Episode 159 of the Institute of Performance Nutrition's "We Do Science" podcast! In this episode, I (Laurent Bannock) discuss "Exercise-Induced Muscle Damage: What is it, what causes it and what are the nutritional solutions?" with Dr Daniel Owens PhD (Liverpool John Moores University, UK) Professor Kevin Tipton(The Institute of Performance Nutrition, UK).
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APRIL 15, 2021
With Dr Daniel Owens and Professor Kevin TiptonPhD
[00:06:13] LB: Hi, and welcome back to the Institute of Performance Nutrition’s We Do Science Podcast. Today, I have another – well, we could describe this either as a double act, or as a triple act, depending on how much I contribute to this conversation. Today, we're going to be talking about exercise-induced muscle damage. We're going to talk about what it is, what causes it. Because this is a performance nutrition focus podcast, we're definitely going to talk about the nutritional solutions, which is more or less the title of the paper that I'm using for the framework for this conversation. The lead author on that was our guest, Dr. Daniel Owens. Dan, welcome back. It's good to have you here.
[00:06:59] DO: Cheers.
[00:07:00] LB: We've got Professor Kev Tipton, our Director of Science and Research, who is also an expert in this topic. Of course, is to back me up. Before I get into this topic and just briefly explain why it is I wanted to do this podcast on this topic, Dan, just super quickly, who are you? What are you up to? Tell us about yourself.
[00:07:27] DO: Yeah, so my name is Dan Owens. I'm a lecturer at Liverpool John Moores University in the School of Sport and Exercise Science. I've been working here now for the past three or four years, just flown by. Yeah, my research interests really are all around skeletal muscle adaptation, and how skeletal muscle repairs itself after damage. That's what this paper is about. Yeah, that's where my research focus is mainly focused. Yeah.
[00:07:55] LB: Of course, people would have to be more or less new to this podcast if they're not actually familiar with you, because of course, you did a podcast with me not so long ago, back in November of last year on vitamin D, and the athlete, which is another area of expertise of yours. I recommend everyone has a listen to that.
Actually, we will touch upon that topic a little bit, because it is relevant to today's chat. Thank you, Dan. I appreciate you coming back on. I always appreciate your knowledge and insights, both as a researcher, as a lecturer and as a practitioner. There's that additional skill set that you have in actually translating that information into what is of value to the bulk of our listeners, which is in itself a skill set. That's great.
Kev, welcome back. It's good to see you again. There's a bit of a link between you guys, I know. You might as well tell us about that, Kev, because you were recently given a new appointment, weren’t you?
[00:08:55] KT: I'm very happy to say that I have a three-year appointment as a Visiting Professor in the Research Institute for Sport and Exercise Sciences at Liverpool John Moores University. Dan and I are colleagues to that extent. Now, I do want to point out based on the responses on Twitter, this is not a full-time appointment. I'm not getting paid a cent for this. I just have to do some work, so I can have the colleagues and friends and hopefully, get to see Dan and Graham and James and these guys a few times to do some work together.
On Twitter when I put it out there, people seem to think that I was moving to Liverpool and all that. No, it's a temporary thing. I'll hopefully get to go there and see people and do some lectures and stuff, but I’m not raking in the dough or anything.
[00:09:42] LB: No, no, no, no. Well, you're with us at the IOPN, of course.
[0009:47] KT: Aye, I've got a full-time job.
[00:09:48] LB: Exactly. That's what this is all about, isn't it? It's about collaboration. I'm particularly keen on that. Obviously, for many years now. I've been talking to lots of people who are from lots of different institutions, or professional sports teams, or private practices all around the world. It is an incredibly valuable way to share knowledge and disseminate that knowledge that isn't necessarily done, or at least isn't as practical to do, through traditional research or traditional publications, which is a huge advantage of these podcasts. Ultimately, we are interested in these things for a reason and there's no point being selfish about it. It's all about spreading the knowledge and furthering the field and so on.
Now, both of you, of course, aren't just people who happen to have a lot of knowledge on this topic of exercise-induced muscle damage. You have both done original research in these areas. Maybe, Dan, it would be good for you to kick this off then with why was this review that I've referred to, which I will link to this paper in the show notes, which was published back in 2019 in the European Journal of Sport and Science. It's safe to say that as it relates to efforts to describe where we are on this topic, what we know, what we don't know, and particularly, the nutritional interventions, there isn't that much out there, which is why I was particularly keen on doing this podcast. As Kevin pointed out, before we started recording, there are a number of things that we want to make clear in this conversation, which I'll leave you guys to bring up shortly. What led to this particular review? Why did you initiate that process?
[00:11:42] DO: Yes. It's a great question and nice to reflect on where it started really. I think, the idea came about when I was doing my PhD, actually back in school around about 2015. I was doing my PhD on vitamin D, and the latter stages of the PhD were focused on muscle damage and repair, and potentially how vitamin D might have a role in that.
During that time, Graham and myself had been talking about exactly what you just said, that there wasn't really anything out there in the literature to say, where are we currently at with nutrition and muscle damage. We know it's a big thing that athletes talk about, as we'll probably come on to in the podcast. There wasn't really anything out there that summarizes where we're at as a field.
We started writing it when I was still doing my PhD. I didn't really get to finish until I was doing my postdoc in in Paris, actually a couple of years later. It was really nice to finally get it across the line and bring in some really awesome authors onto that as well, who just contributed really cool, different perspectives on it, which we hope we got across in the paper.
[00:12:48] LB: Yeah. Kev, you've got more than just a passing interest on this topic as well, haven't you?
[00:12:53] KT: Well, yeah. I've been involved in a few studies, using these types of muscle damage models to try to evaluate some nutrition, potentially valuable, nutrition interventions. There are some issues and I think we can get into that as far as how these studies are done and how to interpret the results. I think, well, a general statement would be, I believe that results from these types of studies are often way, way over interpreted.
[00:13:22] LB: Yeah. That is exactly why I wanted to get into this, because quite simply, when you're working in, whether it's practice, or research, or education, or whatever, in sports science, exercise science, sport and exercise nutrition being our focus, obviously, anything to do with exercise, or training, you start talking about adaptations to the various types of training. You'll certainly get into the concept of muscle damage, or soreness, DOMS, delayed onset muscle soreness, and so on.
Inevitably, there are going to be questions about whether or not that is simply just an unpleasant side effect, or whether it actually does impact performance, or does it impact the adaptations to training? Is the muscle damage and the symptoms that we get from that, is that something that is something that we should be trying to get rid of? Or is there a trade-off there between the symptoms, the unpleasantness of it or, ultimately, what we're trying to get out of the training that led to that event. That's the stuff that we need to get into now, because, of course, on a very simple level, particularly in nutrition, there's a lot of conversations about things, like antioxidants and the impact that they can have on oxidative damage, for example, which is something that might come up in the phraseology, if you like, that you might come across in papers and topics, and so on on this.
It's very easy to go, “Oh, this problem is occurring. I've read about this topic somewhere else in a different context, albeit. Therefore, the solution is going to be to take all these antioxidants and so on,” which is something that we will, of course, talk about today. Before we get into that in any great detail, Dan, I think it's probably worth first, just defining what muscle damage is and what exercise-induced muscle damage specifically is, so that we're all on the same page on this topic.
[00:15:28] DO: Yeah. Exercise-induced muscle damage, anyway, is really characterized by these symptoms that last from the bout of exercise, up to around about 14 days after the exercise. The length of time that you see the symptoms for is really dependent on the duration and intensity of the activity. Probably also, the person's susceptibility to it as well, which is something we can come on to.
