Today, I've got a rebroadcast of a special interview with Dr. Keith Baar from June. We talk all about everything from the effects of testosterone, cortisol, and the role of collagen protein in building muscle. What Dr. Baar has to say may surprise you. Stay tuned for more information on the Flex Diet Certification, which will open for enrollment the first week of the new year. Go to https://flexdiet.com to sign up for the waitlist. You'll be the first to know when the course opens.
Find Dr. Baar:
https://health.ucdavis.edu/physiology/faculty/baar.html
References:
Baar K. (2014). Using molecular biology to maximize concurrent training. Sports medicine (Auckland, N.Z.), 44 Suppl 2(Suppl 2), S117–S125. https://doi.org/10.1007/s40279-014-0252-0
Baar K. Stress Relaxation and Targeted Nutrition to Treat Patellar Tendinopathy. Int J Sport Nutr Exerc Metab. 2019 Jul 1;29(4):453–457. doi: 10.1123/ijsnem.2018-0231. PMID: 30299199.
Davidyan A, Pathak S, Baar K, Bodine SC. Maintenance of muscle mass in adult male mice is independent of testosterone. PLoS One. 2021 Mar 25;16(3):e0240278. doi: 10.1371/journal.pone.0240278. PMID: 33764986; PMCID: PMC7993603.
Halson, S. L., Shaw, G., Versey, N., Miller, D. J., Sargent, C., Roach, G. D., . . . Baar, K. (2020). Optimisation and Validation of a Nutritional Intervention to Enhance Sleep Quality and Quantity. Nutrients, 12(9). doi:10.3390/nu12092579
Jerger, S., Centner, C., Lauber, B., Seynnes, O., Sohnius, T., Jendricke, P., . . . König, D. (2022). Effects of specific collagen peptide supplementation combined with resistance training on Achilles tendon properties. Scand J Med Sci Sports. doi:10.1111/sms.14164
Lis DM, Baar K. Effects of Different Vitamin C-Enriched Collagen Derivatives on Collagen Synthesis. Int J Sport Nutr Exerc Metab. 2019 Sep 1;29(5):526-531. doi: 10.1123/ijsnem.2018-0385. PMID: 30859848.
Lis DM, Jordan M, Lipuma T, Smith T, Schaal K, Baar K. Collagen and Vitamin C Supplementation Increases Lower Limb Rate of Force Development. Int J Sport Nutr Exerc Metab. 2022 Mar 1;32(2):65-73. doi: 10.1123/ijsnem.2020-0313. Epub 2021 Nov 22. PMID: 34808597.
Langer, H. T., West, D., Senden, J., Spuler, S., van Loon, L. J. C., & Baar, K. (2022). Myofibrillar protein synthesis rates are increased in chronically exercised skeletal muscle despite decreased anabolic signaling. Sci Rep, 12(1), 7553. doi:10.1038/s41598-022-11621-x
Paxton JZ, Grover LM, Baar K. Engineering an in vitro model of a functional ligament from bone to bone. Tissue Eng Part A. 2010 Nov;16(11):3515-25. doi: 10.1089/ten.TEA.2010.0039. Epub 2010 Aug 28. PMID: 20593972.
Pechanec, M. Y., Boyd, T. N., Baar, K., & Mienaltowski, M. J. (2020). Adding exogenous biglycan or decorin improves tendon formation for equine peritenon and tendon proper cells in vitro. BMC Musculoskelet Disord, 21(1), 627. doi:10.1186/s12891-020-03650-2
Steffen, D., Mienaltowski, M. J., & Baar, K. (2022). Scleraxis and collagen I expression increase following pilot isometric loading experiments in a rodent model of patellar tendinopathy. Matrix Biol, 109, 34-48. doi:10.1016/j.matbio.2022.03.006
Shaw, G., Lee-Barthel, A., Ross, M. L., Wang, B., & Baar, K. (2017). Vitamin C-enriched gelatin supplementation before intermittent activity augments collagen synthesis. The American journal of clinical nutrition, 105(1), 136–143. https://doi.org/10.3945/ajcn.116.138594
[00:00:00] Dr Mike T Nelson: Welcome back to the Flex Diet Podcast. I'm your host, Dr. Mike T. Nelson, and today we've got another rebroadcast. We've been doing a few more rebroadcasts here since we've got a lot of new people listening to the podcast that may not have gone back into the earlier library, and in reality, it's December, so trying to get guests has been a little bit difficult with scheduling and I'm buried past my eyeballs in correcting stuff for finals with classes and projects and everything wrapping up towards the end of the year.
So I thought it was a perfect time to do some rebroadcasts of ones I think were super impactful that you might have missed. And today on that, we've got Dr. Keith talking about the effects of testosterone, muscle mass, cortisol, and the use of collagen for soft tissue repair. This is a podcast I've been working on.
It took me quite a while to get it a couple years but I was super excited. Dr. Barr was very helpful and. All the questions in great detail. We've done a lot of very cool research in this area and wanted to let you know that the Flex Diet certification will be open the first week of January, 2023.
It'll be open for one week. So be on the lookout for that. You can sign up right now to get on the wait list to be the first person notified, including cool special bonus items. Also go to flexdiet.com, for all of the details. So thank you for listening to the intro before the intro.
And here is the entire episode of a Rebroadcast with Dr. Keith Barr.
[00:01:59] Dr Mike T Nelson:
Hey there. Welcome back to the Flex Diet Podcast. I'm your host, Dr. Mike T. Nelson. Today on the podcast, we've got a super special interview with Dr. Keith Barr. We're talking all about testosterone, cortisol, and the role of collagen protein. As always, this podcast is brought to you by the Flex Diet Certification.
So if you're listening to this right after this podcast came out, the Flex Diet certification is now open for enrollment. It'll be open from now when you're listening to this through June 13th, 2022 at midnight. So go to flexdiet.com, for all of the details and the information. If you're listening to this outside of that time, you can still go to flexdiet.com and you'll be able to put your name on the waiting list so the next time that it opens, you will be notified and you'll get lots of great information for free deliver right to the old inbox there.
So go to flexdiet.com for all of the information. And speaking of the flexdiet.com, we've got lots of great expert interviews there in the certification from the likes of Dr. Stu Phillips, Dr. Hosing Antonio, Dr. Eric Helms, Dr. Dan Pardi Dr. Hunter, and many more. So I tried to include lots of expert interviews in addition to all of the coursework there, which is over 20 hours.
So that if you wanna take a deep dive and talk to actual researchers and practitioners on different topics within that's all included there also. Coming up next here is an interview with Dr. Keith Barr. This is one I've been working on to do, honestly, for several years. I read his research and been following it for quite some time, and.
It turned out great. It is very technical at times, so you may have to listen to it a couple times or if you have any questions, drop me a note. I did try to include as many of the references here as I could, but I was not able to get all of them. And we talked about everything from the effects of testosterone.
This is if you're in a normal level versus a super physiologic level. And you may be surprised by what he says about the effects of testosterone for building muscle in a normal range. And the surprise is, Probably not really needed, which is pretty crazy. We talked about the effects of cortisol and in research what you find is those who have the highest levels of cortisol are actually able to add more muscle, even though cortisol is considered a catabolic hormone.
We talked about nutritional strategies you can do to manage that. Differences between men versus women, especially related to cortisol, how this impacts intermittent fasting and other periods of stress. And then we talked a lot about collagen. So collagen has been an, I've written about this in academic textbooks and papers before.
It was pretty useless. And this was looking only at a muscle centric approach. So it is true that collagen doesn't really stimulate muscle protein synthesis at all. But Dr. Barr and others, Dr. Shaw have done some really interesting research showing that it may be beneficial for soft tissue.
