle spindles and from the Golgi tendon organs. What that means is when we use a muscle contraction to get this type of stretch on the tendon, we’re going to get a different overall system effect than if we just use a passive stretch of the system. Does that make sense?
Joel Smith: Yeah, and I really like the gymnastic illustration, too, because I think that illustrates it very perfectly, and it makes sense with everything else you’ve been talking … in context with this whole show as well, just with how different tissues are acting under load. I mean, like I said, it’s an interesting topic. Look at the science, but there’s definitely people who are still talking about it, and so I’m glad that you’re able to put it under the context of everything that we’ve been talking about so far.
Joel Smith: I have two other questions for you, and one of which is kind of a follow up. You’re talking about the isometrics for health, but what’s your take on a slow eccentric, maybe loaded or unloaded but slow eccentric stuff?
Keith Baar: Yeah. The key to the offense in protocol is the slow component. Again, all you’re getting … and there’s beautiful studies out of Copenhagen comparing the Alfredson eccentric protocol to a heavy strength training protocol. There’s no difference between the two. Really, what you’re seeing is you’re seeing the velocity. The key of the Alfredson isn’t that it’s eccentric, because I could do a plyometrics eccentric. You’re not going to do that as a health movement for your tendon because the velocity is very different. Really, what you’re doing is it’s the slow isometric component. When they say slow isometric, the slow is the part that we’re really interested in. Again, you can do a slow concentric, a slow eccentric, or you can do an isometric. All three seem to be very similar.
Keith Baar: The reason that we use the isometric is because that’s really allowing the most creep to happen within the tendon, especially when we’re looking to change the functionality of the tendon, because most of what we’ve talked about, or all of what we’ve talked about, is when the tendon is healthy. The real problem happens when we get a tendon injury, because when we get a tendon injury, basically what happens is, evolutionarily, the reason that we have these beautiful structures is because we don’t have to pass load through the whole tendon. We can shield any injured tendon bit, and all this stress or all the load goes around it, like putting a rock into a river. The water just goes around the rock, the same way that the load goes around the injury. That’s great for not rupturing the tendon. The problem is that if you don’t load it, the cells don’t know which direction to make collagen, then they make collagen in all different directions, and that’s what we call a scar. It’s a non-directional collagen.
Keith Baar: What you have to do in order for the collagen to reorient and to regenerate a functional tendon, what you have to be able to do is you have to get load through that tissue so the cells know, “We’re supposed to synthesize collagen in this direction.” That’s where having the creep is really important, because what creep is, is it’s all of these collagen molecules relaxing the fascicle sliding, but what it does functionally is as the load goes down … Remember, we talked about if I pull on it, the tension goes up within the tendon, and then it drops, and it drops so far that the whole tendon is now weaker than the scar area. The scar then gets a pull on it, because now the whole tendon is weaker than the scar, and the result is that you get a little pull on the scar, directionally oriented along the line of force, and now the cells say, “That’s where the force goes. That’s the direction we need to synthesize collagen.”
Keith Baar: That’s how we use the long isometrics, or you’re using your slow concentric, but the slow concentric and the eccentric aren’t giving you as much of a creep because there’s movement. As soon as there’s movement, you don’t get as much of the creep effect.
Joel Smith: Yeah. It kind of de-simplifies it and just adds more components and more forces in more directions to the whole equation.
Keith Baar: Exactly.
Joel Smith: Cool. Okay. Last question for you, and I know this could probably be a whole show, so maybe like a 10-minute answer, but just role of nutrition in all this. You’ve alluded to it before earlier. Role of nutrition for people who are dealing with knees and Achilles and trying to get that better, or just optimize their own tendon health and performance?
Keith Baar: Yeah. There’s definitely a role for nutrition. We know that from the first nutrition study ever performed … The first nutrition study ever performed was in the 1700s by this Scottish doctor who was on a ship. Basically, all of these sailors were getting scurvy, and they were losing their teeth, and their scars were coming open, their hair was falling out. He did an experiment where he gave all kinds of really disgusting things to 10 of the sailors, and two of them got a lemon and two other citrus fruits. Within days, those two that got the lemon and the citrus fruit got better. So there’s obviously a vitamin C component to it.