Typically, the direct impacts are a loss of functional capacity of the muscle, so the ability to produce force is an easy way to think about that; an increase in muscle soreness. You also get this disturbed sense of limb position, and also how much force you're actually producing. There are some other things that can occur as well. You can get swelling of the affected limb, a decreased range of motion and so on and so forth.
Of all of those things, the best marker that correlates to the damage is the loss of function, so the loss of force. Typically, you'll see in the literature reports of anywhere from a loss of 15 to 60 odd percent. Again, there are a number of reasons that account for that which we can get into.
[00:16:44] LB: Why are we feeling that this is a topic that we really need to understand in greater detail, and in particular, from a performance nutrition perspective, surely, just take some painkillers, or you just – to use a politically incorrect statement of just man up or whatever? I know you've mentioned loss of function and so on, but just how significant can this be? Maybe a bit of a deeper dive into what actually is going on?
[00:17:10] DO: Yeah. I mean, in terms of why we're interested in it, I think that there are two reasons and you touched on both of them. The first one is probably, how it directly affects performance. I mean, if you've got a loss of functional capacity of the muscle, that's exactly how it's going to affect performance. You're not going to be able to produce the force that you need to in the type of event you want to do. That's just a given straightforward one.
The soreness is another issue with that. I think that’s in a way, it's almost a little bit separate, because soreness is so subjective. It doesn't really nicely correlate to the amount of damage. The management of these things around training and competition is really where we're interested in. I think, something we can get onto later on is considering recovery versus adaptation.
If this happens and we need rapid turnaround before we perform the next bout of exercise, it might be another competitive bout, you're going to try and maximize the rate of recovery. so you can go again. Is that always necessary when the goal of the session is to bring about adaptation? Maybe not. An answer to your question, the reason that I think these things are interesting is because of the direct impact it can have on performance, but also the way the athlete is able to train and compete, I think.
In terms of what's going on, do you mean the mechanisms that drive exercise-induced muscle damage?
[00:18:40] LB: Yeah. Well, let's get there in a second. Because, I just want to bring to the front of mind that this situation that's occurring isn't just simply an inconvenient symptom that results in soreness. Likewise, one has to think very clearly about what's going on to understand whether or not we should try to intervene with our various strategies, whether it's, do I do some manual therapy, massage or whatever, give it a good rub, so to speak? Do I stick my limb or whatever the area the body is into a vat of ice? Or am I going to chuck back a bunch of anti-inflammatories, or some of these novel nutritional compounds that we're starting to learn about?
I've got a phrase that I use regularly on this podcast, which is you can, but should you? It's very much that stop think about this, because your solution may actually be worse than the problem, which is something that I'm looking forward to revealing. In order to understand all of this, we're going to need to underpin it, of course, with an actual understanding of the mechanisms behind this muscle damage. Maybe you could take us down that path now, please.
[00:20:00] DO: Yeah, for sure. Thanks for bringing up the point that it's potentially just an inconvenience. The soreness, yes, potentially is an inconvenience. The actual process of muscle damage and the events that are occurring are real physical changes to the muscle. Usually, we can think about muscle damage, exercise-induced muscle damage in two phases, the primary and secondary damage phases.
We didn't mention before, but damage is really caused mostly by eccentric contractions, or lengthening muscle contractions. They produce a higher force, but for the same motor unit activation as you would get for a concentric contraction. As a result, you've got a higher amount of stress placed on a smaller number of fibers. They're being put under a lot of stress effectively. When that happens in these eccentric lengthening contractions, what can happen is the contractile machinery, the proteins that are responsible for muscle to contract, reach a point where they go beyond overlap. Essentially, we have disruption to the machinery that allows our muscle to contract.
Not only that, we probably have some disruption to some scaffolding proteins as well. Also, to the to the proteins responsible for keeping all our muscle fibers together, so these extracellular matrix proteins as well. On top of that, we tend to see what's called excitation contraction coupling, or a disruption to excitation contraction. That is effectively how we turn a nerve impulse into a muscle contraction. That seems also to occur during the primary phase.
All of this is occurring, basically, during or immediately after the exercise bout has occurred. That's the primary damage phase. The secondary damage phase is what is occurring as a consequence of those primary events. Because we get disruption of the different contractile machinery, disruptions to the muscle fiber membrane, we're opening up the muscle fiber to have a uncontrolled increase in calcium into the cell. That's one of the main things that happens. Usually, calcium is pretty well controlled in terms of its concentration in different places in the body. This influx of calcium into the cell is a bit of a problem. It starts to activate different systems that will break down proteins within the cell.
The mitochondria within the cell can mop that up to some extent and take care of it. Even the mitochondria at some point are going to become overloaded with this calcium. Then we just end up with more calcium pouring back into the cytoplasm, the space within the muscle. That's one issue that happens during the secondary damage phase.
Then, of course, we have the inflammatory response. This is something we can definitely get into, because we might think of it as something that's going to cause muscle damage, but it's also something that's super necessary. It’s absolutely essential, but it happens for muscle to be repaired. During that inflammatory response, we have our innate immune system, that rapid part of our immune system, and we get neutrophils and macrophages coming into the muscle to try and take care of all of the mess. They're just going to come in and start to try and engulf all of the stuff that's been left behind and start to clear it off.
Well, as a consequence, they also release some of what we would call cytotoxic substances and also, some reactive oxygen species or ROS, as you'll often read them. That can contribute to, or is thought to, contribute to further damage.
In summary, we have these two phases. We have the initial event, where we have disruption to contractile and non-contractile proteins. Then we have the secondary damage phase, where we have a bit of calcium that's all over the place and we have the immune system, which is trying to do its job, but it's also causing some secondary damage.
[00:23:58] LB: Thanks for that. That was a fantastic overview. One issue that can come up when we're looking at these sorts of things, of course, is the way in which the muscle damage has been induced in a laboratory setting. Kev, I'm going to bring you in on this one, because I know that these are the sorts of things that drive you pretty crazy with how these types of studies are performed, and then the assumptions that come from them and how that ends up influencing this body of knowledge on this topic.
Ultimately, and my concern is how that influences practice and decision-making, and so on, where we don't necessarily have the knowledge and the laboratory experience that you guys have. We wouldn't necessarily know the difference between a real-world scenario that induces muscle damage, as opposed to this highly controlled set up. As there aspects to what I've said there that need further discussion, Kev? What do you feel, where are we at with this anyway?
[00:25:00] KT: I think so. The models that are used to induce muscle damage are often, quite artificial, maybe, or definitely not directly applicable to a sporting situation, especially an elite sporting situation. A lot of the studies, if you read the studies, I mean, you're using the old sledgehammer effect, right? Where you're just going to do something really bad, just to see the worst-case scenario and then see if something works; some nutrition intervention works.
You take untrained individuals. We used to use a – well, in Birmingham, we had some homemade kit - but basically, you do these eccentric contractions on a dynamometer or something, eccentric contractions. You do 10 sets of 10 or something on untrained guys. They are just completely shattered. I mean, these guys were walking in circles, because one of their legs wouldn’t work.
Then you give the nutrition intervention. What you've done, of course, is set up the scenario where you've got this really, really big effect. If you do the intervention, you have your best chance to see it. From a proof-of-concept standpoint, it's good for something. I think, the problem is when people see that and then they see a situation where you've taken untrained individuals, you've really, really whacked their muscles. Then you see some effect, which is really relatively marginal, most of these studies, and then all of a sudden, it's trumpeted as, hey, let's give them whatever the latest high fad nutrition is.