So if you have some soft tissue injuries you're recovering from, or you just wanna reduce your risk of them this is something that I've been using with my one-on-one clients for almost like three years now. . So again, I don't publicize everything that I do with one-on-one clients. But I think enough time has passed with this that I wanted to share all this information with everyone and I wanted to get it directly from the source who's done a lot of this research.
So we'll learn how do you use collagen specifically for soft tissue? Should you change your training, should you do different types of training? Now, this can be especially beneficial for recovery from some kind of niggly injuries. This is something that again, that I've used with one-on-one clients for quite some time, and again, anecdotally found that it works really well.
So Dr. Keith Barr talks all about that and a bunch more. Sit back and grab your favorite beverage and enjoy this wide ranging talk. From Dr. Keith Barr. Hey, welcome back to the Flex Diet Podcast, and I'm here today with Dr. Keith Barr. Thank you so much for taking time on the podcast today. We really appreciate it.
Absolutely. Pleasure to be here. Yeah. Today we're gonna get into all things collagen, a little bit more related to maybe injury, recovery and performance, but people may not have heard of you. Do you wanna give yourself just a little background about how you got into research? And I know you do also very much applied stuff too, so I'm always fascinated by that of people who are running research and then also applying it in the, shall we say the real world at the same time.
Yeah.
[00:07:25] Dr Keith Baar: So what I did is I started. I started in the applied field where I was undergrad at the University of Michigan. I became a, an assistant strength and conditioning coach. So I started as in that kind of applied vein. And then I went on to do a master's at Berkeley, a PhD at the University of Illinois, and then a post-doc at the, at Washington University.
And along the way I was really focused on how exercise, nutrition, age, and disease alter the adaptation of muscle musculoskeletal tissues. So how do we improve and optimize performance using exercise, nutrition and and maybe hormonal interventions throughout the lifespan. So how does it change, how does our response change as we get older?
All of those types of ideas and some of the best things that we can do are manipulate. The loads that we use as well as the nutrients that we supply our body with.
[00:08:19] Dr Mike T Nelson: Great. And I know you did some early work on testosterone also, if you wanted to touch on that. Cause I think its role a lot of times is misunderstood and there's a huge difference between are you hypogonadal, so you're real low?
Are you in the middle? What we'll say, quote, natural area, and then if you use, other special supplements to get to a supra physiologic level, because I think humans, we tend to think that everything is linear, but it's very much a non-linear dynamic.
[00:08:48] Dr Keith Baar: Yeah so we had shown some of the work that Eric Dividian had done in mine, Sue's labs, where he was manipulating testosterone both in male and female animals.
When he did it in male animals. Basically what he could do is he could castrate them at different ages and without testosterone. Had no effect once you reach maturation. The only time they really had an effect is when they were during growth, so at their puberty. So they were still growing through puberty.
Same thing is really true for the females when you were supplementing with testosterones. When we add external testosterone, you need a secondary stimulus. You need either resistance exercise, or you need pubescent growth in order to see an effective testosterone floor. So for most individuals who are adult, so they're fully mature skeletally mature, we're not seeing a huge effect on muscle mass until you're really super physiological.
The kind of thing that you only get when you're supplementing quite extensively as a performance enhancing drug user. When you're in physiological ranges, it doesn't really have that much of an effect, largely because, most of the steroid effects are seen around 5% occupancy of the receptors.
So most most people who are not hypo or they're going to be able to reach that level as men without really having to supplement, without really having to worry about it. As you get older. That didn't seem to have an a, a really positive effect. And the thing we always see with testosterone is it decreases breakdown in muscle and that's this primary thing that's happening in muscle and that's just making your muscle quality go down.
You might have more muscle, but that muscle doesn't have as good quality because that turnover rate how quickly we can get new proteins into to, to replace the old proteins. If we slow that down, all we're doing is accumulating. Damage. So we accumulate oxidative damage lipolytic damage, all kinds of different things that happen to your proteins post translationally that can have a negative effect on how that protein performs.
So if we decrease protein degradation in the short term, yeah we might have a beneficial effect, but in the long term it's gonna have a negative effect. And we see that cuz men's muscle quality isn't as high as women's when we take it down to the per cross-sectional area.
[00:11:13] Dr Mike T Nelson: So if you're, if we throw rules and ethics aside for right now, and you're getting close to, let's say the high end of a weight class sport, we're speed and power are primary, eminent, would using anabolics, at least testosterone will keep it to that.
Could that be a negative at that point? Because you may be. Weight that doesn't function quite as well per se. It's not
[00:11:36] Dr Keith Baar: So in a situation like that, the benefits are actually not happening really from your muscle. They're happening from the central changes. . So the aggressiveness that's happening.
So when you're gonna do strength, speed, or power, if you're hyper aggressive because your brain is easier depolarized, which we know that happens with testosterone so you can activate things really quickly, that's gonna potentially have a beneficial effect. The other thing that we see in our connective tissue work is when we add testosterone, it makes the connective tissue stiffer.
And that's really where we think a lot of the performance benefits are happening. Those two components, the brain is gonna allow you to make a decision quicker and to do a movement faster, and the stiffness of your connective tissue is gonna go up. And so those two things together are gonna increase your rate of force development.
[00:12:23] Dr Mike T Nelson: Ah, very cool. And I like the part you said about if you're in the normal range, going from say four 50 to eight 50, you're not gonna see a huge difference, which I think is probably kind surprising to most people. I would agree in most of the literature supports it, even though we don't have a ton of data on that in humans.
I think Bain did some stuff in the nineties where they chemically castrated some males and then tried to supplement 'em back in a couple different areas. But there's
[00:12:51] Dr Keith Baar: good data from prostate cancer patients where if you if you use Drugs to block testosterone completely.
They are still able to grow their muscles just the same as people who don't have that negative effect on their testosterone. So you could be at zero testosterone or very low testosterone is a man, you can still gain muscle mass from the resistance exercise. And the rate at which you gain that mass is the same as somebody who hasn't been altered by those drugs.
So that's that from the prostate cancer literature when people are going through chemotherapy that are designed because that, that the prostate is and androgen intensive. So it's so dependent on the androgens for growth that's a you it's commonly used to drop testosterone as low as possible.
You can still gain muscle mass in that situation. And so there's good data there. There's good data in the rate at which women add muscle mass and strength. That suggests, yeah, that was my next
[00:13:44] Dr Mike T Nelson: question. Much. Because I think in mature males and females, the rate of gaining muscle is similar if you control for other factors, even though they have much, much less testosterone than males.
[00:13:58] Dr Keith Baar: Yeah. And there's good work from keratin where he showed that their strength that women's strength will increase faster or greater than males. The baseline is lower, but they respond to resistance exercise as well, if not slightly better than men.
[00:14:13] Dr Mike T Nelson: And are they responding better cuz they're at a little bit lower of a baseline or is there some other factors there?
Maybe
[00:14:19] Dr Keith Baar: you're, they're at a little bit lower of a baseline, but they're also, and so that's probably sociological that we don't encourage women as much as men to, to perform strength exercise. So they're not necessarily starting with as much muscle mass. But then screener has shown that women have a higher protein synthetic rate.
And like I said, the testosterone lowers breakdown. So that women have a higher breakdown rate as well. So the turnover rate of in a woman's muscle is actually higher than a man's. But one of the things that testosterone is doing is it's binding to the glucocorticoid receptor and inhibiting cortisol, some of the cortisol effects.
So one of the things we see is under stress or under high levels of glucocorticoids. So these mineral, or sorry, these steroid hormones that are supposed to drop muscle mass far more effective in women at dropping muscle mass than men because without the protective effect of testosterone, the glucocorticoids, the cortisol in the system is going to.
