#68 - Muscle fiber types revisited with Professor Wim Derave

hello and welcome to inside exercise I'm ameritus Professor Glenn McConnell from Victoria University in Australia and I'm also currently a Danish diabetes and indine Academy visiting professor at the University of Copenhagen in Denmark the idea behind inside exercise is to bring to you the absolute who's who have exercise research so exercise physiology exercise metabolism and exercise in health and what I really want is for you to get your exercise research information from the research experts rather than from influencers and indeed today I bring to you Professor whim Dava from gent University in Belgium he's an

expert on muscle specifically muscle fiber types and muscle adaptations to exercise he's doing some really interesting studies that are challenging our prevailing view about muscle fiber types so we tend to think of muscle fibers in humans as being of three types so type one which is slow twitch so slow oxidative which is good for aerobic metabolism and then the fast twitch fiber type 2A which is fast oxidative glycolytic so has aerobic and sort of anerobic Sprint type performance and then type 2x which is your fast glycolytic which is not very good at aerobic metabolism at

all produces High forces and is very good at producing lactic acid now in very interesting findings wom is showing that most people have no 2xs so no 2x muscle fibers at all so this is very interesting whim makes the good point as well that that we don't really use muscle fiber type enough whim talks about how in the 1970s and ' 80s people like David costal and Bank saltin who are legends in the field of exercise physiology were using muscle fiber type for talent identification Etc but he makes the point that we haven't really progressed

on from that and there's very little use muscle fiber type so as he says there talent edication but also he's got evidence that the likelihood of having hamstring strains is affected by your muscle fiber type that you can potentially use it for tapering and perhaps overreaching so he's saying a lot more work needs to be done to use muscle fiber types more optimally he also talks about non-invasive ways of estimating muscle fiber type and then towards the end of the chat we talked about something very different which I was totally unaware of which is the

fact that antihistamines May reduce your responsiveness to training so if you take antihistamines you not may not adapt as much I found it really interesting I think you will too so stick around now what I wanted to point out to people is that um you'll see in the notes so whether you're on YouTube Apple podcast or Spotify or whatever that I have description of all the different things we talked about and next to that I had the time that we spoke about it so obviously I encourage you to listen to the whole thing but if

you wanted to you could skip around a little bit what I tend to do is start off with the basics and then we get more complicated as we go so you know if you don't want to hear the basics you can look at the timestamps and go straight through so if you're on YouTube you can click on the time it will take you to that point but on Spotify Apple podcast Etc the timestamps are written there but you just have to take note of them and then fast forward you can't click on them the other

thing is please um do me a favor by liking subscribing also uh leaving some comments if you're on YouTube that all helps to get the message out hi whim how are you welcome to inside exercise how you doing fine thanks by yourself yeah good it's great to be on this on this series of of talks I I really um look forward to it because it's a very prestigious lineup of all kind of scientists I have looked looked up to and and admired over all the years so it's I think it's a great initiative thanks oh

thank you very much I think you're the fourth one in a row um talking of of prestigious scientists so we had Eric RoR who was your PhD supervisor on a couple weeks ago yes and I think you're the fourth one in a row that's had link to the University of Copenhagen we'll probably probably get to that soon all right so what I like to do at the start is get a bit of a background on you and ask know you like a scientist who then took an interest in exercise or were you quite quite often

I think probably on average most of the people I've had on were sort of sports types exercise types who then thought oh I can actually study this what was it like for you well I was I was a a sports uh person but not in a in a in a high performance level in any way uh was a bit of a generalist I would say um but the thing is that uh very early in my sport science studies I I really got intrigued by um by physiology um and already during my students period in my

third year I I had an erasmic ex arasmus exchange to Copenhagen so then I I first got to uh well was yans bangsbo who was my teacher for exercise physiology and so on so I was I was intrigued even more and then I mean after I graduated I started in a in a PhD and I immediately knew that I had to go back to to Copenhagen to do some some real science and so I ended up with Eric RoR which who it was um it was a colleague from Len Peter hasel who advised me who

was also been a post talk with Eric to go with him um and I mean I I really think that this has been one of the most defining moments from for my own career yes so some people would have seen I've mentioned that I'm actually doing my fourth research visit with Eric so he's he great and the methods you can do and things are amazing all right so we're going to talk about um muscle so we've had had some talks about uh blood flow the last couple we had Ilia Hanson two two times ago talking

about blood flow and muscle and we had V2 Max with um Jose calar and you know capillarization and fiber type and things got mentioned here and there but but not really you know thinking more I guess about sort of central like blood delivery and things but not really thinking about the fiber types so today we'll be talking about the importance of fiber types and we'll get into some really interesting stuff you've been finding for example that there may be only be you know realistically only two types of muscle fiber in humans rather than pardon in

humans yeah in humans exactly H compared to other species and we'll talk about all that but why don't we just start off you know before going too hard to give a bit of a background so a lot of people would have heard of you know a that person's fast that probably fast twitch in that person's endurance I think theyy slow twitch why don't you just tell us what are the different fibers in humans and and what do they do and why is it important yeah so so we can well scientists and even non-scientists have always

seen that there's different types of of meat or or muscle so to say there there's red and and and white muscles that you can find like in in chicken or in doves or whatever so we've always SE that there's different um types of muscle it seems that within within organism this also can differ like our the the muscles that are important for posture and for balance keeping that have to be active for hours and hours a day up to eight hours or more uh they are also from this for this from this rep R muscle

or slow muscle and then you have this more burst like activity muscles who can produce much more power but they are uh also fast fatigable and and this is the white muscle so so we've had this in the animal kingdom and and we we clearly saw this also in the in the humans not so much the color but when you have specific techniques to stain muscle fibers we could EAS see that there was a a mixture a mosaic of white and red fibers or the the fast twitch and the slow twitch fibus yeah that's that's

very interesting I I often use the example of you mentioned the chicken so you know chicken walking around all day um you know their thigh muscles are more sort of red um and even more oily so you you may talk about how there's more intramuscular fat and things in in those sort of red slow you know less fatigable type muscles and then the then you know if they get a fright or something they they fly for about you know five seconds then drop to the ground and that's the more the um the breast muscle which

is very white very dry not very fatty and you're saying that's the fast which they can produce a lot of force lot of power but they fatigue quickly yeah and you also see that between species so so you have this entire species that are fast TCH and entire species that are slow ttch um um so that is I mean we we we see that this specialization towards speed for example in a cheetah uh which can produce fantastic speeds for a couple of seconds only and then these other animals like migrating birds who can uh produce

the same Force for days without fatiguing so so that that is really something that has been observed consistently in many species yeah yeah and why is it that um because I guess we're going to talk about how humans tend to be 5050 but it can depend you know like sprinters will be more fast twitch and Jance will be more slow twitch why why is it that this that the the species differences obviously okay cheat has to be fast as you said migrating bird has to be slow but why is it that we have more sort

of 5050 how's that worked out do you think yeah we have 5050 but actually we are slow we are slow T endurance species um there's almost no other land animals that have so many fast fibers even if we we would have about on average 55% of these slow T fibers uh all the other big Apes would have uh 70 80% uh fast fibers and if you go to antilopes and all the big cats and so on they they have like 95% fast fibers and so on so so we are really a slow uh species or

an endurant species and that is something that uh I think most people uh don't really realize but we kind of in course of evolution we have decided almost to to make uh a strength or or a talent our our endurance a talent and it's it's it's even more than a talent it's a weapon um because we hunt down our prey before even before we had weapons and and we were hunter gatherers we just ran down our prey for hours and hours especially in in hot um climate as in Africa where where life for us started

um we can run down every animal from the Savannah as long as we keep doing it for hours and hours we the fact that we don't have hair or fur or it's it's all part of this machine or this fantastic weapon we have that is endurance so we as a species should really look at ourselves as a a slow slow specialist and um an endurance type of of animal okay I'd heard I'd heard that I remember with the they were talking about with the Australian Aborigines they could Chase maybe this is wrong the thing I'd

heard was that they could chase the animals chase the animals and and then the next day they'd be like sore the animals would have you know muscle sess and then they could grab them but you're saying you would actually wear them down over hours so um the muscles as you said most animals have quite a lot of fast fibers so they tend to fatigue and and we would wear them down and then and then grab them or stab them yeah pick them up Pi pick them up they are completely exhausted and and fatigue it's probably

a combination of of fatigue and uh heating um so so we have we have more um SWAT glands per square millimeter and we have uh a very good system to to sweat and so on so so where other animals uh would have to take a rest in the shadow and and and cool down we can keep on doing that so this is this is really our strength we can run marathons in in the Heat and if you would do a an Olympic Games and all animals can take part and you do it in Nairobi for

example we would win only one discipline that is that is the uh we are lousy in in speed and and when you're lousy in something you you can as well forget about it like in school you're you're good in in Ms and not in languages then then skip the languages and completely specialize on the MS that's what we've done we we realize that we we are really bad in speed we can't even catch a single animal by hand I mean we cannot even catch a rat or Mouse we can we are super slow and then