I think that's where the problem is, is taking these proof of concept studies, and then really just skipping all those steps in between and go right to, we're going to apply this to elite athletes. There are so many problems with that, based on lots of gaps in between. I think that you often see it, when you read the muscle damage papers, you often see this mentioned somewhere in the discussion. There might be a paragraph or something on limitations and it's buried in there.
Often, I've seen it get ignored many, many times. I think that's where the problem is. It’s not necessarily that these studies aren't good. They are what they are, as long as people interpret them appropriately and apply that information with a fair bit of caution.
[00:27:47] LB: Yeah. it's, I guess, I mean, we obviously have to respect the fact that the further back in the past we go, there was a lot less knowledge on this topic, of course. There's also less technology that you guys now have available. Of course, that should all be factored in in the appraisal of that knowledge today, which of course, is how you approach your reviews, and so on on this topic.
Before we get into the whole nutrition thing, I just want to sit in this area for a bit in truly understanding what exercise-induced muscle damage is, so that we can truly respect the need for not getting into any strategy or trying to influence this. Dan, just quickly take us through, because Kev has given us a very important need to be – we've got to be cautious. There's a warning with this. Having done some of these studies yourself, maybe you could just give us an idea for the listeners, how these studies are done nowadays, or how they ideally would be done, at least from your perspective.
[00:28:56] DO: I think, yeah, ideally how they would be done is a better way to think of it, because we still see studies being done that don't control for a lot of factors. Kev touched on the main problem, which is that they are sledgehammer approaches. You're seeing really pretty excessive eccentric loading of the muscle, which you, I guess, unless you do in ultra-running, a lot of downhill running, you might not see something similar to that.
Another thing which really muddies the whole thing is this repeated bout effect as well, which is not adequately controlled for in a lot of studies. That is this phenomenon where you basically, once you've done one bout of eccentric exercise, you get some adaptation, as you'd expect to the eccentric lengthening and which actually protects you from future bouts of loading. That's due to a number of different factors. you get some remodeling of that extracellular matrix. You get neural changes, neural adaptations, and you also get changes in the way the immune system responds as well.
The take home message there, though, is that you don't see the same loss of function and the same severity of soreness, if you repeatedly do the exercise. One way that we tried to get around that. We've had a project that we've had sponsored by Solomon Running, looking at different compression garments and different things like this. The way that we've designed the study and ran the study is to basically, have all the participants do a month of progressive periodized downhill running training first, before we've actually analyzed any of the compression stuff, so we could be pretty sure that there's been some adaptation to the type of exercise, before we even look at anything.
By the time they get to the damaging downhill running type exercise, they should have had the basal type of adaptation you might expect to have more trained people. We think that is a least a step in the right direction to mitigate this repeated bout effect. Interestingly, from that study, we haven't published the results yet, but a lot of the really interesting data have come from the training adaptation phase. We're going to try and publish that by itself, just to show how adaptations to eccentric contractions from downhill running actually happen on multiple different levels. We've got ultrasound data. We've got some biopsies and bloods and stuff as well. Obviously, some functional outputs as well.
I think, if you really want to translate any of this information, you have to – I think, we need people who are used to doing eccentric exercise first, or we at least need to give them some adequate familiarization, before they get involved in the experimental part of the trials, just because they're going to adapt. That really is going to muddy the data. There's no way for us to predict who's going to respond in what way to the type of muscle damage and exercise. Yeah, in addition to what Kev said, I think this repeated bout effect is something that we have to consider as well.
[00:32:02] LB: Yes. Clearly, this is very much still in the learning phase on this topic, isn't it? Look, I just want to fixate on the word damage just quickly, because when you look up the word damage in the dictionary, the quick Google response to that dictionary Google is physical harm that impairs the value, usefulness or normal function of something. Of course, you think of damage, you think oh, car crash, or somebody damage something and it's a negative thing. It was unintentional. It was an accident. That isn't necessarily the case, is it?
There's a situation here, where the exercise-induced muscle damage is a necessary strategy, if you like. Then also, it's more like, due to an excess, for example, overdoing something. Can you help us understand what the difference is between these different situations and when it actually is necessary? Why is that the case?
[00:33:04] DO: Yeah. I mean, when we think about exercise-induced muscle damage, we also have to differentiate between an injury. We're not talking about a muscle tear, or something that is going to keep you out of action for a long period of time. We're talking mostly about ultra-structural damage to mainly, to the stuff that's inside, the muscle that contract our proteins, and potentially due to the membrane and the extracellular matrix.
Really, it's probably a better way to think about it as remodeling. I think, damage doesn't care, that thought, as you say, that it's unintentional, it's an injury in a way. There's a difference between a tear in the muscle and exercise-induced muscle damage. It's also not that clear, because there's no good relationship between soreness and physical damage to the muscle itself. When people report soreness, following different types of exercise, there might actually be no real markers of muscle damage, at least at the structural level of care.
That is something that is not so clear. Has any damage actually occurred? We're not always so sure about that. Yeah. I think for listeners, it's important to know that we're not talking about here is an injury. It's a remodeling of the muscle in response to lengthening contractions. That's the easiest way to think about it.
[00:34:34] LB: That's why I find this so interesting, because we use words and phrases in the science of this, when articles are written, or conversations are had between experts and researchers. That, of course, is an area where things can get lost in translation. When I take us back, Kev, to our podcast we did on muscle protein breakdown in response to nutrition and exercise back in December, which is relevant to this conversation as well, potentially. If somebody stopped you in the streets, Kevin, and said, “Well, how do we differentiate muscle protein breakdown and muscle damage?” Where do things differentiate and where are they similar?
[00:35:18] KT: Well, I think Dan's nice description earlier about what's happening with some of these proteins being disrupted and that sort of thing. Then, some of these proteolytic, the macrophages, etc., bringing in their proteolytic systems and enzymes. Essentially, what happens is you get some of these proteins are disrupted and damaged, and then they're broken down. Then the amino acids are re-utilized for something, possibly recycled into proteins in the muscle, or out into the system, into the liver for other things. Yeah, there's going to be some protein breakdown involved there, for sure.
Then, Dan alluded to this earlier, one of the things that always bugs me about these papers is, especially if the intervention has anything to do with amino acids, or protein, they're going to attribute the whatever success they have with soreness or something to muscle protein synthesis. Then these guys in this paper, touched on it. It just seems so unlikely, based on the slow turnover rate that we're talking about, that even if you do the math, and I've done this for people. Try to make something with it. You just cannot come up with any reasonable amount of protein that synthesized in the time it takes to start seeing improvements based on these nutritional interventions. It's just not realistic. It doesn't make any sense.
It's not protein synthesis is what – For example, we had our study in 2010, Sara Jackman study, where we saw some lessening of the soreness with branched chain amino acids. People wanted to attribute that to protein synthesis, since the stimulation by the branched chain amino acids. We're seeing the soreness improved in hours. You're just not going to see any reasonable amount of protein made in that short period of time. It can't be that. It's got to be something else.
[00:37:11] LB: Also, an elite athlete is going to report soreness in a different way than a recreational athlete, right? It's going to be a completely – I mean, I'm sure there's examples either way, but that's a factor here, isn't it? Because soreness is, you don't have digital display on your forehead that gives you a specific indicator of muscle soreness. It can be quite a self-reported process.