Drop muscle mass much faster. And sine and Dave furlough here at Davis showed that really nicely in animal models where when you add, any of these glucocorticoids to males and females the females drop muscle mass much faster than the males.
[00:15:31] Dr Mike T Nelson: So would a kind of an extrapolation of that be that females may be more sensitive to the effects of overall stress in, related to muscle mass?
Or is that a little too much of a leap? ,
[00:15:42] Dr Keith Baar: Insofar as that cortisol will go up with stress there, it, the bigger issue for your listeners, if they're looking at metabolic flexibility, I'm sure that a lot of them are doing things like time restricted feeding or some fasting. That means, what it means to us is that the cortisol levels in a woman are gonna go up the same as they are in a man.
They're gonna reach their highest rate before breakfast, right before whenever you break your fast. And it means that the women's muscle are more prone to losing muscle mass in from fasting than men are. And so they're not necessarily gonna see this as much of a beneficial effect as a male would from doing some of the time restrictive feeding or intermittent fasting that a lot of your male listeners will have tried at least
[00:16:26] Dr Mike T Nelson: Oh, that, that's super interesting.
Cuz I have had. Some females do shorter, fast, but only maybe once a week, once every other week. And I can't think of a single circumstance where I've had females do longer, fast, like a 16 eight or those types of approaches where I've had some guys have some pretty good success with that. I would say in general, at least anecdotally, males tend to do better with longer fasting.
And I've always wondered if that was something more physiologic, which sounds like it could be, or other factors.
[00:16:58] Dr Keith Baar: It's definitely physiologic. You can see it from the cortisol effects, but you also see other hormones that are really important in protein fasting as well, like FGF 21. So I have a colleague, Karen Ryan, and she injects FGF 21 into the brains of males and females, and then she gives them access to the individual macronutrients.
So she puts a plate of protein, fat, or carbohydrate out, and when you inject FGF 21 into the brains of males, they will go and almost exclusively eat protein. the females won't do the same thing. So we actually have very different drivers for both. Both our adaptive response, so our metabolic response so fast, but also in our in our cravings that result from the fast.
So whereas males might crave a little bit more protein-rich food, females don't have a specific as much of a specific crave in that way. And that could also play a role in how much muscle mass is maintained in these longer or intermittent
[00:17:54] Dr Mike T Nelson: type fasting. Oh, that's very cool because again, anecdotally, I'll ask clients like, when you get super stressed, like what foods do you crave?
And guys typically will be, some foods, but it's not uncommon to hear, I just want like a big steak, right? Where rarely do I ever hear females say that. I've always wondered if there's something physiologically or if it's just more a societal convention. So sounds like there may be something to that physiologically.
[00:18:19] Dr Keith Baar: Yeah, it's probably a little bit of both, but there is definitely a hormonal a neurocognitive change that results from some of these hormones that are usually produced by things like the bile acid components that you get FGF 21 from. And so because there are these kind of cues that we're getting from the physiological response to either feeding or fasting, there are gonna be sex differences that are going to have significant effects on our muscle mass, and as a result on our base
[00:18:48] Dr Mike T Nelson: of metabolic rate and other things.
Awesome. And if someone wanted to, let's say, gain muscle or lean body mass, I know I'm using them interchangeably at the fastest rate without any exogenous drugs. , is there some types of strategies they should do around cortisol or other methods?
[00:19:08] Dr Keith Baar: Yeah, absolutely. So the interesting thing is that the cortisol is probably the best predictor.
So the higher the cortisol, the better you are going to be at gaining mass.
[00:19:17] Dr Mike T Nelson: It's basically, that seems like the inverse of what most people would guess,
[00:19:21] Dr Keith Baar: right? It is the inverse of what people would guess, and the, probably the best predict, the best reason, the best rationale as to why is that what you've done is you've done the hardest exercise.
So that's the greatest stress. And so what we know is if we want to build our muscle mass, what we're going to do is we're gonna lift any weight to failure. So it doesn't, you don't have to lift a huge weight. You can lift a relatively lightweight for yourself, but as long as you keep going until you can't lift it anymore.
And the key there is that you, you don't rest at any point and you just keep pushing. Keep pushing. Cuz what we know is that, and what St. Phillips has shown quite nicely is that what happens when we get a muscle to failure is that's the only time in humans where we recruit all of the fibers within the muscle.
So all of the fibers within the muscle will get that molecular signal, that's gonna tell the muscle, it's going to now want to get bigger. And so if we don't go to failure, we're only getting part of the signal. So many of the fibers don't actually get the signal to grow. But at failure, we're recruiting all of the muscles, we're giving a signal to all of the muscle fibers within the muscle.
We're working. And that's what, that's why we use any weight to failure. So it doesn't matter light or. You can get bigger by using anything and lifting it to failure and then supporting it with a good high quality proteins that have com that are complete proteins. So weigh is the gold standard because it's easily digestible.
But anything that's gonna be ellucian rich protein that's gonna have all of the nutrients, it can be plant-based. It can be animal-based. It doesn't, it's not a huge difference. But what you're looking to do is you're looking to support that strength training with that protein dose and those two things together, we know the molecular mechanism.
So what we had shown very early on during my PhD is that how big your muscle get is directly is gets, is directly proportional to the short-term activation. Of a protein kinase called mTOR Complex one. And that one's also activated by amino acids and they activate mTOR complex one in different ways.
And so what we know is that the two things together are additive. So when I do my lift and I get that signal, I get that failure, I get that signal of tension across that muscle fiber. That muscle fiber is gonna change that tension into a chemical signal that's gonna turn on mTOR complex one.
And the way that it does that is, is different than the way that amino acids are going do it. And so the result is when we do them together, we get an increase further increase greater than we would get with either feeding alone or with strength training alone. And so combining those things together is gonna give us our biggest growth response.
[00:22:02] Dr Mike T Nelson: Very cool. And I think some of the stuff from Nick Bird's lab or Nick Bird when he was working in Stu Phillips lab showed. As light as 30% of one rm, which I, it's much lighter than I think most people would realize, but they did that with leg extensions again. Yep. That exercise was taken to, momentary failure or you couldn't move the weight or whatever definition we're using for failure in this context.
[00:22:24] Dr Keith Baar: Yeah. They go to positive failure, and when you get to positive failure, you got. That beneficial effect, the biggest effect, whether it was 30% or 90% of one rep max. And then they did the follow up study looking at 30% or 80%. They trained them and they found that the increase in muscle mass was the same between them over, I think it was an eight or 12 week training period.
But what they found was that the increase in strength was greater for the 80% groups. So they had a couple of 80%. So when you're lifting at 80% of your one rep max, you got a bigger increase in strength. But the muscle mass was the same.
[00:23:02] Dr Mike T Nelson: Yeah. And I saw Stu here a couple weeks ago. He said to say, hi, by the way,
Very good. And he was saying there's some even newer studies where they then took the group that did say a low, like 30% of one r m and then gave them a couple practice sessions on what they were gonna test them on. And then he said that the strength, the difference between those two groups got to be even less than, so there's even some debate about if you use some other method and maybe you can add some muscle that way, how long would you need to train that quote new muscle to impart strength changes to it then too.
[00:23:35] Dr Keith Baar: So the neurological adaptations are gonna be a very quick, they're the fastest adaptations that we have within the strength paradigm. But once you make those neurological adaptations, you're also gonna have other structural changes that are gonna be important for how well you transmit the force.
And yeah, so what we say is that if you want to get stronger, you lift the heavy weight. If you wanna get bigger, you lift any weight and you go to failure.