we said okay let's uh let's specialize in this in this low twitch thing this endurance thing this is really what we are this is our middle name um and that is something that to me is also the reason why we are losing the the super fast fibers we are we are dropping that part but we can go into that later yeah yeah we will we can't help talking about the marathon and mentioned I don't know if you saw Calvin TP kiptum two hours two hours z z minutes and 35 seconds yesterday in Chicago which is

just yeah and then two weeks ago in the the women's marathon it's it's really amazing that's that's probably one of the uh most um typical activities for Homo sapiens to do all the rest is a little bit artificial and so on but I really like that the marathon is the last um event in the Olympic Games and that's the one where the where the medal has given at at at the closing ceremony it's the most important discipline in sports it's it's what we are as a species is is this endurance running that's that's really how

we Define ourself and if we ever skip our name because we call ourselves Homo sapiens but I'm not sure with all things that are happening in the world whether it's so smart uh so if you want to drop the stapan name maybe we can uh we can bring something in about running or Marathon or whatever because that is what we that really defines us as a species yeah so what about you know we have to survive and reproduce so survival can be wearing down an animal to get the food yeah um but what about getting

away from prey surely that's important so you know sprinting to a tree and building up your lactic acid and then recovering in the tree and hoping the cheetah can't climb up and whatever you're saying we're not too good at that and we just didn't evolve that way we used our brains to yeah yeah I mean there was this there was this story a while ago from it was on on the BBC News website of a a Kenyan village where there was uh cheetah actually messing around with with the with the goats that well taking goats

from this farming Village in in Kenya and uh they were fed up with that and they said well but let's run after these cheetahs which makes no sense of course they are so fast but what they did is the whole village and children and everyone with with uh just by by being uh in in a majority they they they made the cheetah go away and they started running after them and after a few kilometers they could just pick them up from complete exhaustion so that is really what we what we still do um not so

much and not so often of course uh but uh this persistence running or persistence hunting is has been something that is done up to today there's even a documentary of BBC of David atenor where he explains this um this persistance hunting that's still happening in the S people in the south of Africa so there it's still it's still actual even in in in mhm in groups that don't have weapons or whatever you can still run down animals um quite easily so slow is our is our solution to okay and as as you said we we'll

talk about the you know the the intricacies about what sort of fast which fibers we have but if we just been up till now we've been talking about slow versus Fast how much of that is um are you born with and how much do it change because I mean along the way there was a lot of talk about how cently change whatever you're born with that's pretty much it and my thinking I guess was always that you could change it maybe a little bit so um but not massively if we talk about slow versus fast

and then we'll talk about the the 2A and the 2x's later how much of of the endurance so Calvin kipped him if he's you know running two two hours and 35 seconds and we biopsied him and find he's 80% slow twitch would he have been born that way or would he have been maybe 65 and then a little bit changed 80 or yeah there's no there's no consensus really uh it's quite difficult to to prove that um because what what you do is you have to take a biopsy and that's a very small piece of

muscle it's 100 millgram or 200 milligram it's a couple of hundreds maybe 1,000 fibers of for example U veps or vus lateralis and that vus lateralis would have like half a million or one million fibers so you take a very small piece of that and there you count the number of fast and slow fibers um and then a couple of weeks of training later you do that again but then you have to take a different part and then just by random methodological variation that that can be completely different so we've done studies where we did

uh four biopsies um in in one person and then you can really see that that there's quite a a big variability it can change 10 20 30% between one biopsy and the other so that makes it really difficult to to study this question can fiber type change and for that reason probably there's still no consensus there's still no agreement on whether it can change um what we know is that for for example the twin studies indicate that monozygotic twins so identical twins they have mifiber type composition that is much more likee than uh diotic Twins

or non-identical twins so we know that heritability is playing an important or really important factor here um that's said I think there's some cross-sectional um data that indicate that it's probably can change a bit like you say maybe a 10 20% can change for example when we look at the upper body of swimmers muscles in the upper body deltoids and so on they seem to have much more slow fibers than an average person and and that that is very difficult to explain that that would all be um um because it we don't see that in

the leg so so it seems to be something that is adapted uh along the way uh so I think there's a little bit of shift that can be done but you cannot move from one end of the spectrum to the other so you cannot make a a race horse from a farming horse and the other way around and uh so so you have a little bit room for for change probably uh but not so much the other thing is now I guess it's making me think a little bit because you were saying the variability between

biopsies but I remember when I did my masters with David costal uh he did one where he did like eight biopsies and he found that you know if you just did one it was very variable and then if you did two you know it dropped off and then it became slightly better so if you assume that eight biopsies was correct you know the percentage you got then the biggest drop is from one to two and then it was was dropped off a bit but as you say most people probably just do one biopsy before training

one after training Etc but I guess one stage David costell said he thought if you had 65% slow totch fibers then you could pretty much do whatever you needed to do you didn't have to be like basically he was looking at all these marathon runners way back and he wasn't finding that oh the ones that were better had you know 80% than than 65 and then a if you've got 65% you won't be as good as someone who's got 80% he kind of felt like if you had 65% you could probably pretty much do whatever

you needed to do you didn't have to have like oh I've got 68% I'm going to be quicker than you you know what I mean yeah um that we also saw that in in our study where we did non-invasive um measurement of of muscle topology we we saw that uh well International level or or like National level endurance Runners we saw like the same muscle topology but for sprinters we did see uh so there it seems there's seems to be no limit the more fast drivers you can get the faster you will become uh but

whereas for endurance running it's not really the case but if if you see M for for example um he runs 400 meter in I don't know 50 seconds or so so you cannot do that on pure slow fiber so the whole thing about this endurance running it's also it's become a really fast event in the end uh and you can oxidatively train your fast fibers so you can make them have a lot of um mitochondria um so it's it's true and we also saw that in our data that um the the the more the better

only counts for the first end of the spectrum okay so so so with fast with the sprinters the more you have the better but with the endurance if you've got at least I don't know you know 65 I just pulled out of that that shouldn't be much different but but as you said another point was that the the your fast fibers can become more aerobic now I guess we're we're starting to get to the point where we need to store talk about the types of fast fibers because if you're talking about the 2x which is

the fast fast that's probably not as much of the case as the two A's so what don't you tell us um about this so yeah we've always been and I was saying to you before we started you know that when I learned it it was always you had type one you had type 2 a and you had type 2 B and then it became 2x um why don't you just tell us I don't know the difference between 2B and 2x I guess to start with and then talk about you know the the what are the

balances of type two fibers and and how you think there really only probably two types in humans yeah so so the the first studies in the 60s and 70s of the last century a lot was done in animals in in rats and also in cats so if you look at the at the motor unit so you have a motor neuron with a lot of fibers all attached to it which are fired by this motor neuron then you have this motor neuron in three different types it's called slow then fast um fatigue resistance so fast resistance

so to say and fast fatigable um and then we if we look at the muscle fibers we saw the same it's like slow and then we call it fast oxidative glycolytic and we call fast glycolytic um but that is in animals um and for some reason we have always thought well it must probably be the same in humans as well um and we started staining fibers based on on a method which is called atpa staining where there's an enzyme which is uh labile for for acid or base uh environment and by like destroying this enzyme

in an acid or in a base we could see the difference between fibers and there was if I look at these pictures I always think it's 50 Shades of Gray it's a bit of it's a Continuum of a bit of everything but then after a while um the technique became more molecular and what we looked at was mein heavy chain mein heavy chain is a is one part of of the muscle fiber or the sarir that actually produces Force it's like a power stroke that that is produced by by this head of the misin molecule

and we could see that this comes in uh different um versions and actually in in rodents we saw there was or the scientist saw that there was four types it was type one type 2 a type 2 B and then there was another one type 2X and it it appeared to be in between Type 2 a and type 2 b um so that is um how it works in in rodents and then we checked what is actually present in humans and there we saw uh the type one and type 2 a myin was there but

type 2 x was there and type 2 B was not there so we we still have that Gene uh but we don't express it um so the four basic misin based fiber types that are in in rodents uh we only had three and we had to rename type 2 b2x because the B was already given to another protein which we in the end didn't have okay can I just I guess summarize that yeah so okay so we're all good with type one yeah and which is the oxidative which is the slow one yeah but then

you've got your 2A because we're sort of change we're switching around a bit terminology so 2A I was saying was was what you were saying was the fast um oxidative so it's got the it's a fast it can produce a lot of power but it also has quite a lot of mitochondria it can use aerobic metabolism and then you've got the two B yeah um which is which is which is a very quick contraction and you're saying that the the mice and rats have that that's your fast glycolytic yeah yeah but we don't really have

that we have one that which is 2x which which the Bon rats have as well but it's not as fast not as glycolytic yeah yeah so we don't have the super fast where we have the uh medium fast and and the normal F to say so so we don't have this super fast anyway so this already shows us that that we are a bit moving away from speed as an important uh thing for for evolution so sorry were you saying that with so the 2B which is the super fast which is in the the rodents