[00:37:38] KT: I mean, that goes back to what I said a few minutes ago, which is the models that we use. Again, in that study that I just mentioned, the guys that we used in that were completely untrained. They were really, really, really sore. Then you got to think about what's the mechanism of the soreness? Well again, the soreness doesn't really have anything directly to do with the disruption of those muscle protein, just more likely in the paramecium and epimicium in the muscle fascia. You don't have any pain receptors, actually, in the belly of the muscle.
In fact, when we do muscle biopsies, that's what we rely on. We only anesthetize the fascia of the muscle. We don't mess with putting lidocaine (an anesthetic) down into the muscle belly. It's because there are no pain receptors in there. All that soreness. Again, to attribute and I've seen it in papers and I've seen people present and say, “Hey, it's muscle soreness is being improved by protein sensors.” You don’t know. I mean, there are all sorts of reasons that that's just not – doesn't make any sense.
That's separate from the model, or the population that you're studying, which is what you very correctly alluded to, which is elite individuals are very different from the untrained people that are often used in these studies.
[00:38:50] LB: Yeah. Yeah. No, absolutely. It's important that the listeners understand that, because we can often make decisions, or choices based on how we feel that day. “I'm a bit tired, or I feel I've got the sniffles coming on, or I feel a bit sore. I must have over done the training.” In order to actually interpret that symptom, if you want to call it a symptom, it does require a bit of knowledge.
[00:39:16] KT: Let me just jump in.
[00:39:17] LB: Yeah. Come on.
[00:39:17] KT: That being said, you're absolutely right. When you do these studies, especially with these untrained individuals, the change in the soreness is so dramatic that it's not just to how bad I feel today thing. It's real. You can get a lot of variability around the mean. They have really, really dramatic increases in soreness. It's real.
[00:39:40] LB: Where I was coming from actually, is rather than somebody look, we just came out of lockdown, literally. People are back in the gyms as of right now. There's going to be quite a few people who are suddenly experiencing some soreness. What I'm trying to do here is differentiate that scenario from somebody who's months into their training program, and as a recreational athlete, or as an elite athlete. This problem is occurring where, Dan, right at the beginning, you mentioned there are some very important risks, if you like, some consequences to this, which is, it can literally reduce the function of the muscle. For an athlete, that serious. Almost every kind of athlete, that's going to be serious, of course.
And/or there might be an influence on adaptations to training, which is further down the road. It's not just a loss of function, it's a loss of performance, which for most athletes is the ultimate goal. Dan, just quickly, because you did mention briefly, but if we accept that exercise-induced muscle damage is not specifically a freak accident as such, it is something that occurs. What are the types of activities then that are most likely in the real world, with people who are not newbies to exercise, what are the types of exercise and factors that are going to make this conversation more relevant going forward when we talk about strategies?
[00:41:11] DO: Yeah. I mean, the main one is the type of contraction that leads to this is going to be predominantly eccentric. There's not much evidence to suggest that concentric shortening contractions are going to result in damage. Or any movement that's resulting in a lot of high-force eccentric contractions performed at slower speeds are really going to be what determines the degree of damage.
In terms of real world, I mean, downhill running, where you've got the deceleration forces that where the muscle is having to contract while lengthening, is going to cause some muscle damage. If you think about eccentric motions in the gym, when you're doing the eccentric phases of lifting movements, performed with a high weight at slow speed, these things are going to result in muscle damage.
For those who are maybe a bit less trained, unfamiliar movements that have got eccentric components are going to cause some damage as well, less so the more trained you are. As I say, that the more trained the individual, it's going to take a lot more to actually see any signs of exercise-induced muscle damage. Not to take us off piece, but the type of muscle soreness that some athletes might report, at least in contact sports is probably more due to the actual – the type of contacts that they go into, rather than the actual movement itself. You're going to see it less so in a more trained individual. If it's a unfamiliar activity, that's where you're going to see most of this happening, because you're just not adapted to the type of contraction.
[00:42:56] LB: When we read about, or talk about as has been done on this podcast, I think about conversations with Stu Phillips and Kev, of course, Luke Van Loon and those guys, Brad Schoenfeld, we talked about methods, the whole concept of hypertrophy. There's all sorts of mechanisms at play in responses to lifting heavy and the importance of calories and protein and so on. One thing that you talk about in this review, which has come up in the past is specifically, the role that satellite cells have in this process, which is something you don't tend – you certainly don't hear about that in the lay literature. It doesn't come up particularly often in the general conversations of this topic. Of course, it is relevant when we're talking about nutritional strategies. Maybe you could just tell us a bit more about that process and how that leads into nutritional strategies being a potential strategy.
[00:43:52] DO: Yeah. Well, for those who maybe don't know what satellite cells are, they're essentially just the stem cells of the muscle. Muscle doesn't have its own ability to keep dividing and repair itself, because it's what we call postmitotic, going through its differentiation phase, and then it's terminally differentiated structure. It relies on some stem cells in order to be able to remember to an extent, and certainly to repair itself.
What most of the literature shows is that following eccentric lengthening contractions, you have an activation of satellite cells, which essentially involves them waking up. They usually lie around in this dormant state, ready to take action when they need to. They get activated, and then they'll move to the site where the muscle has been damaged. This actually can be triggered by the immune system. Once the immune system has done its job, it can release some factors which signal the satellite cells to reach the site of damage and contribute their nuclei and to the muscle and start to repair it.
They're really important for muscle repair. The literature has gone through different phases of are they essential for repair? Are they not? I would say, the most recent evidence on this, from really, really cool experiments where they've removed the ability of satellite cells to actually fuse the muscle fibers, shows that the muscle doesn't fully repair itself if they can't do that. They are really important for skeletal muscle repair.
In the context of some of the nutritional interventions, we can get into individually, there are some nutritional interventions which seem to have an effect on satellite cell activation. As with everything, the methodologies used to look at this can be open to interpretation at this time. We have to take that with yeah, with a pinch of salt at times. Nevertheless, satellite cells are very important for the repair and remodeling process.
[00:45:56] LB: Yeah. Thank you for that. We've been talking, we've been alluding to nutritional strategies, which is something I want to move on to in a second, because people are going, “Come on, let's talk about nutrition.” Obviously, we're trying to add some understanding to this. Kev, before we started recording, you were particularly keen to make sure that there was an area that Dan, your colleagues and yourself point out in the paper, that it is important, or it’s crucial to find that the balance between recovery and adaptation requires perhaps, a periodized approach to this, rather than just a blanket approach to this, which of course, is the temptation with nutrition and so on. I mean, Kev, I'll bring you in on this one. Why is that important? Do you want to expand a bit on that topic?
[00:46:52] KT: I think it's something that is being appreciated more and more, which is that often, some intervention that you're going to do to enhance recovery might actually impair, slow down adaptation. You need to think about what your goals are and what the situation is. Dan and colleagues really laid this out very nicely in the paper. Again, you go back, and I think it's mentioned in the paper a little bit, the old story of 15 years ago, when I would go to conferences. Every other person would be up there saying that endurance athletes need high-dose antioxidants. Because when you cycle for an hour, you get all these reactive oxygen species, and we've got to knock those out.
Every athlete was on high-dose antioxidants. That was just in the days when I think, Dan probably would know better than I do, but I think Malcolm Jackson was one of the first to really start in some mouse studies, suggesting that, hey, wait a minute, when you're doing these high-dose antioxidants, you're actually knocking back the stimulus for the adaptation that leads to the training adaptations in the long-term.