[00:23:58] Dr Mike T Nelson: At some point, can you make up for not going to failure by just doing enough physical volume to compensate for that if you have more time and let's say your goal is of more strength and hypertrophy at the same time.
[00:24:11] Dr Keith Baar: Yeah, so you can go, the volume component is important for size. It's not important for strength. So it doesn't look like we need to do a lot of volume if we want to increase strength. But if you want to increase size, you can do less weight and do a lot more volume. And a lot of people in the field know this cuz a lot of a lot of bodybuilders, that's exactly what they do.
They love to be in the gym. That's their job. They in between sets, they talk to every single person in the gym. They're gonna spend five, six hours in the gym. Frequency, intensity, and duration is what we manipulate. So if you wanna have your duration be super long, you just do it with a lower intensity.
And so that's basically still right within that overload principle that's really the key to growing muscle bigger and stronger.
[00:25:00] Dr Mike T Nelson: On the catabolic side, is there anything we should look at nutritionally to maybe mitigate that? I know there's always a bunch of talk about carbohydrates immediately after training, and then I think it goes, thz lab again showed in terms of insulin release, if you're just having 20 to 40 grams WHE protein, you have enough insulin release to stop the catabolic process.
So maybe from that side, it's not as important as we thought. Obviously you'd be replenishing glycogen if you're gonna do a session within a short period of time, right after, which would be a different circumstance.
[00:25:33] Dr Keith Baar: So the classic study there was. By Kevin Tipton, Stu. Stu was on that paper as well where they fed either all amino acids or essential amino acids.
And when they just fed enough of the essential amino acids, they got a decrease in degradation. Because a lot of times what we're looking at for degradation isn't something where we're driving degradation or we're inhibiting degradation through the insulin stimulation. Cause insulin stimulation for the first six hours after exercise is inhibited.
And so after resistance exercise, and so what we're actually getting as far as the degradation is used to drive synthesis after strength training. Because what we're looking for is we're looking for essential amino acids. If we don't have a source from the diet, because somebody's doing it as fast, we have to break down protein.
In order to free up amino acids, specifically the essential amino acids. And so what Kev Tipton's 1999 paper showed that is if you bring up the essential amino acids, you drop protein degradation. And that doesn't necessarily need any insulin response. There is some arginine in that essential group that he gave to give maybe a little bit of insulin, but the insulin component because when we do heavy exercise or we do strength exercise, we get that load across the muscle.
Troy Herm Kornberg's shown that when you do that, you activate a different system that's parallel to the insulin system and that's activating m. In an in a way that doesn't need insulin or IGF one. And then what you get is you get feedback inhibition. And so my former PhD student Lee Hamilton had shown that after exercise, the association of either IRS one or IRS two, these two insulin signaling substrates goes down.
The association with the insulin receptor goes down and with the PI three kinase, they go down. So what you're doing is and Renny Kuman showed long time ago, now that what happens after lifting heavy weights is you get a period of insulin resistance that lasts maybe three to six hours while you're getting this feedback, inhibit.
On insulin signaling because you don't need it because you're able to activate these systems independent of insulin. And then 24 hours later you actually have an increase in insulin sensitivity because you, this whole system is reset insulin since insulin signaling to some degree. And so it allows you to then re to get a bigger stimulus from the same from the same amount of insulin.
And so we think that's one of the really important things that resistance exercise does, is it resets a lot of the signaling cascades that are downstream of insulin or downstream of some of the metabolic flexibility. Things that we look at. Because we just had a paper come out where we did four bouts of exercise over two weeks, and then 70 and two hours after the last bed of exercise, we looked at protein turnover and we looked at signaling through mTOR.
And mTOR signaling is significantly lower. In the muscle that you've exercised four times over those two weeks, but your protein synthetic rate is higher. So what we're doing is we're dropping a lot of the baseline level of IOR activity is going down. The baseline level of certain aspects of insulin signaling are coming down.
But then what we're doing is we're returning the ability to signal the next, at the next meal or at the next bout of exercise. And so what we're doing is increasing this, the, what we call the dynamic range of the system. What we do is we have a go really, we activate the system really at a high level.
And then for two or three days, it's going to actually go down below baseline and then we're gonna be able to activate it again. And every time we have a meal, because we've got this greater dynamic range, we take more of the protein that we eat, we make it into muscle in that space. And Stu again has shown that 24 hours after your last resistance exercise bout you're still better at building muscle than if you didn't do the exercise bout yesterday.
And so a lot of that is because what we're doing is we're modifying the dynamic range. We're dropping the baseline of things like mTOR activity and insulin signal. And then when we get that signal comes back because we eat, we get insulin, now we're gonna have an insulin signal. Now we've got this much greater range.
We go from a lower starting point to the same level of stimulation. That change is much bigger and that means we get a bigger biological effect from the same state signal.
[00:30:09] Dr Mike T Nelson: And so the main insulin effects you're talking about are related to the non-insulin mediated uptake category, I guess you could say.
Is that correct? So
[00:30:17] Dr Keith Baar: there's a lot of the non-insulin mediated stuff yes. We know that the insulin signal for a glucose uptake can be mo, can be basically replaced by an contraction based signal. We know that a lot of what insulin does is change blood flow, get blood flow to go to the tissues where it's supposed to, where we're supposed to store amino acids and sugars and that's to our muscles and certain fat depots.
When we do exercise, we're, we don't need the insulin to change blood flow. Now that exercise is changed blood flow by producing metabolic byproducts so we have greater blood flow. So we don't need as much of the insulin effect to get more of the substrate into the tissue that we wanted to go to.
[00:31:01] Dr Mike T Nelson: Very cool. And the new study you were talking about, were they. I think they did heavy stimulation for a shorter period of time. If you were to translate that into humans, and assuming that's the same, would that be an argument for doing maybe less frequent, but more intense bouts of exercise then to try to raise that ceiling effect?
Or what would that look like if you could translate it into humans? In what group? In probably like intermediate level athletes, so not beginners, but people who have been, training for a while, but not elite level athletes.
[00:31:38] Dr Keith Baar: Yeah. So yes, I think that people get into the same routine of their exercise training.
And so we adapt to that and so it's less and less of a stimulus each time. And there's a Japanese group that shows if you do the same exercise over time. And our new paper as well showed that even the second bit of resistance exercise, where we saw mTOR activity go up 20 fold after the first one, six hours.
After the second one, it goes up five. Or three, three to five fold. So we're not seeing that huge response that we saw, and that Japanese group showed that over time, that those individual responses to the exercise are coming down. But if you take a two week break and you do the exercise again, bang it, there goes the, that molecular signal comes back.
So there's two ways you can do it. You can take a little time off and then come back and hit it with that, with the same type of exercise, you'll get a bigger stimulus from that? Or what, what's more, what needs to happen more for people who just go out and train the same way every day is you just have to throw in, say, 20% of your sessions or 20% of the time that you're going to be exercising at a much higher intensity.
So adding those high intensity intervals is gonna have a huge effect. And we know that from work, from the Buck Institute, Simon MEK had shown that when you lift weights or when you do high intensity interval training, that the transcriptomics, so the, all of the messenger RNAs within your muscles, if you're older, they look like you're younger again.
Because that high intensity exercise that's getting outside of the comfort zone, that's giving you a greater stimulus to see things like muscle growth, response genes, insulin signaling genes, mitochondrial genes, they have a much bigger effect, especially in an older population if you do high intensity interval training.
And so yes, I do think that manipulating manipulating that intensity is a really important thing to do for. All levels of athletes and even athletes who are just training for life. So they're not going to train for any competition. They just want to feel like they're still making progress. They're still making the changes towards their goals.