we did you say we actually have the gene for that but we don't express it that's interesting that's correct that's correct and and my point is that also for the type 2x we have the gene and we some sometimes express it a little bit uh but we we we are getting rid of it also so we're moving away from we're dropping the fast the super fast fiber types we lost the type Tob and now we also losing the type to eggs because if you do physical activity you actually silence the you suppress the expression of

type 2X and then a phys Al active person uh usually we don't see any typ to act so so the way to get rid of this super fast fiber type the way we do it now is is simply to suppress it by physical activity and we know that in in the past 100 thousands years uh hunter gatherers have always been active so always suppressing the type 2x fiber type which means that uh for the yeah best 100,000 years we have survived with only two FIB types because we were suppressing the third one now sometimes we

see in biopsies that there is type 2x expression but that is mainly in people that are have a a low activity level or for example spinal cord which is an extremely low activity level which means complete paralysis so we only we failed to suppress the super fast fiot type if we are too sedentary or or sick but in a normal functioning human body which is physically active hunter gatherers farmers and so on uh We've we've probably uh completely supressed that that fiber type and even there's one one of the most typical genes of these super

fast fibers is actin in tree uh we I mean 20% of world's population already have a knockout of acting in three so I think we were in the process of losing it completely and if we would talk to each other and 100,000 years maybe would no longer recall that there that there was an intermediate period where there was some dop direct expression now and then so so you're saying it's only really sedentary people the people or as you said spinal cord injury people that actually have the 2x fiber and we're meant to be hunters and

gatherers we're meant to be Physically Active even doing a 10,000 steps you would not have that fiber you would only have the slow so type one and the 2A which is your fast oxidative glycolytic so that becomes really interesting because it's hard it's it's just like a total flip right because I've always I guess or for me anyway I've just always thought the pure sprinters are going to have the two x's because that's you know they don't want to have fast oxidative they just want to have fast glycolytic yeah and but but they actually losing

it and and it's it's interesting to say that because because I've done some of that Myas and atpa staining so with the acid the acid you where so people may be familiar with this where if you look at a cross-section of a muscle you see that there'll be all these white ones and some black ones the black will be the slow and the white will be the fast and then as you say I guess the Shades of Gray but the ones that are intermediate we'd always call the two well we used to call them two

B's but two x's here and then You' find if you exercise train you wouldn't even find those anymore hardly they'd be gone so so the idea was that 2x's would get a 2 a and that's you there is yeah that's well not everyone will agree with me um but there's a bit of controversy in the literature on that um what we know is that the physical activity uh and training suppresses the expression of type tox that has been I mean repeatedly shown if you do cross-sectional studies on athletes uh you usually well you will not

find type 2 x fibes in in endurance type athletes and usually will you also not find type 2x fibers in in well-trained uh Sprinter or power athletes there's been studies on on Elite weightlifters well world class weightlifters they have 70% fast fibers but none of those is type 2x pure so so um there is only one exception in the literature and it's it's mentioned a lot it's from the traes group um showing that the biopsy of G injection had 30% type 2x fibers um which unarguably is is a top talent of course so I don't

know what I mean it's a case report of course but but most studies would show that well-trained uh Sprint and power athletes will not have this High number or will have zero type direct so so I don't know how to place this this analysis and and that that brings me to to another ideas it's very difficult sometimes or there's there's um problems in how to define a type to X fiber or or pure type to X fiber so to say because the techniques that we use um are usually uh semi-quantitative or or just qualitative so

what we've done in in a more recent study now with proteomics um in collaboration with with a group in Copenhagen from Atul deshmuk um proteomic allows to do a quantitative comparison of how many 2 a and 2x my you have and there in the pipes we could also see no fibers that have in a quantitative measure more type 2xg than type 2 a protein um so so that is probably the reason where there's a little bit of controversy in the in the literature how do you define it like 2x fi and a pure or a

hybrid or whatever that makes it a bit complex so the proteomics just so people know is it's a lot of omix is nowadays is a ways to measure all sorts of different changes in in muscle for example um so proteomics you'll basically look at all the proteins in the muscle are you saying they're doing that on single fibers or pulled fibers or the whole muscle yeah so we do that on on single fibers so so we have a a study now um where we collaborated with with the group of Atul deshmuk and and um we

did we developed or optimized a method for single fiber transcriptomics and they at the same time in the same uh period developed the technique for human muscle fiber or single muscle fiber so not pulled pure single Fiber One fiber yes it's one fragment of a fiber it's a few millimeters long and it's it's 50 micrometers thick um and do the whole transcriptome or the whole proteome which means measuring all the MRNA that's there all the proteins in just one fragment so we optimized this to do it on a high throughput rate and we did it

on a thousand fibers mRNA and dat a thousand fibers for for proteum and we came to the same conclusion that um that type 2x fibers uh don't really classify as a separate fiber type when you look at all the genes or all the proteins wow okay now when you um were in your Tweet and in your paper and also is it Kevin Mara how do you say Kevin uh yeah he also sent a tweet in response to me saying I was having you on saying that that they also find uh very few pure 2x fibers

it made me think remember way back like 20 years ago I think it was like Eva blomst I think it was was was looking at coexistence of different fiber types basically within each fiber yeah is that is that right so saying that that when you look at a fiber it's not some will be just pure type one some will be pure type 2A for example and some will be like a hybrid and she went through and looked at them all is that still considered to be the case so so that within the one fiber you

can have more than one type of thism and heavy chain yeah there are some indications that along the length of the fiber that it can maybe change um this will probably not be the main reason where where why there there is this coexpression that we sometimes have so we have like pure fibers we see that on the proteomics my transcriptomics and then we see some what you would call intermediate or or hybrid fibers who are a little bit on on on the on the crossroads of of the different types um and it could be indeed

that this is because the fiber type changes along the length of the fiber or it could just be that there's a combination of of um proteins that are are expressed what we also did is is look at not only M heavy chain but also for example you could do a fot typing on tropen T C or on cira or on tropis uh and because they all have a fast isopor and a slow isopor and what we see is if we have a a fiber which is fast foring heavy chains usually also fast for troping and

troping light chain and so on so it makes sense that I mean it's like with a car you know if you want to if you want a fast car make all the elements of your fast fast and and just not have one one wheel of a of a of a slow car on on there so you want the whole machine to be to be consistent but still we see that about 20 to 30% of the fibers uh have a deviation from that they may have a fast M of fast trop and so but then for

example a slow Circa so so I think there's still a lot to to discover there on on how this actually is um is functioning this slow versus Fast machinery and in a muscle fi wow okay so that's interesting so you're actually saying the C existence so with Eva bom blom's paper it would be like she'd take a biopsy and you're saying if she sort of had could almost could be like one end of of different ends of the same fiber could be you know of the same fiber you could have bit slow come up slow

one end and 2 a the other end so you get this coexistence that's that's hard to kind of Imagine yeah it it doesn't make any sense because you want you want to Contracting fiber to be consistent right you want to don't be don't want to be so we don't really know what is there but it has also been shown uh quite recently in in rodents where where you can actually see these regions with with different expression level um so that is something we'll have to to have to iron out in the in the next couple

of years what what actually is is going on there hey I was just thinking you sent me um you've got this resource that you make available to people on on fiber types and and we'll get to it a bit later on about how you know how you can you apply some of this understanding um and I saw you had the sloth so you know if someone's lazy you call them a sloth yeah because they do tend to just sort of sloth up there in the tree not don't do a whole lot bit like the Australian

koalas I guess and were like 100% slow twitch but based on your theory of um if you're sedentary shouldn't they have some two exit because they pretty sry on that um no I I think that there's there's a different um evolutionary path uh for all these animals and what we have done is starting from a from an ape um which has like usually this these homonid have like oneir uh of each type uh we are just moving to slow but but every other animal has its own evolutionary part and the slot probably because it doesn't

have any um yeah natural um enemies they they have only slow Fir and they have their their biggest challenge in evolution is not to escape from competitors but to be uh energetically efficient so they hardly well they move very slowly they can escape a movement detector and so on they're they're really slow um and that is something that is also almost forgotten in in physiology but slow fibers are much more efficient um to generate a certain degree of force especially in isometric contractions so in contractions that are I mean not just like holding tone of

muscles this is something that slow fibers do much more efficiently it means it cost less ATP to produce a certain amount of force for a certain amount of time uh so so that's probably why the slot they have such a predominant slow fiber type but this the only one we could find that is slow than humans all the others are faster than hum yeah they went like Bo so I saw figure and we were sort of 50/50 and then the sloth is just bang 100% yeah and there's no variation um yeah I was thinking about

it's really interesting how you mentioned earlier this this the paper I think it's Anderson uh where they rapid switching off of the the 2x's after doing um weight training so yet like within four days um it was all gone yeah what about the other way so if you go from like do people know if you're like a well I guess it doesn't matter if you're weight trained if you're endurance trained or whatever you you're saying you lose your 2x but what about if you stop so you said Sentry people tend to have more some 2xs

if you stop do you do you go back get some two xes again um there was some there is some suggestion in the literature that uh when you do tapering um then the type 2x is come back and that there's even some kind of overshoot of of type 2x fibers um in in your taper and that's that gives you this extra kick after tapering but I'm not sure I mean this this isn't really a consistent finding uh it could also be just an accidental finding because I I don't really think that in these Elite athletes