I remember bringing that up at a conference one time. It was a dieticians’ conference. Of course, this guy gets up there, he's all enthusiastic and all the dietitians are trying to figure out where they're going to go and buy their high-dose antioxidants for their athletes. I said, “You might want to be careful about this.” I was almost shouted out of the room at that point, because I was the heretic for suggesting that this was the case. You see more and more evidence that this is the thing. I think now, it's pretty well accepted. I think the example that was in the paper, if you're in a tournament situation, when you're playing three or four matches in a weekend or something, or even in a week, well then, you might want to think about a little bit more focus on the recovery, so that you can get back and play your game a day later, or a few hours later, depending on when the next one is.
If you're in this normal course of your training cycle, well then, you need to think about the balance between, “Okay, in this training cycle, it's more important that I slap together five really hard workouts. I'm going to do a little bit more recovery. On the other hand, maybe I want to do that and just suffer, so that I can get the training adaptation I need.” I'm saying this in generalities, because I'm not the person to talk to about how to apply this. It's others who work with athletes. The name that comes to my mind right away is Trent Stellingwerff, who's probably one of the leaders, Inigo Mujika, people like that, are really good at the balancing these things. They've written some really nice things about that.
I think that's really, and like I said in the paper here, that's laid out very nicely as well. That's going to be the challenge is how do you balance those two? The most important thing is to recognize it and to acknowledge it and say, “All right, here's what we have, and we've got to come up with this balance. How are we going to do it?” Rather than just go and rough shod onto, “I'm going to give everybody branched chain amino acids, because this paper shows it reduces soreness.”
[00:50:08] LB: Dan, before we move on, is there anything you wanted to add to that at all?
[00:50:11] DO: No. I mean, that's a really a nice summary. I'm glad that that message is what's got out, because that's what we were trying to get out. What we outlined in this paper a few years ago, there's still no clear answers for all of this. We're seeing more and more papers talk about periodized nutrition strategies and how over the course of the season, you can implement certain approaches when they're required and as Kev talked about, really. We do really need the researcher practitioner to drive these studies and show how it can be applied in the high-performance setting.
I think, as we'll get into as well for some of these strategies, despite the fact that they say they may act in this particular way to have an effect on oxidative stress. They may not even do that. You have to be super critical of the conclusions they've made, the types of assays they've used. All of this comes into consideration. When you actually nitpick it, you're actually not really left with much. You're really left with only a few things that you say, yeah, this, this might have an effect one way or the other. It's just important for you as a practitioner then, to figure out when it is you want to use it. Yeah. I mean, I guess we can get into that as we talk through a few of the different particular nutritional strategies.
[00:51:32] LB: Dan, it just so happens that that very issue is something that we're dealing with on our program at the IOPN, which we only launched last week, didn’t we Kev? Our journal club, which is specifically aimed at our audience, which is people wanting to become effective practitioners. They need to understand the science, but they need to understand how to critically appraise that information and contextualize it.
It's not an easy thing to do. As you guys know, you guys have been at this for a long time, one way or the other and it's still difficult to do. Even after your PhDs and all that research and all that applied experience, it’s still difficult. I don't think any of us can say that it's not.
Right. Kev, let's talk about dietary solutions for these exercise-induced muscle damage situations that I think that we've done a pretty decent job of getting into. Of course, one of the first things that comes to mind is the role that protein and amino acids can have in this process. I can think of no better a man right now to give us the overview of how protein amino acids play a role in exercise-induced damage. What do you want us to take from that knowledge that we have to date?
[00:52:51] KT: Yeah. It's a difficult one in a way. Like I said, a lot of those studies were done in these sledgehammer type models. It seems like, if I had to make an overview, I could say that probably, sucking in fair bit of extra protein after a damaging situation, that damaging exercise bout in this a model, seems to have some effect on soreness. That's what we found in our branched chain amino acid paper, that is we saw a pretty good amelioration of the soreness.
Again, you have to take that with a grain of salt. The mechanism is by no means, it's just really difficult to come up with a mechanism. We didn't see much of an effect on muscle function. Then there's the argument of, well, if people are sore, then they're not going to do as much. That's potentially true. In that case, in that particular study, we actually did electrical stimulation of the muscle, so that it took the soreness out of it. It was just what the muscle could do. Now, on a practical level, I'm sure that's a little bit different, that people are probably less likely to do something when they're sore, but y’all have both worked with elite, or high-level athletes and you know as well as I do, that people work through all sorts of pain.
It doesn't even have to be high-level. Even on the level of rugby that I played, I saw guys get their nose smashed all over their face, put a little cotton in there and go back in and play. You can overcome the soreness pretty readily. What does it really mean? Most of the stuff with protein and amino acids that I've seen is, I mean, there may be some that have some effects on. Dan, maybe since you've done this more recently, but mostly, soreness that I see that's affected and I'm not sure how that is applied, to be honest.
Now, there is one interesting study that was done by Katherine Black, down in New Zealand. It wasn't with protein, but it gets into the soreness versus function thing. Instead of doing a one-off, heavy-duty bout, she tracked – these were professional rugby union players down in New Zealand. She tracked their soreness over their pre-season training. They came in. I mean, nowadays, they don't really come in ever untrained, these guys, but in less peak, I should say. There seemed to be something, this was with omega 3 fatty acids, but there seemed to be something with soreness there.
Then, because of that, that does translate into training, what's the right word? Sharpness? Would that work? If you're less sore, then you're probably going to be more likely to push a little bit more. That was the theory anyway. I suppose there is an applicability to the soreness, but it's round-about. It's not direct. I'm not sure what the protein and amino acids in that case really mean. Again, going back to the models, the model of supplementation that we used in those studies is often very artificial as well.
[00:55:55] LB: Let me ask that question from a different perspective. Where I'm thinking is like Dan, for example, I mentioned, this could certainly be in it. Yes, it's an issue in the gym with people lifting. Endurance athletes, ultra-endurance athletes. I've worked with a few that are running crazy distances across mountains, and so on. There's huge amounts of issues here. Lots of scenarios, where muscle damage is going to be induced. Another thing that is an issue there is they can barely enough to keep up with their activities.
Not specifically energy availability type conversation, but we're about eating enough protein and about proteins sufficiency, or amino acids sufficiency. Because of course, in those athletes, there is a possibility that they may be under eating protein, particularly in the endurance athletes. It's an area that does require some convincing sometimes, that they should consume more protein relative to the other macronutrients. Is there anything there?
[00:56:57] KT: I mean, I don't know. Dan, maybe you do. I don't know of any studies showing that in a low-protein intake, that there's more muscle soreness in certain athletes. I don't know if I'm ignorant of anything. If there is anything out there.
[00:57:11] LB: I'm just talking about soreness. Just the process of the damage itself, which may not necessarily result in the symptom of soreness.
[00:57:21] KT: Sorry, I was using soreness as a catch-all term there. But, for damage, no. I don't know of any. Dan?
[00:57:29] DO: No. I think, the way I would look at it is first of all, it's unlikely to probably have any protective effect. Whether or not the muscle is going to be damaged, I think is independent of the protein intake. Kevin will tell you. I think we know anyway, that the best way to adapt to repeated training bouts is coupling, the training session with adequate protein intake.