Those are the and the goals could simply be healthy body and low body fat or whatever it is. All of those things, the idea of going high intensity, throwing in 10 to 20% of the work that you do as high intensity work is absolutely essential.
[00:34:02] Dr Mike T Nelson: Yeah. That matches a lot of Martin GABA's work.
He's done some stuff on that for several decades. And so for practical area, would you look at 20 to 30, 40 seconds, like a windgate type protocol where you're going as hard as you can more on the complete rest, and then try to keep that quality of work high again when you do the second interval. So you
[00:34:22] Dr Keith Baar: can do it.
There's any number of ways you can do it, what you're looking to do. You, there's three areas that we're adapting really well to, to endurance exercise. One is our long slow endurance exercise. And the other two windows are sprint intervals and our high intensity intervals, sprint interval is between six seconds and 30 seconds.
You do those six to 32nd intervals, you're using ATP faster than you can produce it because you're going from stored phospho to glycolysis. So you're at that transition point between two metabolic systems. It's if you are driving your manual transmission car and you're accelerating, you have to pause for a second while you put in the clutch and you shift.
That's what your body is doing to some degree. So at those transition points, you're using a t p faster than you can produce it, and that's gonna give our body a signal. The second transition point is between glycolytic and metabolism and oxidative metabolism. That's happening about. One to three minutes.
So we're looking at those intervals at like 32nd intervals, two minute intervals. Those are great intervals to do, and those are the intervals that are gonna give us those metabolic signals. Those things like at, so a t p consumption, ADPs going up, ADP activates the a p activated protein kinase, and we get a really important signal from that.
When we go long for a long time and we go at a relatively low intensity, that long slow distance, we get a different signal that's driving the adaptation that we're making. And that's a calcium-based signal. And so that signal is likely cam kinase based. So now we have two different signals. One's an intensity signal, one's duration signal.
We are, we tend to be really good about the duration signal, especially if we're cyclists or swimmers or we can get in there and go for a long time. Getting that intensity signal is something that we're less. Proficient tap cuz it's more painful. It hurts to do, it's not fun. And so it is not the fun one, it's the one that makes you feel like you're gonna vomit at the end.
And so people shy away from that one. So when we're trying to do this, we're trying to mix these two signals in and we mix these two signals in such a way as we can maximize the adaptation and minimize the mechanical IPO impact. Cuz especially if we're running, if we're gonna do a lot of high intensity running, the impact force is gonna be much higher.
So our mechanical load is gonna be much higher. The likelihood of us getting an injury is gonna be much higher. And so that's not necessarily where we want to do it. We want to do it when we're rowing or cycling or swimming where we're not having as much of an impact force. You can do it with the running, but now your percentage of your overall percentage of high intensity work has to be lower if you're a runner than if you're a rower, a swimmer, a cyclist.
[00:37:08] Dr Mike T Nelson: Yeah. I'm a big fan of the rower because a lot of my online clients, they're not training to be sprinters and I don't know how much I trust them to run full out at 90% . Yeah. And even if they could the impact over time, it's like you're looking at the cost of benefit ratio. If you're gonna be a sprinter, then yeah, of course it's specific.
But if you're not gonna be a sprinter, I think you can use other modalities and still get that high intensity point without mechanical trauma also.
[00:37:35] Dr Keith Baar: Yep. No, exactly.
[00:37:37] Dr Mike T Nelson: And probably a good time to shift gears towards collagen. How did you get interested in collagen?
[00:37:43] Dr Keith Baar: Yeah, so we've for years and years we've been engineering musculoskeletal tissues.
So I started doing this with Bob Dennis at the University of Michigan where we would make little muscles in a dish. And Bob was, this is this crazy engineer guy who's smarter than anybody else in the world that I know. And he had come up with this idea that when you do deep space flights, you are gonna need a motor, and that motor needs to be able to repair itself.
So what would be perfect is if you had a muscle that could produce all of the movements that you were gonna need in order to have some 10 year long flight. And if something went wrong with the motor where it didn't work, it would actually repair itself. And so his idea was if we could create, if we could engineer these muscles, we'd have these motors that could be tuned to do different things within.
A body or a spaceship or whatever. And so he is got great videos you can still find online where he is got little fish that are floating in a and he's got two little engineered muscles on either side of it and he then could contract them alternatively and cause the fish to swim around . So I went and worked with him for a postdoc and I was engineering muscles.
But when we put those muscles onto those little fish or onto any other kind of machine, they would always fail at the interface where we just tie them on. So they would always pull out or they would always have failures there. And we realized that what we didn't have is we didn't have a working tendon.
And so what a tendon does and so with Eleanor rooted there at Michigan, what we had, what we showed was that tendon is a variable mechanical tissue. So we were doing these things where at the muscle end of the tendon, it's very stretchy, the bone end, it's very stiff. and that allows me to attach that stretchy muscle to a stiff structure.
And so we started to think about, oh, we engineer all these muscles, we should engineer some tendons and ligaments. And so we started doing that. And then I moved my laboratory, my first lab to Scotland, and I had a PhD student there named Jennifer Paxton. And what we were doing was engineering.
We were trying to engineer these ligaments, these tendons, and we said if we're gonna have a bone, a tendon, and then a and a muscle that's three tissues, it's really hard to do. So let's just start by making a bone, a tendon and a bone and a, that's a ligament, bone to bone. And so she started engineering ligaments.
And what we found really early on is that if we wanted to make a strong ligament, we had to add proline. And we had to add some of these other essential am or amino acids that aren't that. Aren't necessarily found as at a, as high a level as we need it. And so when we added Proline into the mix, we got a big increase in, in the strength and the stiffness of our ligaments.
And so I did some simple searches around to see what our proline rich foods and gelatin came up as a prolene rich food. It's, it's just collagen itself, where the collagen has been boiled to produce the gelatin. And so it still forms a gel and it's really good that way.
And so what we had figured is that if this works in our little engineered ligaments, that these, that when you give proline or when you give glycine at high levels there's a group from from Brazil who just gave lots and lots of glycine and they saw that the tendons and labelings got better.
So we figured that this might be a way to do it just by giving dietary collagen. And so we started by doing that. We would take, we would feed people collagen or gelatin. We could take their blood and put it onto our engineered ligaments. Before you had the collagen and the vitamin C with, so your overnight fasted that blood made ligament that's really weak.
But the ones that you got an hour after eating the collagen or the gelatin, that made a much stronger and much more collagen rich tissue. So that was telling us that maybe there's something interesting there. And then we did a study together with Greg shot the Australian Institute of Support. Yeah.
Where we fed people for three days. We fed them either a placebo, five or 15 grams of gelatin. We had 'em jump rope six minutes an hour after. And that's because we had, using our engineered ligaments, we'd shown that connective tissues adapt really well to short periods of activity. That if you do an hour's worth of exercise, your connective tissue is gonna turn.
Get maximal around 10 minutes and then turn off by the, even though you're continuing to exercise by 60 minutes, the cells aren't getting a signal that's positive. And so we were just doing those short periods of activity and over the 72 hours, when we gave them 15 grams of gelatin, we could double the rate at which the bones within those subjects were producing collagen.
And so that was telling us that there was, potentially something there. We hadn't done other proteins, we just did placebo control versus gelatin. The five grams didn't give us enough. But the 15 grams gave us a nice effect. And so we're actually starting a study right now where we're gonna do pretty much exactly the same thing.
We're gonna compare. Our hydrolyzed collagen to whey protein. And to the third thing we have is we have a vegetarian collagen. Made by this, made by a company out of the Bay Area here called Gel Tour. And what it is it's recombinant collagen that's made in bacteria, ah, that's the only form of collagen in the world that's actually
[00:42:50] Dr Mike T Nelson: Vegetarian.