Keith Baar: We know from some of the studies that we’ve done that the vitamin C, the reason that it works and the reason it’s essential is because it is a mandatory co-factor in this prolyl hydroxylase reaction where we’re making collagen. What it does is you can’t export collagen from a cell unless you have that reaction, and every time you have that reaction, you consume a molecule of vitamin C. It’s not that we use it and we can reuse it and reuse it and reuse it. It’s that every time you use it, it’s gone. When you wake up in the morning, what we’re finding from some of the studies we’re doing is that it looks like your vitamin C content in your tissues is really, really low. That’s one component that you have to have. You have to have some sort of a vitamin C component.
Keith Baar: The other thing that we’ve been looking at quite extensively is the role of just dietary collagen or dietary gelatin. The difference between them, gelatin is basically … It’s all collagen. It’s all coming from skin or bones or connective tissues from either cows or pork or chicken or fish, so there’s not a vegetarian source of it. That’s the number one thing. What we’ll find a lot with our athletes is, “Oh, you know what? I went vegetarian, and now I’m getting all these niggles, these tendon injuries, these ligament problems, and my knees are hurting me more.” It’s not surprising because they’ve lost all of their dietary source of collagen. The reason that this is potentially interesting is because collagen is essentially three amino acids. It is glycine, it’s proline, and it’s lysine to a large degree. The glycine is every single third amino acid. It goes glycine, any amino acid, and then a hydroxyproline. One-third of all collagen is glycine, so you need a good amount of glycine.
Keith Baar: There’s a group out of Brazil who’ve shown that if you supplement with glycine, you can have these great effects. They were giving just globs of glycine. It’s not physiologically possible to do that in a human. The glycine and the proline are really, really important for building this collagen material. When we get up in the morning, we know that we don’t have many of these nutrients around. We can break some stuff down, but as we’ve talked about before, collagen isn’t something that’s breaking down all the time in our body. It’s one of the more stable proteins in our body, so we’re not getting as much turnover there, so we potentially have this need for it. What we’ve shown is that as you increase the dietary intake of either hydrolyzed collagen or gelatin … and the hydrolyzed collagen is just taking the gelatin that you’ve isolated out of the skin and bones and all of those things, and you just use an enzyme to cut it up so that it no longer forms a gel. That just means that you can dissolve it in water. You can dissolve it in whatever you’re looking to do.
Keith Baar: What we’ve seen is that … When we did the first study on this in humans, we showed that if you give 15 grams of gelatin before you do an activity that’s going to increase collagen synthesis, what we found is that we got a nice, robust effect that was probably twice as much as we got from a placebo control, where we got twice as much of an indicator of collagen synthesis based on having the 15 grams of gelatin before we did our exercise. The reason we do it before is because tendons and ligaments, unlike muscle, they don’t have as much blood supply to them, so the tendon is relatively avascular. The ligaments are completely avascular. They get their nutrients from the fluid that’s around them.
Keith Baar: If you need the nutrients from the fluid and it’s a dense material, you’re not going to get in there unless you’re actually squeezing out the liquid that’s in it, and then as it recovers … Every time we pull on a tendon, the tendon gets longer, but it gets skinnier. We squeeze out all the water that’s in it. That’s one of the things that causes the creep, and then when we relax, it’s going to suck up the liquid from the environment. If we have the nutrients, the glycine, the proline, and all of those things, in the environment, it should be able to suck those things up while it brings back the liquid, and that’s going to bring in the nutrients that the cells need to make new collagen.
Keith Baar: So we gave those supplements 30 minutes to an hour before we’re going to do training. Basically, then you combine that with the loading of the areas that you need to target. So if you’re worried about your Achilles, we do six minutes of jump rope. We don’t do 20 minutes of jump rope. We do six minutes because you only need a few jumps in order to maximally get the stimulus for your tendons to adapt. It only takes about five to 10 minutes of activity, and then it takes another six to eight hours of rest before those cells will respond again. Ideally, we do something in the morning, we do something in the evening. If you’re going to do a long training bout and that’s going to be in the morning, I’m going to do my little protected session in the evening.