that that type 2x fibers really have a a meaning alog together um but if you go to really sedentary people um we do see that people with a lot of this type 2x fibus which is like in my opinion a failure to suppress the fiber type that we don't longer need as humans um so if if there there's like a resurrection of these type 2x fibers that this has a metabolic consequences in a way that we see a lot of type X fibus in people that are with type two diabetes uh and also insulin resistant

relatives of people with type two diabetes we see a lot of these type 2x uh fibers so so I think it it could even have a a metabolic um consequence or a penalty almost um to to have this this fiber type reemerge and I guess is that partly because you know type 2 diabetes is partly genetic so do you think they they may pass that on to their so you know this this type two act we're meant to be suppressing and getting rid of you think if if someone's sedentary they could pass that on I

guess that's epigenetics so yeah we don't really know but it could be that from a genetic point of view there's well like we know with athletes the fast versus slow I'm not even saying the type to X but even the fast ver slow um fiber type we see that um well there there's quite some literature it's since the last 40 years I think showing that the chance to become insulin resistant is higher when you have a lot of fast fibers I'm not even talking to X just fast fibers yeah um there was a recent study

by a group of ab Cuts in in Stockholm who um measured fiber type in in a non-invasive way Al something can talk about the relaxation time of muscles um and then they saw that people who are identified based on a Rel a fast relaxation time so a fast apology that they have uh much uh poorer insulin sensitivity or they have some well early insulin resistance almost uh so I really think that that is that is an important aspect of trying to predict who is um well prone to to metabolic disease it's probably not only insulin

resistance also obesity and cardiovascular disease that part of this reason why some are more prone than others is because they have a they have an innate or um yeah inherent fast topology in muscle it's it's a project that that we are going to start um next year um with some new people in my lab and and we we're going to try to have a a very a big study rolling on um whether that is indeed the case that muscle typology uh can be a predictive factor in in in the chance to get the metabolic disease

so maybe um so that sort of fits I guess with what you were saying earlier evolutionary wise that um not just getting rid of the two x's but across time we should be getting rid of the two A's as well right because if you're saying that we're we're built to be slow to wear down animals with persistence hunting and then also we're going to die off by getting diabetes and things if we have more fast fibers as well so you're saying across time we should end we should end up I guess we don't want to

be like a sloth but you know the having more slow twitch is protective in terms of being able to hunt and not get things like diabetes perhaps yeah the thing is that we will probably I I don't think that the type 2A will will also be suppressed I think there's always this this um two roles that that you need to have you need some for some actions you you really need power uh even just to survive and for others you need endurance so we we we always going to have both um but the the fact

that we get uh insulin resistant and diabetes and and obesity and so on it's not really a driving force for evolution it usually happens after we reproduce so it's we're not going to select this out it's more like how I see it is like if you're born with a lot of slow fibers uh and we know slow fibers are insulin sensitive much more insulin sensitive than fast f so that's the reason why we we people with all slow fibers can handle glycemia much better is that um that it probably means that if you're lucky to

be born with with slow fibers you could probably well do without exercise and still be healthy and if you and if you have a lot of fast fibus you probably need to exercise and take care of your diet to stay healthy uh but that is more of a provoc idea at the moment yeah it makes sense we need both fast and slow because I guess if you're trying to wear it at an animal you want slow but if if if something does come at you whether it's another human or or a cheater or something I

know cheaty you you got to be any like 20 meters away from the tree but you still want to be able to get there quickly and fast fibers help you to do that now we've talked about invasive ways of measuring muscle fiber type with biopsies and things but um I know you've been looking at and you mentioned the abcat study why don't you talk to us a bit about some non-invasive ways of measuring it so I remember when you first uh um sent me some dot points or we sent each other some dot points I

remember the old classic sort of 30 second Sprint so you do a wind gate you know in the lab and you'd look at the ones that had the highest Force but then they would fatigue the most that would give you an idea that they had a lot of fast fibers now we weren't thinking about 2A and 2x just fast and the ones that didn't produce as much force and then didn't didn't um fatigue as much were slow yeah so that's I guess one way what don't you tell us is is that a good way of

measuring it still and and what are the other ways you can try and work it out yeah well I think think the the reason why we eventually want it is because these biops is just invasive and so it's not never going to find the real way to the to the Elite Sports scene so to say or challeng identification and so on uh so we need to go for for non-invasive proxies or estimators of this well well we call it muscle typology it's very fast or slow um there's there's been measures um relating to um relaxation

time where you have electrical stimulation of of a muscle and then you you measure the the time you need to produce force and then to to it's it's actually the twitch so to say like fast twitch slow twitch you measure the slow twitch or the fast ttch in an electric stimulated muscle that's something you can do in humans um it requires a little bit of technique and that is a very uh yeah sensitive way to do it if you're G if you go to other techniques um that are more functional like uh sprinting for example

you could say well I just just look at my stopwatch and say I I can recognize a fast athlete I just see if someone is athlete or I can measure it if it's atly but there's so many factors that that influence running speed so if simply measuring running speed is not a good way to measure the topology of of an athlete um so the best thing because and and there's also other techniques like jumping uh like these these Bosco jumps that that used to be uh popular to to measure um muscle topology there so because

you are if you have a lost of lot of fast fibers you're explosive and and you can have more uh height in in your vertical jumps like a vertical jump yeah that is something that reasonably correlates with with muscle topology but for all these functional measures a lot is dependent on the on whether you're used to do it right if you're trained to if you have a good technique of jumping and so on so I can I can work on your jumping technique with plyometric training and so on and make you jump 5 cm more

in in in a couple of months that is not that is showing that it's it's it has its limitations in in in non-invasive uh measurements so what we wanted to do is is develop a technique that is um independent of any form of skill of or exercise or faque just measure uh the characteristic of a muscle add rest uh you can sleep or you can be trained or you can be tired doesn't matter you just measure that and and the way we did it is um there's a noninvasive way to measure the chemical composition of

your muscle with uh with an MRI scanner so MRI is is just a magnetic scanner that you usually use for um Imaging uh but you can also measure the chemical composition of your tissues it's called Mr spectroscopy so we use that to measure a molecule called carnine in muscle and that is a a molecule that is typically present in fast fibers and much less in slow fibers and we thought well maybe if a people has if someone has a lot of carnine in his muscle which we measure non-invasively just addressed in a scanner that means

has a lot of fast fibers so we compare it to the biopsy technique and we've done three different studies now to validate that and we could indeed see in all those studies men and women that um the nonivasive estimation of carnine is is a good estimate of your muscle fiot type composition you can do it at a relatively young age so you could even I think use it for talent identification so just of interest so you did I guess four biopsies or something yeah to to get your fiber type and that's probably the gold standard

and then and then you do the caros scene with the Mi MRI and how how close was it how are we talking five or 10% or well the so we did in three different occasions um so the the correlation is um um are our square of 50 so so 50% of the of the variation was explained um but we know that the biopsy in itself or the gold standard is also so variable so what we did then is instead of worrying too much about whether it exactly uh correlates with the biopsy technique which is varable

as well to to do the same studies that have been done for the biopsies so we we checked whether Elite athletes in short distances in athletics would have more um carnosine than than endurance and that was indeed the case it's about twice more and we done that for cycling as well um and we couldn't see it on swimming and that is another story why we couldn't really see it also in the biopsy studies people cannot really see that um short distance swimming requires more fast drivers and longdistance swimming and we also could not see that

in in the the cares measurement for but for most other sports we could confirm that it is a good non-invasive proxy of of muscle topology that's interesting I wonder if the swimmers is partly because they they all maybe not all but a lot of them do so many hours a day training even some of the sprinters maybe they um I think it's because they don't they never perform at at um near maximum power requirements because when when you when you go through the water I mean it's a very s maximal um effort because if you

do it too fast you just slip away through the water so so the the the maximum power in in like 1500 or 2,000 Watts that you see on a bike in tracks cycling or you in in a 100 met Sprint and so on the in swimming it's it's only a fraction of those maximal powers that you use even in in a Sprint because you cannot I mean Your Capacity to produce power is much higher than you need to just move water away that's true that's true and I often think of I'm picturing Ann Thorp who

is our famous swimmer way back in the two 2000 Olympics he he'd be sprinting it but he'd have these slow beautiful you know strokes and I I picturing that I'm thinking yeah that looks like if he was doing you know weights or something he'd probably be generating a lot more power each stroke yeah so that was one one reason that I I went to to Australia in the Gold Coast in the group of of CLA minan spec specifically because it's the highest concentration of top swimmers you could find in in world are actually training in

on the go Gast um and then we did these scans um on all these swimmers and we still couldn't we still couldn't see it in these absolute world class swimmers so then we we knew for sure that it's if we can't find it there it's probably not an issue in in swimming as much as it is in running and cycling I guess it's so much technique as well yeah running and cycling is is just not as much technique okay now I I do want to I still want to I'm still thinking about that 30 second