If someone's not getting adequate protein intake, they probably haven't adapted that well over time anyway, or as best as they could. I mean, in terms of yeah, I would just back up what Kev said in that the studies that are out there, basically show that a start, that the protein synthetic rate between eccentric and concentric contractions isn't really that different at all. When protein, extra protein is provided in these studies, we don't really see any changes to mechanisms within the muscle. The best study I can think of, the most recent one was done from the guys down at Exeter Uni. Now they did combine protein with a poly phenol supplementation.
They've done the most in-depth dive into the muscle following damage to see what's going on. this was published after – only in the past year or so. Essentially, they showed that there was an improvement in the rate of recovery with the protein in polyphenol drink. There was no change in myofibrillar protein synthesis. There was no change to genes associated with inflammation. Those processes are unlikely to have contributed to that acceleration of recovery. I think that is the most in-depth study. Where we're at with this is you would never want to compromise adequate high-quality protein intake. It might help you recover quicker, but it's certainly not due to mechanisms that we can see directly at the muscle. I mean, that that's where I am with it anyway and what my understanding of present is.
[00:59:25] LB: No, that’s great. The reason why I asked simply is again, when you hear people talking about muscle damage and remodeling of muscle, one starts thinking about throwing protein at it. I think, it's quite clear that that isn't necessarily – what isn't what we believe is necessary. You've mentioned a bit before, you guys were delving into this issue of this balance between recovery and adaptation and repair, and so on.
This is where like as Kevin was saying, there has been quite a lot of interest in the role of things like antioxidants, whether we're talking the high dose stuff that you get in supplements, that are very much at supra physiological levels. Those are not levels found naturally in the diet. Of course, that's often how it's marketed, as being potentially a better solution, because it packs a bigger punch. It's going to wipe out those reactive oxygen species and so on.
Or, perhaps, we can go food first. We love using that phrase, food first. There are substances found in fruits and vegetables, like polyphenols, for example, proanthocyanidins and all those sorts of things that may potentially have a role here. Because you guys have talked about this, maybe we could just quickly just talk about this role of Cox-1, Cox-2 production and wanting to put the fire out and why that may or may not be a good idea. Bearing in mind, we are talking about athletes as well, where there's a point to this training.
[01:01:09] DO: You've alluded to the first point, which is that there are these functional foods, which offer some additional health properties above their basic nutritional value. They contain high levels of polyphenols. The most common are flavonoids and tannins. The same with the direct antioxidants. Vitamin C and E, which are the main ones that are usually touted. If we take all these things together, the reason that people tend to promote them in a exercise-induced muscle damage perspective is that they've got anti-inflammatory and antioxidant properties.
What I would like to start with saying on this is that these things should be the basis of a good diet anyway, because we know that, for example, with vitamin C and E, we have a requirement to get this from the diet. In that respect, we shouldn't be compromising these things. We absolutely need them in the diet.
When we're talking about high levels and using them to try and direct them at different components of muscle damage and recovery, that's a completely different perspective. What most of the studies on this area try and do is that, because of the fundamental way in which these different things work by trying to scavenge free radicals and potentially limit the effects of inflammation, that we say, okay, that's the basic mechanism. If we give them in these exercise-induced muscle damage studies, if we see a change, it must be due to changes in reactive oxygen species, or inflammation or so on.
Based on the evidence, and James Cobley wrote the part in our paper on this, which was really interesting to me and definitely opened my eyes to a new perspective on this was, it's really unlikely that the antioxidant properties of these foods are going to outcompete, first of all, our own antioxidant systems. It's also unlikely that they're going to accumulate at the right place at the right time, in the right quantity to take care of what's being produced. James also made a really good point, based on really sound theoretical knowledge that if for example, some of these antioxidants, let's say vitamin C and E, if they could accumulate at the site of, let's say, an inflammatory cell, which is engulfing what it needs to engulf, it's producing reactive oxygen species, it would probably facilitate the immune cell, rather than dampen any of the response. It's super unlikely that these things are having an effect in that direction.
I think, a pitfall with the research on this as well is that oftentimes, they remove a lot of the, let's say, polyphenols, or the amount of antioxidants that people are getting in the diet, right down to a really low level, so that then they're replacing it with a known amount. Whether these things actually have any effect on top of a well-balanced diet, that's another question in itself. There have been some studies that suggest, particularly on vitamin C, Graham Close here, that was some of his postdoc work with Malcolm Jackson, as Kevin pointed out before, and Carmen Gomez Cabrera published a long time ago, showing that potentially, high doses of these things might actually blunt the training adaptation response. Through what mechanisms? We're not entirely sure.
What seems to be the case is that from potentially modest effect on something like muscle soreness, there is the risk that you might blunt the training adaptation response. Throwing the kitchen sink at things when it comes to antioxidants and anti-inflammatory type stuff, I think is definitely not the way to go. You're probably more likely to have a detrimental effect than you are to have any positive effect.
My take home from all of the information I've collected over these years is that we should be promoting a polyphenol-rich, food first, eat a rainbow, all the different things that we talk about approach. I don't see there being a real need for having real high doses of these anti-inflammatory, antioxidant type compounds.
[01:05:36] KT: That's boooorring.
[01:05:40] DO: Yeah, it doesn't sell.
[01:05:42] LB: Yeah. You're right. When I read your review there, that section was interesting, because I didn't know so much about this. This makes sense. What's happening is in a specific area of the body and a specific parts of the muscle as a localized situation, is contained, so to speak. Because when you're ingesting these things, it's very much more system wide. We don't have heat-seeking missiles for these strategies.
If you only look at it from a very simplistic perspective, it's very easy to understand how those strategy, solutions have been suggested. Like you said, now that we know more, specifically with these techniques that you guys are using in the lab, it's obviously clear now that that's maybe misguided. Unfortunately, the supplement companies don't necessarily want us to know that, but that is very much where we're at.
Kev, there's a similar topic. We did a podcast, only a few podcast ago about omega 3s, which is very interesting, the emerging research in that area, particularly as it relates to things like muscle protein synthesis and hypertrophy and so on. Specifically, on this topic of exercise-induced muscle damage, what do we know about omega 3 polyunsaturated fatty acids, Kev? What should we take home from it?
[01:07:08] KT: The omega 3 fatty acids, as far as muscle damage goes, I think the main rationale for it is an anti-inflammatory effect. Omega 3’s fatty acids are anti-inflammatory. That's the main rationale. We did a study when I was in Stirling a few years ago in footballers. These were semi-pro footballers. we had a little bit of success in ameliorating some muscle soreness, as I said earlier in that situation. The interesting thing is, well I could say, the rationale is that it's anti-inflammatory. But, in that study, the indications, we didn't really see any amelioration of systemic inflammation. We measured C reactive protein, a marker of systemic inflammation, but didn't see any difference between when there was fish oil and when there wasn't.
We did see some more local effects. Through deduction and some – Jordan Philpot was the first author and he laid this out very nicely in the discussion, that there seems to be some sort of protective effect on the structural integrity of the cell membrane. Going back to this notion of that the omega 3 fatty acids are incorporated into the cell membrane. In this study, we had the supplementation for four weeks, I think it was. Might have been six. Anyway, several weeks before the muscle damaging exercise, so that would have been the case.
We didn't measure muscle biopsies in this study. We didn't have the wherewithal to do that. We did have the red blood cells, and that was incorporated in red blood cells on a time course, that the muscle biopsy should have – I mean, the muscle cell membranes would have had more. It looks like, from the evidence in there that whatever effect we were getting was in the cell membranes, rather than overall systemic anti-inflammatory effect.