So they'll just mimic the amino acid profile in different Yeah. It's got same amino
[00:42:54] Dr Keith Baar: acid profile. So they build up is the, and they use it already for cosmetics where the collagen is used in cosmetics. And so now what they're looking to do is see whether that could be used as a supplement in a dietary supplement in people.
And so we'll have those three proteins compared to placebo controlled in a bunch of men and women, and we'll be able to see. Is it just any protein will work? So the whey protein's just as good as collagen, or is the collagen important and is there something special about animal collagen? Or can we just take in this recombinant protein, which has never been in an animal, and can we get the same thing from just having those amino acids in it?
So I think it's gonna be a super, it's a super cool study. We're starting to recruit, so if your listeners are yeah, in the Bay Area, in, in the Davis area and wanna be part of it, they're more than welcome to, to reach out and join the clinical trial. We should have the clinical trial up on clinical trials.gov this month so that we can, and our recruiting is starting.
[00:43:55] Dr Mike T Nelson: That's awesome. And it sounds like that may settle the debate between you and Stu about collagen versus whe .
[00:44:01] Dr Keith Baar: I don't have any debate with Stu because I agree with him that it's not great for building muscle. Yeah. Cause it doesn't have any, it's got almost no leucine, it doesn't have, it's not a complete protein.
The question that I have is whether there's something that the cells within connective tissue are getting from either the amino acids or some of the other kind of limited amino acids that you see in collagen that you don't see in any other, that you don't see in any other protein. And those are the hydroxylated forms of amino acids.
So hydroxyproline and hydroxy. Some of our data would suggest that those modified amino acids are actually giving a signal to cells, which could be important for the synthetic response that we see in, in response to dietary collagen.
[00:44:45] Dr Mike T Nelson: Yeah, that is my next question. How much do you think of that is providing raw materials for building blocks and then you've got the stimulus of exercise and potentially more blood flow to areas that don't get a ton of blood flow and or is there some other downstream effects from the collagen that's signaling different things to go on or combination of both.
[00:45:09] Dr Keith Baar: Yeah so the interesting thing that I told you is that when we take people's blood before and after they eat dietary collagen, and then we put it onto our engineered ligaments, the ligaments get stronger. Yeah. And this isn't a situation where we've actually got five times the physiological level of amino acids in the media already.
So we're adding 10% of the me, we're adding 10% of the volume is the serum, and we're getting more collagen synthesis. We're getting stronger ligaments, but we're not adding a lot of glycine or proline. And so what that's suggesting to us is that something else in the collagen is actually having the the beneficial effect.
And so we know that the vitamin C is important, but that's in all of the different groups. So the question then becomes, what is it? Or is there something special about some, something that's within that dietary collagen? The. Is driving this increase in collagen synthesis. And I think that's the really important question that we re, we're really keen to answer with this study that we've got going on now, cuz not only are are we going to have whey protein, but we're gonna have this collagen that doesn't have hydroxylated proteins in, right?
And so if those hydroxylated proteins are important, we should see that what collagen is better at stimulating collagen synthesis than whey protein. And it's also better than stimulating something that has the exact same amino acid profile, just doesn't have the hydroxylation. So it's gonna be a super cool study in that way because it has the potential to really pull out mechanistically what's going on.
[00:46:46] Dr Mike T Nelson: Yeah. That's awesome. And so one thing I've done with clients based off of your research, especially with Dr. Shaw, was add 15 grams of collagen to their whey protein, about 40 to 60 minutes before exercise with some vitamin C thinking, eh, maybe I'll hit two birds of one, two stones. I'll get the, potential soft tissue effects per se, and then get some of the muscle effects per se.
I assume you would generally agree with that in terms
[00:47:13] Dr Keith Baar: of practice. So it depends on what we're trying to target. So if you're trying to target muscle, we're totally fine with adding it afterwards because the reason that we put it in beforehand when we're looking at bone and tendon and ligaments is cuz they don't get the same kind of blood supply that the muscle does.
So if we're looking to fix a say, we have a hamstring pole, so somebody's pulled their hamstring, it's pulled off, or it's been surgically repaired, or whatever, and we're repairing that tissue. Now what we want to get is we want to get both a muscle signal and a connective tissue signal. There's gonna be blood flow after the exercise that we do because that muscle is already pulling in blood flow.
And so now we can do that as a supplement that we just do after, together with the protein. No problem. If we want to target it specifically to tendon, then what we're gonna do is we're gonna put it in beforehand. And you can do it together with whatever you want to do it together with. But yeah, we're gonna try and get it in about 40 minutes to an hour beforehand, just so that when we're pulling on that tendon and we're squeezing all the liquid out of it and then we're relaxing and we're squeezing and we're relaxing, we're getting that rhythmic movement through that tendon.
We're gonna get more fluid flow and that more fluid flow is gonna pull more nutrients into the, to the proximity of the cells. And we're gonna get more of whatever signal we're hoping to get there, using that kind of load as a way to target our nutrition to where we want it. Yeah, the way that you're doing sounds fine.
The way that we would tweak it a little bit is if we're looking for a muscle signal Yeah. Fine. To give it afterwards. If we're looking for something that's more tenant or ligament based, we're gonna give it, or cartilage based or bone base, we're maybe gonna give it beforehand.
[00:48:50] Dr Mike T Nelson: Got it. And would there be any downside to adding like six to 10 grams of essential amino acids with the collagen beforehand?
[00:48:58] Dr Keith Baar: Not at all. Not at all. And it might be something we're adding the whey protein together with the collagen is gonna give us a better response. Sure. Because the whey protein are gonna have all of the other amino acids that are necessary. The thing to remember is that collagens are really simple protein.
It's basically three, it's basically two amino acids. It's glycine and proline make up two-thirds of the amino acids within collagen. So the sequence goes glycine, any amino acids and the any amino acid then proline. So most of what we see are glycine and proline. So that's one of the reasons why we are giving a dietary collagen, is because if we give whey protein, iss a dairy based protein.
It's a great protein, it's a complete protein. But what happens is after exercise you'll see a drop in glycine within the body. And it's possible that we're getting a little bit of a limitation based on how much glycine is there because it's not as glycine rich as some of the connective tissue. And there's some really nice work coming out of Glu van Loon's lab that's showing that after resistance exercise, there's higher rates of protein turnover in the matrix than there is in the muscle.
So the matrix has actually got more protein synthesis response to exercise than the muscle does. And we've seen that in a number of our studies that where when we give a stimulus for a muscle to grow bigger, we actually see collagen concentration go up, which means that the collagen is increasing at a faster rate than the muscle protein is.
And we've got a colleague in France who inhibits collagen synthesis when he does that. And what he shows is that you drop 50% of the strength gains are lost by inhibiting the increase in collagen synthesis. So we really think that the matrix is important. Whether it's sensitive to collagen as a dietary supplement, we, it's far too early to know.
But we do know that the matrix is really important for the functionality of that muscle, the muscle's ability to transmit force and to become stronger.
[00:50:54] Dr Mike T Nelson: I think it was Van Nuns Lab that also had a study looking at different tissue turnover rates that they did from some surgeries showing that basically, Turnover rates were much faster than at least what I thought.
Cause I had heard the old thing, which has been disproven now that, muscle will turn over in, know, 90 days and soft tissue takes nine months where all the newer data, and you're suggesting that might even be inverse, that some of the collagen processes may turning over faster than muscle.
Yeah.