Sprint um so how does that how does that go when you correlate that because I remember was it thorn senson thorn senson or something they did 302 Sprint they did 30 contractions on the I kinetic dyn dynamometer the sort of I don't know if people know that sbck kcom sort of things and they they correlated that with with fast and slow twitch fibers how does that work out because that that seems like an easy way to do a measurement yeah it's it's true so we we before we set up we we set up a big

study to compare all the different techniques that had been proposed uh and we first did a literature search and we we came up to over a 100 studies including the one you mentioned um that have a kind of functional measure related to um to mus fiber type composition so then we did a study on on 40 people 21 21 women many biopsies and then did all these techniques and one technique test we did was the 302 Windgate test and there's two elements of that that really correlate well with muscle topology and one is the the

slope of the fatigue which makes sense right so if you if you start low and you keep you keep your level quite good then it means you're a slow twitcher and if you start high and you have a steep decline means that you're slow uh you're fast switcher so that makes uh that that is indeed something we could confirm but the second one uh which came out really clear was lactate levels after such a 30 second all out and and you have to wait a couple of minutes so we saw after the value you get

like after three minutes uh correlates really well with with muscle topology so there there are a number of techniques you could use uh and I think what what we have I mean we haven't published a study yet um but uh one thing that we um we want to promote is that there's there's many different ways to sample the muscle topology of your athletes but you have to be aware that some are trainable so and you should make sure that you do it in a homogeneously trained population some are sensitive to disturbing factors like like nutrition

and so on um and so it's better probably to take different aspects of of muscle topologies so one that measures the fatigability and and one that measure the power and the other measure like the contractile Properties or the the relaxation time and so on and if you make a combination of a few of those tests you can get a reasonable good idea of the topology of your athletes and that's when it really becomes interesting because that's what we for forgotten to do with the in this in the 70s and I'm glad you had to talk

with de costell and and I'm sure bank saltin would be alive he would also have been on your on your podcast and they discovered so many important aspects of of muscle fiber type composition in in sports and we don't use it at the moment and part of it is because we we kind of gave up on how to to measure it yeah so I mean is um I'm just wondering so is your carnosine I mean the gold standard is uh you know biopsying four four biopsies or something the carnosine is that is that better than

say a 30 I'm still thinking like so if I would if someone's listening now and saying I want to work out my f fiber type is you know it's probably you'd have to find someone that knew how to measure carnosine and you know and go and have an MRI done um is a 30 second Sprint or um uh something like that is it is it accurate enough to get a bit of an idea and then to then which I want to expand on to then apply it to sports which you just touched on which which

David costal and Bank whole team were doing back in back in the day yeah well one reason why we did that study is we we've done well almost 15 years of of work now on this on this carnine uh which we think as a research tool and in our hands because we're used to do it it's a very convenient way to to do these measurements in populations that are very difficult to access and and in in Sample sizes that are very difficult to get like for example we did we did this analysis in in football

players in Manchester United there's no way you could ever have them do this uh they don't even do V Max testing or whatever they very difficult to get but Mr scanning I mean we just said okay have you have your music on and sleep for 20 minutes and that's we could we could have them do that and and in that way we could we could actually uh discover things we we hadn't discovered before uh like the the hamstring strain injury which seems to be like a thing that mainly happens in in fast reaches so I

think that this this technique of of of carnine measurement in in a mar spectroscopy is is a really good research tool it's used in a couple of places now um but in to make it a broadly applicable Technique we we want even more simple tests and that's why we've done these additional comparisons now just make sure that you you choose the right ones I mean we did a survey with athletes no sorry with coaches and sports science staff on what they think about muscle fiber types do they think it's important for what would they use

it and so on more than 500 respondents so elen leens the postto my lab has has done this survey and sometimes athletes or coaches say well what I use this reaction time to to measure but that that is not a good measure of of muscle is something yeah that is something different right or so so you have to be aware that some techniques are really good and for example a 30 m Sprint is dependent on so so many aspects the morphology the size of your limps the the I mean the muscularity um and so on

running technique so so that is something you should probably not use but some other things like biking for 30 seconds all out is is a very good one so so you you just have to make sure that you don't do anything I mean characterizing a fast apology player may seem easy and and every spectator on in a football stadium knows exactly who is the fast players in the team but but it's a little bit more complex than that okay so so if we pick up um you know you were saying things that David costore and

things were think people were thinking about 50 years ago or so um where do you think we should go so you touched on you know how these things can be used so applying the muscle fiber types so you touched on uh paper you mentioned where you found um people that had more fast ttch based on your muscle carnosine had 5. threefold higher uh risk of sustain of sustaining hamstring strains yeah so so that's something you can do to to look at the risk of a particular injury I guess and then try and what train them

to minimize that what what are some ways you could use the fiber types in yeah so as far as I recall the very first idea in the time of c and saltin and so on to use Fiber types um is to to Talent idea to say well you're a fast Reacher we see that why not choose this discipline and you will become good at it and and in East Germany and so on they did biopsies on 12 year old kids and so on in that period so it was a little bit sketchy but um what

what we kind of discovered in the last 10 years by using this non-invasive measurement to to actually do it in large groups of really professional and Elite athletes is that we came to some new uh applications that were not in I think in the original plan or the original promise of of muscle topology in the in the 70s uh and one is indeed the the hamstring injury risk you it's very difficult to measure so what we did is over 100 professional football players we followed them for three seasons uh but we had this muscle topology

measurement on on all of them and then we we had enough um hamstring range which is the most um common injury in football players uh to actually have a statistical power to see whether it's different in fast T versus slow twitch players and then we could see indeed there's a fivefold difference fivefold higher risk of haming strains in fast SES and slow T we saw that in the Belgian competition four teams and we also saw it in the the Premier League uh competition so it's it's um something that you can only discover I think when

you have high enough power and non invas PS why that this is probably because um f witches they um they have they s they sustain more fatigue so take castill a PhD student in my and my lab has just published a paper last week on on the match profile so he had to GPS data of football players in fast SES and slow Tes and maybe that's interesting to say as well in a football team you have everything you have the marathon runner you have the Sprinter in your team so it's a very henus um population

um and what we see is the decline in in high intensity actions uh is is is steeper from the first half to the second half is steeper and fast reaches so they have more fatigue it makes all the sense of course and we know that fatigue is a risk factor for haming stange strains uh so I think now we we kind of published the the explanation afterwards we first said that there's more injuries and and then we said yeah it's because because there's more fatigue so how can you avoid that that is to take better

care of fast raches to um to give them more recovery to to have the the match uh intervals longer um to yeah to just individualize uh training recovery Cycles to to the to the fast SES in in yeah more respectful way so to say maybe also I had um Christian thorg on talking about Physiotherapy and in sport and he was saying how Ecentric contractions uh can reduce your risk of hamstring strains uh Contracting the hamstrings conent uh eccentrically so maybe you could focus those players and make sure they do that or something like that yeah

yeah I think it's to do with phasical length um which which also seem to be a risk factor so I'm not certainly not saying it's the only one but it's a new one we could add to the to the whole scheme and something you can work on you you can actually um well make sure that the fatigue sensitive players are more taken care of so to say we did we did a study in in um colleagues in in Australia and gold coasts um having an overload of training in in Runners so the normal training load

is is like 100% if you put on 100% And then you kind of give an overload of plus 10 plus 20 plus 30% uh running volume um then what we could see is a slow Wes actually cope with that they can they swallow that they you just add 30% of your mileage and they they're okay with that and they improve and if you have we didn't have any fast riches in that group because they were middle distance and endurance Runners but if you have the intermediate topology Runners they could not go with it they they

started to have signs of overtraining um so that really means that um muscle topology for sports practice I think one of the most important things is that it allows you to understand your athletes and to individualize training recovery Cycles based on these this inter individual differences okay so that fits with your fast saying the fast fibers are more fatigable so the soccer players and the endurance well the soccer players as they get more fatigued they're more likely to do a hamstring strain and then the endurance Runners um when you increase the load they've got more

fibers that be become fatigable so they can't handle it as well as the ones that have a lot of slow fibers that's really interesting so you can really apply it I was thinking my first thought with the soccer players well I should say football I guess the football players in Australia football can be rugby league Rugby Union stting rules football and soccer so we have to say soccer I don't get it yeah you get it good um yeah my first thought I guess was the with with the football players that the the ones that had

the more fast witch would be faster and they'd have more forces that you know they'd have to be slowing their their leg you know because you know obviously you you LIF you're lifting your leg and your lower legs going forward you've got to slow it that's what the hamstring is doing I was assuming that the faster ones would be getting more injuries and they'd have more fast fibers but you're saying it's the fatigue So based on that were they do people have hamstring strains more in the second half of the of the game than the

first half they become more fatigued yeah so the it's even in the first half the last quarter they have uh the the most haming strains and then it get even higher in the second half and it's the highest is at the last 15 minutes of the last half uh so so that is what what had been shown so fatig is certainly a factor but maybe interesting to say and that's also something that people don't know about fiber types is that fast fibers are not so robust or not so endurable that they it's like um a