We did see a decrease in leakage of this, of CK. One of the things that's always done in these – often in these muscle damage models - is you measure intracellular proteins that end up out in the blood. You get a leakage of creatine kinase and myoglobin and other different measurements. We did see an amelioration of that. That, again, would have been at least consistent with the notion that there was something going on in the cell membrane, that there was less leakage.
Now, CK is, I'm sure Dan can tell you that – I mean, we were getting – in some studies, we would get a 500-fold difference between individuals in their response to CK. It's incredibly variable. At least in this case, there was enough that there was difference between the groups. All in all, it looks like if anything, the omega 3 fatty acids are having some impact by changing the composition of the cell membrane. Again, these were high-level footballers. Not fully professional and elite, but they are high-level and training pretty hard. We did the same model, where we did the eccentric – really heavy, eccentric session that they would never really do in any real training or competition.
How to interpret that is again, goes back to how difficult it is, I think, to interpret some of these and to apply practically some of these situations. If you go back to what I mentioned before, the Katherine Black study, there was some amelioration of soreness in those elite rugby players over that training camp situation, pre-season training. How much that really helps them? I don't know. That was at least a more ecologically valid model to use, that's probably more applicable for some of the listeners, if they want to apply some of this stuff.
[01:11:21] LB: Also, a bit like Dan was saying, when it comes to previous conversation about antioxidants, polyphenols, and so on, we should eat a balanced diet, rich in colors, and so on and so forth. It makes me reflect on a overwhelming statement from our recent podcast, Kev, with Chris McCrory, about omega 3s, where he felt there just isn't really anything that would convince him that we should take supplements of omega 3s, apart from scenarios where you're not going to eat oily fish, or so on and so forth. Is that the same on this topic you feel, or not?
[01:12:03] KT: I'm generally against supplements, for the most part. Unless someone is exhibiting, y’know, some sort of – they just won't eat something. Now again, as we talked about in that other pod, in our culture, in Britain and in USA, people don't eat that much oily fish. They're certainly not eating algae to get the omega 3s from that. Regardless, why a lot of vegetarians say that you don't get a lot of transformation of the ALA to – or arachidonic acid to omega 3.
I do know, again, just from conversations with nutritionists with various rugby clubs, a large portion, if not the majority, of these pro rugby players are on omega 3 supplements all the time. Maybe that's why. I don't know exactly what the rationale is. I haven't got that far.
[01:13:02] LB: Oftentimes, I have an idea. That's partly, having worked with a lot of teams over the years. Young guys, young girls can be quite fussy athletes, can be quite fussy. Although it is true. Rugby players tend to be a bit more disciplined in doing what you ask them to do. Even when they're away from the club, whilst you can't see what they're eating, there is this mindset of well, for insurance, I'm going to give them some omega 3s at the clubhouse, because at least I can be sure that they're getting them in, is probably the mindset there.
What I'm hoping is the listeners don't all start rushing out and buying antioxidants, rushing out and buying omega 3 supplements to help deal with this problem, because that isn't necessarily how they should be looking at this.
[01:13:55] KT: I mean, again, I think if hopefully, a message is getting through. Dan said it several times, and I've said it, you said it, food first. Eating a diet with fruits and vegetables with lots of polyphenols and cyanines and tannins, etc., and vitamin C and vitamin E. I don't see how that's a bad thing. Adding lots of supplements on top of it, not ever going to be a fan of that, or if I can't see it. I mean, who knows? Skeptical, but open minded as you know. I don't see it. It just doesn't make any sense in a lot of these situations.
Yeah. Hopefully, you get two messages out of this podcast, which is, yeah, food first. Let's get the diet right, before we start worrying about these supplements. Second, adaptation and recovery aren't the same thing. You got to think about what your goals are. If your listeners go away with those two messages, I'll be happy.
[01:14:52] LB: Yeah. Just because you can find them in supplements, it doesn't mean you should be going out of your way to avoid them in your diet. Needless to say, there's lots of things in food that we get, in addition to these things that we need.
[01:15:06] KT: There's lots of other things in supplements that you get too.
[01:15:09] LB: Exactly. Potentially. Yeah, it's a whole nightmare in itself.
[01:15:13] KT: If you’re taking a high dose of something, you're also more likely to be taking a high dose of some banned substance that might be a contaminant in these things, too. There's another reason to be leery of supplements, which got another big one, their paper out a month or so ago, again, coming out with that message. It's been for 10, 15 years, there have been several these papers coming out with these contaminants. You think these people would learn.
[01:15:40] LB: Yeah. You'd hope. Now Dan, there is a potential exception to this rule of not needing supplements. That would be potentially, the vitamin D, vitamin D, for those on the other side of the Atlantic. What about vitamin D? Now, we've done, of course, a podcast, Dan, where we thoroughly delved into vitamin D. It's an area that you've spent a lot of your time researching. I do recommend everyone listens to that podcast. specifically, with regards to the role of vitamin D in exercise-induced muscle damage, what do we know? As I've just teased, where might there be an argument for supplementation on this particular situation?
[01:16:28] DO: Okay. I mean, with regards to the need for supplementation, as you say, we covered a lot of the details in the other podcast. I definitely encourage people to listen to that for the ins and outs. Essentially, for those of us who live, or live further and further away from the equator, for more months of the year, we're going to see less sunlight, which is the direct mechanism where we're getting most of our vitamin D from.
There's plenty of evidence to show that for many months of the year, if you don't see enough sunlight, you'll have low vitamin D levels, which are associated with a number of adverse health outcomes. During the winter months, in particular, at least where we live here in the UK, we do champion the idea of having a daily vitamin D supplement of around a 1,000, 2,000 international units. That correct deficiency and keeps you in the adequacy zone.
In terms of its role in muscle damage, I mean, there are only a few papers, which tend to show a positive effect on recovery. One of my papers was one of those. We saw an enhanced recovery of force in the later stages of recovery, of the recovery process. 90, set 40. I think it was 48-96 hours between those time points is where we saw the main benefit.
We also did some basic cell culture studies on that and showed in a roundabout way, that we're seeing some effect of vitamin D on the ability of our muscle stem cells to fuse to one another, and to produce muscle. We can't say that a direct mechanism, but it could be one of the ways in which vitamin D might be having an effect on muscle.
There is also the really understudied side of this which is vitamin D in the immune system. There's considerably more evidence on vitamin D and its role in innate and acquired immunity, than there is on direct muscle studies. As an example, we know that our macrophages, that the cells that come in after neutrophils to help out with the muscle damage and start to get rid of all the mess, they can directly synthesize and activate vitamin D from the correct precursors. They also have a vitamin D receptor to be able to utilize it as well.
Vitamin D can act as a really important regulator of our immune system, and enhances anti-microbial activity and so on and so forth. One area that I would like to see more research done on and hopefully, we can do some of that going forward in the future, is to look at whether vitamin D plays a modulatory role, not essentially dampening the immune response, but making sure that if you're vitamin D sufficient, that that immune cascade is doing what it's supposed to do.
Because I imagine that if you're severely vitamin D deficient, there's going to be some negative consequences on the way the immune system acts in response to muscle damage, as it does in other areas of the body. The evidence is, I would say, moderate, but certainly, with regards to making sure that your vitamin D levels are sufficient, the evidence is really good. We need to make sure that that's the take home message. This isn't an ergogenic supplement, by any means. All we should be trying to do is correct for a deficiency.