[00:51:25] Dr Keith Baar: So that, that study that Smz was the first author on, basically what he had shown is that protein turnover in the ACL was actually twice that of the quadricep muscle. . And that the patellar tendon was almost the same as the acl. And we know this load dependent because when he looked at the pcl, the posterior cruciate lament, it had the same amount as muscle.
So the loading, cuz the PCL isn't loaded a lot, the ACL L is loaded quite a bit. That's where we're getting that dynamic difference between those two tissues. But yeah, it was quite, illuminating to see that. We also have to understand that yes, there is real good very good data from Michael Care's group from Kaia Heme using the bomb pulse that shows that, look, collagen turnover in the core of our 10 of an Achilles tendon doesn't happen to a l to a great degree.
We might be, because again, that's using this radioactivity that you would find in the en environment. It might be that we're able to recycle really well all of the protein and amino acids within the core. And so we don't see, say a a breakdown. We don't see turnover overall, but we're able to recycle those amino acids or it means that the core isn't changing and the outside of our tendons is cha are changing quite a bit.
And so we can't make any grand conclusion as to which one it is yet. But we do know that, met metabolically, the outside of a attendant is far more metabolically dynamic than the inside. And so it's possible that we're seeing differences through the tendons from the core to the outside, and also as a function of things like exercise and nutrition and other components.
[00:53:05] Dr Mike T Nelson: Yeah, that's fascinating. And then you also wonder about all the freak case studies of weird Achilles ruptures that, quote unquote appear to happen out of, nowhere. And there's different, like Levaquin and different drugs seem to target Achilles heel injuries more often and yeah.
Yeah,
[00:53:22] Dr Keith Baar: so there's a whole bunch of things within that. One of the ACE inhibitors is got huge numbers of Achilles stent interrupters with it. We know the fluoroquinolones have a huge number of Achilles tend interruptions. So there are drugs that are specifically targeting things and we don't know how they work and it's still very early days to figuring out how they work.
But yeah there's definitely lots of really interesting things as far as how these tissues are turning over, what their turnover rate is and what their, how dynamic they are because there's data, there's really nice data in female soccer players that shows that the a c L gets bigger over the eight months of a season.
So as you, as they trained, the ACL got bigger and then what you would assume is since they were all college level athletes, is that in the four months that they took off, that tissue got smaller again. Again, it's, these are highly dynamic tissues, is what we're learning. And so what we're doing is we're learning how to support them with the proper loads.
Like I just had Camille Herron in here who's the world's greatest ultra marathoner, and she was telling, she had gotten all kinds of bone injuries when she was young runner. She, that made her go into science as a college student. And then she did a master's in bone biology and bone mechanical transduction.
And she learned that the way that a bone worked is it had short periods of load and it needed good amounts of rest, like six to eight hours. And so the way that she trains is she trains twice a day because she knows that by training twice a day, she gets two of the signal. It lasts only a short period of time.
Even when she runs for say, a hour and a half or two hour run, she knows that her connective tissue only gets maybe a half hour of an adaptive signal from that two hour run. But if she does, if she was gonna do a four hour run, which is not uncommon for an ultra marathon, or if she breaks that up into two, two hour runs that are separated by eight hours, she gets two of the stimuli to her bones, tendons, cartilage, to have a positive effect.
Whereas the a different ultra marathoner who's doing that as a single session only gets one. And so now what you get is you get these differences in how the body's gonna respond based on how we're pairing up the exercise. I know that Brad Lin had done some work where he had taken military recruits who get tons of stress fractures, and instead of having them run once a day, you had them run half as much twice a day.
And stress fractures go down massively. Huh. So just. Figuring out how the different tissues responded to loading is really important for understanding what exercise training should look like based on what your injury history is, based on what your capabilities are.
[00:55:55] Dr Mike T Nelson: Oh, that's awesome. And as we wrap up, I know you've talked a little bit about possible user collagen and then certain types of isometric exercise.
And I think that it's interesting, like high level sprinters, you talked about potential hamstring injuries, but if I think about the average gym gore, rarely do I ever hear of a muscle tear. It's almost always a soft tissue related injury. So is there something more for that population they should consider doing related to training?
[00:56:27] Dr Keith Baar: Yeah, so again, that's one of the interesting things that happens because as we, as you train, basically you're training the stiffness of the structures that you're training based on how you train. So if I do a lot of fast training, my, my tendons are gonna get stiffer to do fast training. I can't do it against a lot of weights, so that means my muscle's not gonna get a stimulus for strength.
So I'm gonna get a little bit weaker muscle over time. Now I have a stiff tendon and a weak muscle. That's when I get muscle pulls. Most people don't do a lot of their training fast. We've talked about that already, so that most of the average people aren't getting muscle pulls. What they're getting is they're getting tendon problems and they're getting these types of injuries where the muscle is stronger than the tendon.
And now the, basically when we do a stretch, when we do any type of movement, we're stretching both the tendon and the muscle together. If the muscle is super strong. The muscle doesn't stretch very far. The tendon stretches a long way. If the muscle is weaker and the tend is stiffer, now the muscle has to stretch more.
And so what we're looking to do is balance these two things. So what it would suggest is that in recreationally active individuals, their muscle is stronger than their tenant is stiff. So that when they take a move, now the is stretching a super long way. And so that means that the likelihood of an injury is gonna be in the tissue that's, that strains the most.
And so that's where we get a lot of our tenant injuries and other things. And so what we're doing is what we've found, and I've got a PhD student, Danielle Stephan, who's doing a lot of work with essentially how we should be loading to fix tendon problems. Because a lot of times people get, oh, even though people say, oh, Achilles tendon rupture came out of nowhere, you talk to them and they're like, yeah, for a couple weeks now I something going on.
There's something going on. It didn't feel quite right. And then I took a step and bang, Aquin. And that's the issue. And so what we're doing is we're addressing those early or those tendinopathic areas where I've always got pain in my, in the front of my knee or in my Achilles or in all of these things, or for a lot of throwers in their elbow, ucl, in their elbow, the golfers in their, in the inside, the tennis players on the outside.
And all we're doing is we're doing these 32nd isometrics where if you've got a lot of tendon based pain, like if you're super painful in your first few steps, and then it warms up and you'll get out of it, that's a good sign that it's a tendon problem because the tendon super stiff first thing in the morning.
As you get moving a little bit more, it's going to be a little bit less. and if you have those types of things where, yeah really sore for the first few minutes. Or if I go out for a run, I can barely move in the first few steps, but then I eventually warm up. Those are the things that are telling you that.
The problem is with your connective tissues, you like your tendons, and that's where we come in. We use isometrics. The reason we use asymmetrics is the, that our tissues, our tendons are super dense connective tissue, and so when we get an injury to it, we get a little bit of damage to it.
The load doesn't go, the load doesn't stop going through the tissue. What it does is it goes around the damaged area. It's basically like taking a big rock and throwing it into the river. It doesn't stop the river just goes around it. And that's basically what happens to the load that we're putting onto that tent.
The only time that we're going to get, and that's what we call stress shielding, because the strong part of the tendon,
[00:59:44] Dr Mike T Nelson: sure it's taking all the load,
[00:59:45] Dr Keith Baar: yields the load from going through the weak part of the tendon. And so what we want to do is we want to fatigue the strong part of the tendon so that we can get load through the scarred part of the tendon.
And so the way that we do this is we pull and we hold on the tendon. So we use an isometric contraction. 30 seconds causes about, 80% of the relaxation that we're gonna see within that tendon. Even if you go out to two minutes, three minutes, it's only gonna go 10 or 20% lower in the tension through the strong part.
But as that strong part starts to relax, now the weaker part has actually got, More stiffness than the strong part. And so what we get is we get load going through the weaker part and that load is gonna give the cells the signal they need to reorient and to start making aligned collagen the way that we want it to be.