Formula One car I mean it's it's really everything is made in a very light and very for optimizing speed so the the Z diss are much smaller thinner and the whole Machinery of f fibers is is like it's more brittle it's it's not so robust and that's maybe also so reason if if you just put a mechanical stretch on a fast fiber is more likely to break than on a slow fiber so so it's it's probably also that factor and that is something you cannot change with individualizing training prop s so maybe there's other factors

as well uh leading to to more injuries in fast fibus okay just other things just thinking about other ways to apply uh your fiber type topology that you've worked out so we've talked about um hamstring strains and what was the other one we just talked about forgotten already um yeah the training recovery cycles and Trover yeah over what was the one overt trining that's right and what was the one you you had tapering something about tapering as well yeah but there's not a lot of information on that uh but what we could see in that

in that same study um with overtraining we could we could also see if what they had a a week of taper that that um in that period the the slow riches could really rebound quite quite well their performance um but it's more it's more um a research idea I I don't think at the moment we can say there's sufficient um information to say that to people that the taper in slowes can be shorter that's my hypothesis but but we don't have that direct evidence yet okay I guess that would fit with them being able to

recover quicker as well right yeah you must realize that that a slow fiber cannot fatigue um it's it's maybe strange to say but it cannot grow into acidosis um I have a colleague in in Poland who does um electrical stimulation of single motor units so what you do is you dissect in a live rat um in the in the spine you dissect one motor unit motor neuron and you electrically stimulate it and then um you you look how much um you can continue the contractions uh if they hit if they they don't know in advance

but if they hit a slow motor unit and a slow fiber and they contract it IT contract all the time at the same force it you can simulate it for hours and hours and it never fatigues I mean if you could go on for days probably and it slow fiber you cannot fatigue so we have to realize that's exactly what we do we have these slow fibers who are active for hours a day um so so they are so different fast and slow fibers and that that we must realize that if you have an athlete

in front of you that has a lot of slow fibes or a lot of fast FIB that makes a lot of difference for many things so we have this hypothesis that it also impacts um nutrition um I I think that some nutritional supplements only work for fast ttes and other supplements only for slow Tes that's another project that we recently started in a in our lab so I think the applications are are in many directions and when we asked these coaches for what would you use it why do you think muscle topology is important over

20% said well to individualize nutrition and we like we were like what this no science on that oh yeah yeah yeah to to individualized nutrition so um I think the field is in ahead of us on on that that's interesting so what would what would they say what would they say and and what are you what are your I know the science isn't there yet but what are they saying like uh why don't you tell me what are they saying yeah I think it's it's in two directions it could be the fueling uh we know

for example that um well fast tribes you can increase the oxidative capacity you can make the mitochondria but you can never make them good in burning fat uh that is something that's like like almost exclusively Dawn in the in the slow fibers so so that is certainly one part the the the micronutrient uh combustion the fueling I think is is One Direction and the other is yeah the supplements for example the dietary nitrate supplementation you had Andy Jones in your in your pocat series as well um they well was a Swedish group um who showed

that only fast virus have have a um a benefit from from nitrate supplementation so that means that if you have a fast apology will probably benefit from beet juice and if you slow topology you will not um so I think also for that to have these nutritional supplements effectivity uh to explain why there some people are responders and non-responders I think quite quite a bit will be explainable by by most of topology I think but but all that is still to be done you know what sorry for being Australian Centric as I mentioned Ian Thorp

earlier Australian swimmer when you talked about slow fibers you can't fatigue them it reminded me we had this great Marathon run of Robert De castella along in the 80s anyway he I remember his his 400 the idea is when they tested him at the Australian sport they couldn't get his lactate up just couldn't you know do a Sprint whatever just no lactate and then it makes sense because because I remember one stage at the end of this Marathon I think it was the Rotterdam Marathon he um he did 60 seconds for the last 400 meters

when his best ever like fresh on a track for 400 meters 57 seconds it's just like one speed you know and and can't produce lactate so just same speed the whole way probably yeah yeah and also the other way around you have those stories of these extreme fast Rich athletes who have never run more than 400 meter in their life right It's amazing And if you would have them go all out on a on a 400 meter they would probably have to recover for a week or something like that so so it's it's a true

thing and I was talking about the homo sapiens being slow Rich that's true but we we must realize that we still have a a big variability a big range uh and that is something that I think is um it's also hypothesis I'm I'm throwing a lot of hypothesis here uh I think the variability in slow TD fast TD within a community has an advantage as well I don't know if you know about chronotypes uh but there's people who are early birds and and night owls um and I think the combination having the combination in your

group of or your small population is very valuable because then you always protected from uh from predators during the night because there's always some late night hourl still still awake and and then they are replaced by the by the early birds one hour later and and I think it's also the case for fast lowd a a tribe would probably be stronger if it had and an endurance Runner and printer and the tree climber in in the community to to um to take all the the specializations and maybe that is a reason why um in in

in humans there's still a big range there's still a big variability and we exploit it and we we we enjoy it in in sports and in Olympic Games uh but maybe it's a deliberate choice and evolutionary uh strategy to to be broad ranged definitely you you'd know when you do these pracs in your you know undergrad classes and things you'll get people doing 30 second Sprints I know I keep talking about that the wind gate so just so people are clear so 30 second Sprint on a on a bike is the wind gate is where

you go as fast as you can from the very first pedal so you don't pace yourself you go as fast as you can then you hold on for de life for the 30 seconds it's probably the longest 30 seconds you've ever had to endure but the funny thing is you'll see and you're talking about this variability you have you just get a bunch of students you know one from each group does a 30 second Sprint one one person massive force and then they die like crazy and you got to watch them you know they they'll

go to the bathroom you got to get someone go with them because they can faint in the bathroom hit their head whatever and then you've got the the other one that generates nothing fatigues like nothing and then two minutes later they're oh can I have another go and the person with the fast W person's throwing up and what do you be they're fainting and whatever so yeah very very different and and and just so hopefully people would get this by now but the person that does the high force and fatigues a lot it's gonna have

more fast fibers the person there wasn't much yeah there was one study in in our lab from El Le who is now pook she um she did three RNG Gates so I mean if you do one RNG gate you regret it after five seconds that you ever started that so that 30 second all out and then you give them four minutes of rest and do another ring game formit as a FRS and do another Wingate so majority would then formit and everything it was it passed ethical committee and then we um we did that in

a in a group of fast SES and slow Tes we had defined beforehand we had taken we left the middle part out and we just did the scan on y this is group of fast Tes and slow T we did the three wing Gates and then we we also looked we we indeed saw these fatigue Pro profiles to be very different but every looked how much time would it take to recover and the slow Tes they recovered within 30 minutes uh and the way we measured the recovery was a the maximal voluntary contraction of the

knee extensor so just isometric knee extension and and that was back to normal within 30 minutes but uh this the fast SES uh and we only measured for 5 hours so we don't know what happened after that but they were still not recovered at to to Baseline within five hours so it it could probably take many more hours or days for them to really recover and they did exactly the same total power so so it was distributed differently but they did exactly the same amount of work it was heavy for all of them and they

they didn't like it all of them but but the way they differed in their recovery was so massively different and as a coach we don't realize how much difference there can be in how when you ask something run a couple of rounds I mean that that is that is can come in so differently from a physiological level uh from physiological point of view can come in and kick in so differently in athletes so and you have to take care of this individual variability and learn to understand that this these are not weak at AET these

are just athletes that have a very different physiology just the way their muscles are composed that's that's basically it that's interesting because I remember again talking about some sports people don't know about but Rugby Union during high school and then early 20s I played rugby union and now and back then because I'm 61 now so you know early 20s everyone train the same sorry the coach would get everyone everyone do you know three laps of the overall and then everyone do these Sprints and everyone do this it's like and then later on we people start

going well hang on a minute they're very different the fullback stands there does nothing and then Sprints and then the Fords are like running around all day and you know just like in soccer I guess so then we got to the point where we start training them sorry we start training them differently but we now you're saying I guess that we've got to get to the point that that even within those so you got the forwards and the backs and whatever even within those you're going to have some that are going to have more fast

ttch and their slow twitch and you've got to think about their recovery will be different as well yeah it's in some sports it is the case that different positions require different fiber typology um but not in in soccer um we don't see that um we've done it in many teams now and there is not a clear pattern uh we've done 150 professional players so if there is is a difference it's probably very small difference if you need many more hundreds of players to prove your point it's probably only going to be a marginal uh difference

um so there's two things you don't need to be of a certain type to be a professional football player and the type of um your most apology is not going to Define where you play in the team M um so it's it's other factors it's it's can be morphologically I mean length and so on muscle mass this kind of but but not so much muscle topology yeah but in other sports it is of course I mean in rby it's quite clear that that if you run 100 met Dash in in 11 seconds along the line

that's that's not going to be for everyone right MH all right so I think we've we've talked a lot about fiber types what I'd like to do is ask is there anything else you're doing in the lab that you're excited about so I know you sent me something through so why don't we talk about that a little bit you're talking about the histamines and yeah yeah yes so I'm I really focused my my research on on the muscle fibers the myof fibers um and a colleague of mine Kine de Bok who was also so she's