Keith Baar: When I’m going to get my nutrition, I can do my nutrition before any session that I want to, but if I’m going to do a protected session that’s only for my tendons and my ligaments and my connective tissues, it’s going to be a short session, and I’m going to do an hour before I’m going to have the gelatin or the hydrolyzed collagen. In that way, what we’re trying to do is we’re just trying to provide a loading stimulus, this creep, stress relaxation loading that we talked about, together with the amino acids that are necessary to build new collagen. Now what we’re trying to do is we’re trying to fix any damage that’s occurred within the tendon.
Joel Smith: I got you. That’s awesome stuff. Well, one question with all that. Vitamin C and then, I think, collagen. Is there a specific … or gelatin. You said you were giving these athletes that. Is there any guidelines about going out and … I know I do a bone broth collagen supplement. I mean, is there any guidelines on supplementation?
Keith Baar: No. A lot of them, it doesn’t necessarily … We don’t know that there’s a difference between brands. We don’t know that there’s a difference between gelatin and hydrolyzed collagen. It does seem like, in different people, some of them respond really well to gelatin and not as well to hydrolyzed collagen. Again, maybe some people can absorb it and digest it better in one form or another, but we haven’t done all the tests necessary to know … We haven’t even done the test to say, “Look, collagen is better than, say, whey protein.” We have to do those things. It’s still very early days for the collagen nutritional supplementation. There’s many more companies touting all of these wonderful benefits than there is actual studies saying that there are actually any benefits.
Keith Baar: We’re trying to stay ahead by doing as many studies on these things as we can, but really what we would do is we would … For a lot of our athletes, they’ll take in a gelatin, 15 grams, that’s going to be in a glass of orange juice. The gelatin doesn’t dissolve in there. They’re just going to take it, and they’re just going to drink it down. It’s going to taste horrible.
Joel Smith: I’m sure.
Keith Baar: I know people who put the gelatin into milk and stir it in, and then they add hot milk and they do it in their morning latte, and then they have an orange juice with their breakfast. Now they’ve got both the collagen and the vitamin C. People can do it in a lot of different ways. One of the great sport nutritionists that I have worked with, he would do it in a chocolate dessert. He would make this really beautiful mousse that had the gelatin in it, and it would be gelatin and hydrolyzed collagen, but it was in this chocolate dessert. You can do it in a lot of different ways. There’s beautiful ways to do it.
Keith Baar: One of the old ways of doing it is just eating steak and actually eating the part that’s chewy because that’s where we used to get all of these nutrients. We’ve become lazy in our food eating, as well as everything else, so we don’t like to actually have to chew on stuff. One of my good friends who used to be the nutritionist for the English Institute Of Sport, Jeni Pearce, she called it her hyena diet, which is you eat the bones, you eat the cartilage off the end, you eat all this stuff that we don’t eat anymore, and that’s where you get it from. That’s a completely natural way to get it. We take it as a supplement because people are reluctant to take in those sources anymore.
Joel Smith: I love it. You can almost liken the … People will show animals who can really jump high. It’s the wild cats, you know?
Keith Baar: Right.
Joel Smith: Maybe there’s something to do with it. I don’t know, and it’s a good reminder, regardless. Shoot, after this podcast, I’m going to go in the backyard and do some line hops for a few minutes and drink some orange juice.
Keith Baar: No, that’s good.
Joel Smith: I feel like I had … Oh, yeah, last question. Okay. Well, it’s just a quick, little follow up, but you mentioned doing this for health, like a companion session for health, or the supplementation or anything. If I’m perfectly healthy and I’m a sprinter, a jumper, I just want to jump higher, run faster, get more out of my tendon stiffness, same kind of effect and benefit?