And so what we've had incredible success with this with a lot of people who, you know, who haven't been able to do their activities that they love to do, they'll do the 32nd isometrics for a couple weeks and they'll be able to return to, to play. We've done it with professional athletes, we've done it with all kinds of individuals to help bring them back.
And so what we're doing is we're doing four 32nd isometric holds with two minutes rest in between. And all we have to do is figure out a way that we can get load through the tissue. So if I have a tendinopathy, my elbow, I'm gonna take something and I'm gonna rotate it out so that there's a heavy thing over here and I'm gonna hold it in that position.
So I'll have tennis players hold up fry pan out. With their elbow a little bit bent. And so now they're getting loaded through these muscles, which are the external rotators that are gonna go through that area where you get tendinopathy. If you're a baseball player, a thrower, or you have golfer's elbow, you just go the opposite way and now you're getting load through the inside.
You're getting that long load hold through the insight, stress, relaxation, the damage part gets that signal to align and to synthesize collagen in a directionally oriented way, and we can repair the collagen.
[01:01:46] Dr Mike T Nelson: Oh, that's awesome. And based on what you talked about with collagen, would you have 'em do that twice a day then for those four rounds?
Because you could up the frequency per day,
[01:01:55] Dr Keith Baar: easily do it twice a day. So again, it depends on how much it's limiting you. So if it's something where you can't do your activities, then yeah, doing it twice a day is gonna get you back faster. and it doesn't have to be like, the heaviest loads you can possibly, you just have to do a load that's going to be sufficient to allow relaxation through the strong part, get load through the weaker part.
The older, the denser the scar is, the greater the load you are gonna need to use because that scar is now gonna take a lot longer to get that directional signal to. Got it. So if we use a heavier weight, it's easier for us to get that signal into the, to the denser scar. So if we have a really old scar or really old injury, we're gonna use a heavier weight to get that load through them.
[01:02:42] Dr Mike T Nelson: Yeah. That matches some stuff I've done in the past with just heavy ish eccentrics for 10, 15, 20 seconds. And I found just anecdotal, I can't remember where I read the study from. , a lot of tendon issues literally within a couple days started like clearing up. So it was probably maybe the isometric e portion of it that was doing this.
This is a slow component,
[01:03:02] Dr Keith Baar: right? So if you did, so that's the alfredson protocol. You do your heavy ecentric, you do heavy concentrics. The heavy component means you go slow. That's the force velocity relationship. So when we realize that, okay, all of these things that are having a beneficial effect are just slow moves.
The slowest type of contraction is an isymmetric contraction cuz there's no movement at all. So by definition it's the slowest. And so that's why we went there and you put that together with a bunch of other data from, from horses or from other things where they decreased stiffness and they saw that the tendons went to looking beautiful again.
That told us that what we're trying to do is decrease that stiffness is important cuz that's how we shield. The injury. So we don't get a lot of tendonopathies in kids because their tendons aren't stiff enough yet to shield that little injured area. Ah, yeah. And so because they can't shield the injured area gets loaded.
And so we don't see that scar formation. As we get older and older, we're gonna have stiffer, connective tissue. We're gonna be able to shield any injury really well. So as I get older, again, I'm gonna have to use a heavier weight cuz the connective tissue is gonna be stiffer at the beginning.
So in order for me to overcome that shielding effect, I need to have a bigger load
[01:04:19] Dr Mike T Nelson: and for isometrics, for people listening. One thing that goofed me up for quite a while I had to unlearn was like strength and condition wise, they're of classically taught and isometric. the muscle, quote-unquote, not really working because it's not moving.
But what happens is I'm like, go do a wall, sit for two minutes and tell me your quads aren't doing anything. Exactly. And it's, the muscle is still contracting, but because there's play in the soft tissue, the joint is isometric, meaning the joint space isn't changing an angle, but the muscle is still doing work because it's pulling on all that soft.
[01:04:51] Dr Keith Baar: Yep. The muscle has to do a lot more work because what we normally use our tendons for and our matrix is to have momentum in the movement and to capitalize on the momentum so that we get stored in returned energy for free. So if you wanna make an exercise hard, if you think a pushup's easy, that's great.
Do a 32nd down, 15, second up pushup, That's actually gonna use your muscle much more because when you're doing a normal pushup, you're storing and returning energy in all of these connective tissues throughout the system, and the result is you get a lot of bounce back where you don't have to use your muscle as a motor.
If you actually want to really test your muscle, you go slow movements because now you're no longer storing and returning energy. The series elastic component. It's all the muscular component that has to work much harder. And that's again, as the series elastic component is doing less of the work, we're gonna get better signals to potentially both the muscle and the tendon.
[01:05:55] Dr Mike T Nelson: And I think that matches, there's an old study, I think from Australia where you had to do a bench press with at least, I think it was a six second pause at your chest to try to eliminate that str shortening cycling effect, which is a much longer pause. And even people doing pause, bench press would be doing, or you can do it from the bottom as like a starting position where now you're already in that position.
It's concentric only. Yep.
[01:06:21] Dr Keith Baar: And that's what we see with a lot of different things that we do with when we're doing supplementation or we're doing training. You're not gonna see a change with a squat jump, but you're gonna see a change on a counter movement jump. The counter movement jump you're storing in returning energy.
So the connective tissue stiffness is really important on a squat jump. You're starting from a one position. You're not storing in returning energy, you're just trying to produce that rate of force development. And so we don't see as much of a performance change for a lot of the connective tissue work that we do if we're only doing a squat show and we're not looking at something like a counter movement.
[01:06:56] Dr Mike T Nelson: Yeah. Awesome. Thank you so much for all your time today. We really appreciate it. And if people want to are in the area and want to enroll in your study, how would they find you? Yeah
[01:07:06] Dr Keith Baar: so once everything's approved on this end from our I Rrb, it's gonna be on clinical trials.gov.
Or they can email me at kb a r uc davis.edu. And that's just a way that if they're in the Davis area and they wanna be part of some of our studies, we're happy to have 'em. .
[01:07:23] Dr Mike T Nelson: Awesome. And are you looking for any more graduate students if people are interested in that
[01:07:27] Dr Keith Baar: route? I've got a good cohort right now.
I'm always interested in supporting young scientists. So yeah, if there's exceptional young scientists, I'm always interested in looking at opportunities to, to increase the number of the individuals that we can get in and get doing outstanding musculoskeletal work so that we can improve quality of life for as many meek people as possible.
[01:07:50] Dr Mike T Nelson: Awesome. Thank you so much for all your time today, Dr. Barr. We really appreciate it and sharing all your wisdom. Thank you so much. You're welcome.
[01:07:57] Dr Keith Baar: Thank you for having me.
[01:07:58] Dr Mike T Nelson: Thank you. Thank you so much for listening to the podcast today. Really appreciate it. Huge thanks to Dr. Keith Barr for taking time out of his busy schedule to come on here to share all the different protocols and different research and everything that he's done over the years.
Really appreciate him being open with all the information. If you've enjoyed this and you wanna learn more about how to use nutrition and recovery tactics to maximize body composition and performance in a complete, flexible system check out the Flex Diet certification. It is open now through Monday, June 13th, 2022 at midnight.
So go to flexdiet.com, for all the information. If you have any questions, there'll be a way you can contact me there. I'll do my best to answer any questions you have if you're listening to this outside of that time period. Then you can go to flexdiet.com also and get on the wait list for the next time that it will be open.
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Thanks again to Dr. Keith Barr. Make sure you check out flex diet.com as it is open now. We'll talk to you again in just a few days.