a good friend she was also on your podcast she always said yeah I'm not so interested in in muscle fibers I said what muscle CLE the muscle I mean the majority is muscle fibers that's what oh no I'm interested in muscle physiology but not muscle fibers so it's she's interested in all the other cells that are in in the muscle um and and now I'm also starting to get really interested in that uh because um there's so many we call the mononuclear cells so the the multinuclear cells or the the myofibers that are like grown

together cells in in a long line but the monuclear cells this is just a cell with one nucleus um you have all kind of um immune immune cells it's called faps and and all these different cell we don't know nothing about them in muscle and they seem to be really important um and what we did is some um and this study is still ongoing it's Tio was a PhD student in my lab he looked at transcriptomic level which means if you have a exercise and you look at a muscle how many genes are upregulated or

down regulated by exercise which is seems to be quite important because that's probably going to predict what's going to happen on the long in training adaptation we see that the majority of these changes in upregulated or down regulated genes are not in muscle fibers but in other cells in immune cells and so on um and that's that is quite surprising I think to to us because we always think about how does a muscle adapt to exercise oh we see the mtor pathway going up and empk going up and so on forget about the myofibers what

we what we've done is we we suppressed um the histamine signal during exercise so histamine is is something that is liberated by m cells it's it's a signal molecule uh and it's it's well known for allergy medications if you have allergy symptoms because you have too much histamine if you block the histamine then you don't have these symptoms H if we give antihistamine during exercise then you don't adapt to exercise you don't have a training effect and we did it in a in a six- we training study we gave them antihistamine with each training session

and hardly anything happened they didn't get more mitochondria they didn't get more capillaries so the all the training effects or health promoting effects were were gone and and the real interesting part is muscle fibers they don't have histamine receptors and they don't produce histamine so the whole thing was blocked the training adaptation was blocked and the my fibers had nothing to do with that because they don't even have histamine receptor so that was the first we did it two years ago and now we started looking into all those other fibers or all these these other

cells and they seem to be the key players in training adaptation we've never thought about even the slightest idea that that it would not be the muscle viribus but it it is mainly the other virus having all all all the all the cells all kind of signals going back and forth and so on so I think a main um thing that we will see in the next years is uh is a discovery of all the roles that these other cells have in muscle I mean wow we we now just saw that there's M cells in

muscle we never knew that there was mus CS in and muscle and they seem to be just part of a very normal training adaptation signal it's not pathology it's not infection it's not muscle damage it's just your exercise a muscle and Mells immune cells start a whole Cascade of signaling that actually leads in the end to more mitochondria more more capillaries and so on uh so that is for me an eye opener and and a game changer in the field and luckily we can now do these studies with single cell transcript and single cell prots

and so on so this is really going to give us a whole new perspective of what exercise physiology is all about wow okay well I'm trying to get my head around this so so you're saying that when you exercise it's not the muscle fibers even though they're Contracting and they're getting these signals and things that are going on you're saying none of that matters it's it's what's happening to these mass cells that are producing histamines and even though and but then you said the the muscle fibers don't have histamine receptors so how does the muscle

fiber even know that the mass cell is producing histamine then yeah histamine is just a first signal from one monuclear cell to another and in the end it will also come of course to the muscle fibers I mean I'm I'm I'm putting it a little bit black and white we also saw a lot of transcriptomic changes in the muscle fibers but these were um proportionally only a minority of all the changes I don't know if you're aware of the metamax studies um so these are just um studies where you have a transcriptomic response in muscle

but that is bulk muscle uh and that is it's a really nice overview of all the transcriptomic studies all combined in one like metaanalysis and Tool you can use um just realize that that most of these changes and up and down regulation is in other cells there's also some in muscle directly but the signal isn't probably starting in muscle H but it's it's ending in muscle it's it's all other cells that are doing this might be things we don't realize yeah this might be out there somehow but I had mark tanapol on and he was

talking about all these different mitochondrial diseases and and glyc glycolysis diseases so people that don't have phosphor fruit their kise so they can't really use glycol so people know glucose and glycogen go to lactate mardal disease where they can't break down glycogens they don't produce lactate whatever but he basically finds that that all of these different diseases can be improved by exercise if you train them so if they can't use glycolysis then if you train them for their fat oxidation they're improve or if you if they don't have fat oxidation enzymes if you train their

glycolytic or their carbohydrate Pathways they can improve so it's hard to see because that looks like it's going straight for the muscle fiber defect and it's you know and they do get these training responses it's hard to see how you know what I mean yeah but but still it doesn't exclude that also in these patients it's the mononuclear cells that set up a lot of the of the signaling um and and start a lot of the of the adaptation um it's what I mean the adaptation is is is well I guess I guess that could

still work because the adaptation is okay so if you don't have phosphate fuit can a you can't produce lactate you train for fat and you get better but it could be that's still just the signal is just to train fat it doesn't matter that you've got that problem yeah I get I get what you mean wow okay well I'm gonna have to look up the the the so you've done that study have other people followed up on that with the so you're saying if you take antihistamines it's not a good idea if you want to

adapt to training so are these really high levels is it the level that someone's taking just for hay fever would that be enough to stop your training adaptations yeah so we've done um studies with with high doses of both H1 and H2 so that's two different types of histamine receptors uh to to completely block all the histamine signaling um now we are following up on a study where we do the only the H1 receptor blockade the one that is used for allergy medication and in the do that is used by by people normally and what

we do is we do a resistance training and and with every resistance training rout we just give them the normal allergy dose and medication H1 just before the exercise or to the resistance training bow to see whether that would also affect so that's of course the question that people ask us a lot I mean this study has been really picked up in in in the popular media for that reason of course um but I cannot answer that whether it's it's uh it's really problem problematic um for people taking antihistamines but it seems to be the

case that we underestimate how much um yeah damage you can do with with drugs uh we we of course always realize that the side effects um but in the case of histamine there was histamine signaling hundreds of million years ago even in single cell organisms long before there was M cells so histamine is a really old molecule that is used all over the body for all kind of signaling and if we use antihist just for one reason to to get rid of your uh Sy symptoms of analogy just realize that all the hist signning the

rest of your body is gone as well and in the case of Muscle it seems to be quite a a problematic uh impact um it's also for glycogen resynthesis and that's something that would be interested for you if we have H1 blockade not H2 but if we have H1 blockade the muscle glycogen resynthesis within 3 hours after exercise was completely blunted by H1 receptor antagonist so the glycogen resynthesis in the first three hours goes up quite a bit after exercise it did not go up in a histamine anti-histamine uh H1 receptor block H1 is the

normal one that people take with their antihistamine medication so so it's not only training adaptation it's probably also simple recovery uh from exercise so that's that's yeah go ahead soorry I know ill said just a couple weeks ago that we were talking about post exercise hypotension so after exercise you know your blood pressure drops and she was saying you could prevent that by giving an antihistamine um well it's along the line of this I mean and UA is also co-promoter of the the PHD student who is working now on this antihistamines but the one who

um who started this type of research on H in Oregon he uh he indeed first investigated antihistamine or histamine signals because he thought there was uh the reason for the postex siiz hypotension that you can get but then he also followed up with a study where he saw that the whole muscle trans cryptone was blunted with antihistamines and that's the part where we picked up and not so much the the cardiovascular um implications or the hypertension or whatever wow so just summarize you're saying that therefore that antihistamines well but again you said we don't really

you don't really know yet if it's just the the doses that people take with their they've got itchy eyes and runny nose and whatever but potentially it's reducing your uh normal sort of blood flow after exercise which is which is why the blood pressure drops you have a r of blood flow uh it's it's maybe reducing your muscle glycogen resynthesis it's reducing your muscle turning on all these genes and things during and after exercise and you're saying more chronically it can be reducing your training responses is that fair to say yeah yeah that's true and

and this is only one signaling molecule and I think there's a lot of others that that are also activating and and this whole training is actually you change the interstitial mure uh your your soaking your muscles and muscle fibers and all the other cells in some kind of exercise bath and then then the whole thing is uh is upside down and all cells are activated and and communicating with each other and you you really create one big um yeah soup of of exercise signal and and all the cells in there start communicating each other and

adapting and that's what eventually lead to training adaptation more mitochondria more capillaries and so yeah and you say messing around with that but say anist me May throw it out some similar discussion we had with um I think it was Katrina debok and uh also uh when I had Christian thorborg on again with physiotherapy this idea that oh you sprain your ankle or you just a bit sore so you take these um anti-inflammatories spraining ankles bit different but you know taking anti-inflammatories then that that's also another thing right because so if you've if you hurt

yourself then the timing can make a difference you know should you just let your your body do its own thing but then it's like I don't want it to swell up too much so I'll take an anti-inflammatory but the timing may be important as well yeah anti-inflammatory but also antioxidants that's also been shown by for Michael risto and so on could take antioxidant then also your training response is blunted uh so so reactive oxygen spe is probably also play a role in this interplay or the communication between cells in the post exercise muscle environment which