I've seen so many papers, which have got this poor research design, where they supplement people who are already vitamin D replete. I can’t understand why we keep seeing these studies and why people think we're going to see some additive effect. For anyone who's out there, students who are going to go into this area, please be critical of that and try and design studies where we're looking at people who have vitamin D deficiency to start with and looking at the effect of that.
[01:20:20] LB: Yeah, it's a fascinating topic, isn't it? We've certainly done a podcast on that. Kev, let's move on to one of the last areas that I wanted to cover, because we are running out of time here, or we're close to run out of time already. Creatine monohydrate is a popular substance, is used by huge numbers of people. When you start thinking about strength, power, hypertrophy, and so on, often creatine monohydrate has been seen to play some beneficial roles. As far as you're aware, is there anything here that argues a case for creatine monohydrate and exercise-induced muscle damage, Kev?
[01:20:59] KT: I don't think there's a great deal of information really. I certainly haven't seen anything that's convincing to me. I think Dan, y'all touched on it in this review a little bit, but I wasn't familiar with those studies at all. I wouldn't go crazy with it for a muscle damage situation. I don't know. I don't see any rationale for that.
[01:21:24] LB: Yeah. Great. Right.
[01:21:26] KT: I mean, people are using it all the time with resistance exercise and training anyway, so a probably moot point.
[01:21:33] DO: Yeah. Those studies that we cited are using the same doses that you would use anyway for creating loading. Yeah, it's almost a case of well, there's no need to do more than you might already be doing if you're taking creatine anyway. Yeah, I think the evidence base for actual direct effects on muscle damage and repair is too limited to make any conclusions.
[01:21:58] LB: Dan, you guys have an excellent, a practical set of considerations, where the focus is very much on being pragmatic about this, which course is spot on with where we're trying to take this conversation, because, of course, it's about looking at the science, unpacking the science. What do we know about exercise-induced muscle damage? Ultimately, what we're interested in here is, what can we do about it from a nutritional perspective? From a practical perspective, what are your final points on this topic?
[01:22:33] DO: Well, I think one of the key things we have to stress first is that food first approach as a baseline. That's not a food-only approach. I’d make that point. We're not saying that there's absolutely no need for supplements, whatsoever. We should be basing this around getting plentiful supply of micronutrients from different sources in the diet. We need to as a practitioner, you should be first of all, just making sure that the athlete is trying to meet these nutrient demands from having a very rich and dense diet.
Then, in terms of intervening with the exercise response, we have to bear in mind that for the normal training session, the normal block of training, as Kev alluded to before, I don't think there's any need to be doing anything extra to try and ameliorate any of the effects associated with any of those sessions, even if muscle damage might occur, even if there is an eccentric components, even if there is some muscle soreness.
I don't think we need to do too much to intervene there, other than ensure that we're on point with all of our basic nutrition strategies. At least in our paper, where we show the conceptual region, where you might want to intervene, is where the dose of exercise stress is very high. That could be in a tournament situation, where you have – you're repeatedly going through these very strenuous exercise bouts. In that situation, you would be trying to recover as quick as possible.
In those certain situations, you might consider things that have got a higher evidence base. There's no real detriment to using some additional cherry juice, for example, pomegranate juice, which are higher in these polyphenols and flavonoids and tannins, and so on. You might get an amelioration of some of the detrimental effects of that high exercise stress. In those tournament situations and repeated high-dose of exercise stress, that might be where a practitioner would intervene with some of these extra things.
For the most part, I honestly think that nailing all of the key things that we've talked about, making sure that high-quality protein distributed correctly across the day in the right amounts is key, making sure that energy availability is where we need it to be, making sure the guys are all vitamin D replete and having a very rich and varied diet is where we're going to see the best benefits. That's going to support the recovery process, the adaptation process, the best anyway.
If people want to see a visual representation of that, on the last page of our review, I think it's figure 2. You can see how we've tried to visualize that and where you might want to intervene. If people want to follow that, I think the paper’s open access. If not, we can send you a copy, no problem. Yeah, I would just encourage people to have a look at that, have a look at that figure and see what they think. Yeah, that would be my take home messages really. Just consider, as Kev said before, that balance between recovery and adaptation. They're not the same thing.
[01:25:41] LB: That's brilliant. Dan, actually, yeah, it's not open access, but there are copies on the university repository. I'll link to those, so they got those, because that is a nice diagram. Actually, before I let Kev have the last word, which is always the right way, I just wanted to come back to something I did want to talk about briefly. That’s this concept of the hormesis theory. Why actually, that is something that you've referenced here. As it just so happens in the blurb under figure 2, you talk about the framework for the hormesis theory and the context and nutritional intervention. Just quickly, what does that even mean? Why is that actually an important concept potentially?
[01:26:26] DO: Well, it's essentially what we were just saying there, that with different biological phenomena, you have this bell-shaped curve, really, where a low-dose of exposure to something potentially stressful is not going to really do much, by the way of adaptation. With increasing amounts of exposure to that challenged homeostasis, you're going to see an adaptation. With too much of it, you're going to see negative adaptation and negative consequences. That's what we're getting out with this curve of, I guess, the dose of the exercise stress and the adaptive response. That's where we've tried to superimpose where nutrition might overlay on that and where we might conceptually be able to have some effect.
[01:27:12] LB: That’s a great illustration of that phrase, or use of you can, but should you? Yeah. Awesome.
[01:27:18] DO: Absolutely. Yeah.
[01:27:19] LB: Kev. Do you have any final points then, you want to raise here about our conversation today? Any thoughts, things that we may have missed, or you wanted to quickly bring to the –
[01:27:30] KT: Maybe not miss so much as re-emphasize again, applicability of the results from these models needs to be very carefully considered. Maybe in the future, we might want to do – change the model a bit to more like what I mentioned before, Katherine Black's where she actually did it in a training camp with elite athletes. Also, think about some of the studies that well, Olly did one when he was a PhD student. We really ramped up the cycling, the stress of as in a training camp for a week, we doubled their, or we tried to double their workload. In that case, it was high protein. Asker did a few studies with a similar model with high-carb and others.
Maybe those are more applicable, or more easily applicable situations that we can apply to looking into these kinds of interventions, to see how effective they are. With the caveat, with the understanding of the overall, what we're talking about this, the hormesis is a potential downside of this, that we're doing this in his particular situation for a particular reason. Not just this blanket, “Hey, we're training hard. Let's all take this stuff.” Hopefully, we beat that horse to death and people will take that home.
As far as these individual supplements go, I think Dan touched on it nicely there is that, yeah, maybe there's some idea about some of them. Mostly, I think, again, if we can just emphasize eating. The first goal needs to be so many people, athletes are suffering more from not eating properly overall, than they are from not having the right supplement. I think that's, I think, all the practitioners I've ever talked to, the best in the world, they've always told me that.
[01:29:23] LB: Absolutely. Well, listen guys, I think we've had a – I personally have really enjoyed this conversation. It's ironed out some creases, I feel that there are in this topic. You guys have done a great job, helping me and everyone else get to grips with what is essentially quite a complex topic. I look forward to bringing you back down again, but on this topic, specifically. When we know more, it'd be great to repeat this conversation and see if we're any – if we deviated at all from any of the things that we've talked about today, which will be fascinating.
I will put links to the paper. In fact, several papers, I think they're of interest here, the various podcasts that we've done with you, Dan and Kev and links to how people can find you and so on and so forth.
Without further ado, I'd like to say thank you, Dan, thank you, Kev, for your time. I'm very much looking forward to bring another podcast back in the very near future. Take care everyone and stay safe.
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