Keith Baar: Yeah. What you’re doing there, by the collagen, is we think we’re increasing collagen synthesis. Remember, there’s two things that go into stiffness. There’s the collagen content and the organization, but there’s also the cross-linking. If you put it in there, if you are eating it and you’re doing your training, what you’re doing is you’re combining the two things. You’re combining the increase in collagen synthesis with the potential to cross-link what you’ve made by doing your training for performance. If I want to take an athlete and I want to combine these things, a perfectly healthy athlete, now what I’m going to do is I’m going to do … Before their high-quality sessions, before their sprint repeats, before they’re going to get in and do their really high-quality work, that’s when I’m going to go in and give them the collagen.
Keith Baar: First thing it’s going to do, it’s going to target to the areas that I’m working. It’s going to target into my hamstring. It’s going to target to other areas. Then what it’s going to also do is it’s going to give me the potential to say, “Okay. Now I’m using my loading to give me lots of cross-links in those areas where I’m putting those things in, because I’m doing the fast movements.” It’s combining the two things. If I want to do it for health and robustness, now what I could is I could do slower movements and target it but not be building up the cross-links, and that’s going to give me the health-based component. I can do it for performance. I can do it for health. In both situations, you’re increasing the robustness of the tissue, but in one situation, you’re making it so that you’re fixing any injuries and you’re making it so that you’re not as likely to get a muscle pull, and the other, you’re improving performance.
Keith Baar: The way that we would do it through a season is we would be alternating these things. Early in a season, when it’s really about getting the volume of sprint or we’re getting the volume of whatever loads we’re doing, now we’re going to do some protective movements, some slow movements, together with the intervention, and as we get closer and closer to competition, now what we’re going to do is we’re going to decrease those, we’re going to increase our fast movements. Every individual, because they have different genetics and there’s a whole genetic component to tendon injury, which is beautifully done by a friend of mine, George Mokone out of Cape Town, now he’s in Botswana, but they had shown beautifully that there’s a number of different polymorphisms that predispose you to tendon injury.
Keith Baar: If I have two athletes and one of them has a lot of those polymorphisms, now I need to know, “Okay. They’re going to get injured more easily. I’m going to keep the protective movements later into the season, or all the way through the season. This person’s never had a muscle pull, or never had a tendon injury. I’m not worried about them. I’m going to keep their health-based movements lower, and I’m really going to jack up their plyometric load or their max power work as they get closer to competition.
Joel Smith: That’s great thought to finish on, just like that spectrum and bandwidth of how to utilize it. It’s just a great way to tie things up, Keith. I really appreciate this talk, your time. I think that the tendon thing … Like I mentioned, my own research project 10 years ago, I’ve convoluted some stuff. I think it easily can be, but I think that, man, you really did a great job. I really learned a lot from everything and how you made sense of everything today, so I really appreciate it.
Keith Baar: Thank you. No, it’s great. I’m glad it was understandable.
Joel Smith: Thanks for joining us today for another episode. Appreciate you guys being here with us, and another gem in the tendon and connective tissue lineup of education. I’ve been so educated by doing this, so it’s amazing to be able to sit down with the world experts and just be able to put it all together. Honestly, ever since I had this conversation with Dr. Baar just a few weeks ago, I’ve already been implementing these things, and they have been tremendously helpful. I’m following the line Jake Tuura. Jake Tuura has done this stuff, and he’s got tremendous benefits and health from it. I’m sure that you guys are going to get some great things out of it as well.
Joel Smith: If you did actually … Any results you guys get from hearing a guest, I’d love to hear stories. I’d love to hear emails, so shoot them my way. I am certainly happy to read them from what you guys are getting from this show. If you enjoy it, be totally stoked if you left us a rating, review, iTunes, Stitcher.
Joel Smith: In closing, our sponsor, SimpliFaster.com, they’ve been awesome supporters of this show. Make sure you check out their website, see what they’ve got going on. We’ll be back next week with another great guest. Have a good one.
Free Speed Training eBook - Velocity 101
Improving speed is one of the most popular topics in the athletic performance equation. Where there are many ideas and thoughts out there, as to particular training exercises, or setups, the more core aspects of speed training often go without mention. These include the fundamental aspects of what makes an athlete fast, specific sprint-power concepts, the relevance of "3D" motion, motor learning and more.
Velocity 101 will help you take a leap forward in understanding of what makes athletes fast, and how to train it effectively