eventually leads to training adaptation we see a lot of the when we do the anti-histamine uh or the histamin blockade in in muscles that have just exercised we see that a lot of inflammatory signals are are reduced and also reactive oxygen species um signals so so I think this there's a lot of players in a very complex interplay and that is one of the big challenges for the coming years is to to understand this better and if we understand this better we will also understand why there's adverse effects of certain medication for um exercise response

right all right so just before we finish up actually I was thinking I didn't ask you about I like to ask about are there sex differences so if we go back to muscle fiber type are there sex differences and also with age do you get we know I mean I know we get changes in bber type with age but why don't you just tell us a little bit about that yeah the the sex differences are subtle but they are there um not so much in the number of fast versus slow fibers but the fast fibers

of men are somewhat bigger than for women and the slow fibers are not different between men and women so if you add that up you actually see that when you have just the muscle weight that um man have about 5% more um fast muscle weight than slow T muscle weight compared to to women um but it's a big range so it's to overlapping gion curves there's a lot of overlap but on the average you see slightly more fast muscle mass inen so with age um there's there's different periods where um where fiber topology changes um

one is in in puberty what we see is the difference between men and women and and fast fibers becoming bigger in men this just something that happens during puberty um and also the the fast typology um really increases during puberty so to say children are like more oxidative slow type um okay individuals you you see that if you if you walk in in the mountains with your kids and they they seem not to fatigue it's It's amazing And if they're fatigu and then they they wait for for like one minute or two minute and they

start playing again it's amazing their their recovery potential um so so the fast the real fastr profile really kicks in during puberty and then um it goes back again then we start um going to a more slow twitch profile as we go into advancing age um and in when you're are really talking with a old day age then you see that actually the the motor neurons of the fast fibus die off but sometimes they are uh re well reintegrated by by by slow motor neurons but then we're talking at a really Advanced state but even

before when you're 40 50 and so on you see that on average that um that slow twitch profile is is taking over again right okay okay so how do we um not how do we Okay so this has been this has been interesting what I like to do at the end is to finish up with some takeaway messages so uh We've covered a fair bit of ground today what would you like people to take away from this well one thing is that the fact that we have been like a bit on on the wrong leg

with this these three fiber types and and there was only two part of it is because we are when we do animal research and animal models we we always think that it's exactly the same in humans and we have to do this translation as well and have a lot of attention in where we do discoveries to also see whether it applies to humans and how it applies to humans and some of these findings are Lost in Translation um and I sometimes find it a bit frustrating so to see I I was looking at cell metabolism

that's a top journal in our field uh and also last week all of the papers are in mice and that's very good but and they have their value but but we should always question ourself can we translate this to humans is it the same and also pay attention to that so that's one thing I think we should never forget um uh the translational part to to humans and then also further to to the field to SP Sports I think the these fantastic discoveries in the the 70s by these Giants on on muscle fiber types I

feel sometimes a bit embarrassed that it's still not used in in sports we should do better and translate it all the way to the field so that's one thing H second is that that maybe people don't really realize so much that endurance capacity is really our thing that's what humans are really made of that's how we want to profile ourselves in in in nature uh and that is probably one of the reasons why we are getting wi of or losing this this extreme fast topology and then well third the last one uh I mentioned is

these these non-muscle cells I mean we're going to see a lot of work in the next years on how to understand muscle physiology fatigue recovery adaptation by looking at the the other cells the cells that are not myofibers but of which we know almost nothing at at the moment um so that is exciting times ahead it's not going to be easy there's going to be a lot of omics and stuff um but we're going to finally understand in a in a completely unbiased way what actually is happening in in muscles during exercise actually do you

want to do you want to just explain the when you you've said a couple of times unbiased do you want to just explain to people if they're not sure because you know you think of bias at the moment of you know your Echo Chambers on on Twitter or something but you're not talking about them that way no no so when I was saying this this um type 2x variables don't exist um there was when looking when you look at all the the the proteins or all the trans the transcripts and you say you ask a

machine can you put all the fibers into two or three categories based on not just one um gene or one protein but on all the genes the whole package that's what's called unbiased biased way is that we say well um I think the most important protein in the muscle is myin heavy chain that is that is that is you already have taken a choice you don't know if that one out of 5,000 why would that one be the best one so so it's you're biased and the re the reason we're biased is because someone has

started Brook and Kaiser have started atpa staining and that measures the enzyme that's me that's present on M and heavy chain and from then on we didn't think for 50 years we stopped thinking for 50 years about what could be a good way to classify fibers uh and now we just say well we just take a blank page every protein could be a fiber classifier uh just tell me what you think is in this database and that's what we call unbiased or unsupervised and that's the only correct way so to say to to classify subtypes

we ended up with two so that is uh well there is one thing maybe and and that is also in this paper um sorry for that but the slow versus Fast classification of viribus is not the most important uh way to classify fibers or explain differences between fibers so that is something that came out of our uh study but it's still not published so I won't go too much detail of that but but what we actually found it there even more important factors than slow versus Fast to describe the differences between fibers and if you

want to uh know what it is you have to look up the the bioarchive paper and and read it you can't just tell us very quickly and then they can look it up okay so it's ribosomes uh ribosomes is a big thing now um what we saw both in the in the trans say what ribosomes are quickly yeah ribosomes are small yeah yes ribosomes are small organel in a cell that uh translate mRNA into protein and muscle cells have an awful lot of them because the whole protein turnover in our body is the from a

a practical point of view the most the most protein turnover is in our muscles so these ribosomes the small machineries that make protein from mRNA are really active in in muscle fibers and what we now see that there's um ribosomes that have a number of ribosomal proteins a certain type of ribosomal proteins and we have cells that have ribosomes with other types of ribosomal proteins and we don't know at the moment what the difference is but we know that if you ask in an unbiased way tell me what the most important difference is between these

thousand fibers then the machine will say us is the ribosomes the ribosomes are so much difference between uh from one end to the at the other and then the second most important difference between all those fibers is that some are slow and others are fast so it's it's a really surprising uh finding and and we're still digging into why that is and it's a collaboration with Atul dasm and rer Moreno and Ben STS uh and it's uh really something we we enjoyed over the last half year to to discover yeah great okay and and uh

the important thing is is is with these things is people don't always think you said that the paper is is what people call a preprint and you often see on Twitter people will say congratulations you know someone will say I've got this finding and they'll say congratulations you hang on a minute it's a preprint which means it hasn't been reviewed it hasn't been accepted it hasn't been published it's a preprint and that's a preprint I'm not saying it won't come out but people sometimes forget that don't you think have you noticed that absolutely absolutely so

um but I also um support the idea that it's valuable to to throw the data out and and so people can start working on this um of course there is a risk that people would spit out data that completely invented but you also can have that with um with data that are published so so it's not really a guarantee it's it's published in a paper so it's it's free of false um but but you of course have to take into account that it can it's still subject to change to critique and so on um and

then in that case I think it's it's worthwhile to to look at who is writing that is that someone who has already had um well a good um or or a valued um expertise in the field or someone that is just coming out of the blue then I would be a little bit uh suspicious I'm not putting I'm not obviously putting down your paper I haven't I haven't looked I did see the title I'm just saying that concept sometimes gets lost because there's one thing you know you said cell metabolism a top Journal if a

paper's published in that it's probably likely to be tighter than something that's published in a much lower journal and and here we've got preprints which you don't even know it hasn't been reviewed hasn't been accepted hasn't been published you don't know what Journal it's GNA get get into but sometimes in Twitter people will be like oh look at this great finding it's like no no it's a preprint so I'm just making a point there that I've been wanting to slip out and you happen to be on the end of it okay Absolut correct well thank

yeah thank thank you very much for coming on but I agree with you it's good to throw it out there and you can get feedback and uh and you can you can get the because it used to be people would be very secretive they wouldn't even mention which thankfully has not really happened on the podcast and you you're happy to mention things but used to be people would be very secretive you know they wouldn't want to talk about what they' found in things I think people have found more and more that there's more to be

gained by actually putting it out there and getting people's other people's ideas to then you know follow up Etc yeah I I just realized I I've thrown all our ideas in the lab in the public now but that's that's what I I think is is the most valuable we have a lot of ideas and we want to well have people think about it and and I mean like this two these two fiber types only the it it will create some debate and critique but by doing so by just saying well wait a minute what if

we started the other way around we say there's only two fiber types then you can throw mud at it and try to disprove it and if we can't I mean then that's probably correct but if we never challenge the idea and never be provocative then then we will never CH challenge the idea that is not three five typ so I I like that that debate and throwing no ideas on on public I was going to say if no one challenged that the world was flat we'd still think the world was flat but some people do

think the world's flat it's making a come okay there's people from all around the globe that think it yeah yeah and you did as you said there's a lot of variation within people okay well thank you very much for coming on it's been great and I'll see you around was a joy thanks a lot Clen okay see you mate byebye I hope you enjoyed this podcast please like subscribe pass it on to your friends and colleagues check out the other podcasts thanks again