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Lateral Gastrocnemius in Achilles Tendinopathy with Gabriel Fernandes

73m 43s

Lateral Gastrocnemius in Achilles Tendinopathy with Gabriel Fernandes

Gabriel Fernandez, a physiotherapist and researcher, conducted a PhD study investigating neurophysiological mechanisms in runners with Achilles tendinopathy. Contrary to previous research that blamed strength deficits in the soleus muscle, his work points to altered neural control of the lateral gastrocnemius. The first study used transcranial magnetic stimulation (TMS) and found increased cortical inhibition in the triceps surae area, associated with reduced plantar flexion endurance. A subsequent study using high-density electromyography to analyze motor unit firing rates revealed that the lateral gastrocnemius did not appropriately increase its firing rate with higher force demands, unlike the soleus and medial gastrocnemius. Further investigation into specific spinal circuits for the soleus showed no differences between groups. Fernandez hypothesizes that running, as an endurance activity, might lead to fatigue in the less fatigue-resistant gastrocnemii, prompting neural compensation strategies that could alter force-sharing within the calf muscle synergy. The research suggests a shift in perspective is needed, moving beyond solely targeting the soleus in rehabilitation to consider the coordination and neural drive of all triceps surae muscles, particularly the lateral gastrocnemius.

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I'm sitting here with Gabriel Fernandez. I came across your work. I don't know who posted on Twitter. Maybe it was Gerard McMahon. They posted your study on the lateral gastroch. Kind of like stop pointing finger at the soleus and maybe start think a lateral gastroch. So I saw it. I read through it. I made a meme. The Saul Goodman meme about the the lateral blaming. We should maybe look at the galato gastroch. Stop blaming the soleus. And someone tagged you in the comments of like, this was your study. And I was like, I didn't even know that this was you. So we got on a phone call had a little chat and now we're going to talk about your work. So tell everyone who you are. Okay. My name is Gabriel Fernandez. I'm a physiotherapist originally from Brazil, I live in the Goku's in Australia now. I've been a physiotherapist for around 16 years now. I worked with many sports. Olympic athletes and you know everyday runner triathlete, you know, soccer and all the sports that you see in Brazil in Australia. I moved to Australia in 2016 just after the Rio Olympic Games. And in 2018, I started my PhD at QUT in Brisbane. At QUT, I was having a chat with my supervisor at the time to try and think on, you know, things to do and, you know, what interests me that he would be able to help me out. And I had, you know, working with sports for a long time. I had this interest in tendons in general, because you see a lot of them, you know, I worked with Beechwellie. So there's a lot of Patelotend and shoulder and a lot of runners through my time. And he said that you'll be more suitable to help me with something coffe-related, because his background was around neurophysiology and mechanisms, specifically associated with coughs. So I said, okay, we'll do the Achilles tendon. I had read this paper that Solias paper from South O'Neill talking about how the strength and endurance deficits found in Achilles' syndrome, the population was related to the Solias. And then my supervisor mentioned that Aburniria had done a study on Patelotend drop fee with TMS measuring cortical inhibition. And he said, we have this here. We can do that in Achilles. And we started talking about, you know, the structure of the PhD and how, you know, neurophysiology, physiologically speaking, the other system controls muscle force through various circuits, cortical and spinal circuits. And then we decided that, you know, we'd look at some of those circuits and try and see, you know, what's happening that is impacting Solias' force capacity. So that's what we started and we'll be with up on studies on that. The first study looked at the brain with cortical, the cortical circuits, specifically the cortical inhibition circuit. And then we looked at the more neuron via the more units with like a very high-tech EMG system that breaks down the raw EMG into more specific more unit action potentials. And you can, you know, specifically assess and quantify the neurodriver or the amount of input arriving at muscle. And we can talk about specifically each one of those studies, but I think the idea was to look at, you know, the potential mechanisms that could be impacting the solias and the deficits that were seen in this population. Okay, so yeah, I think probably up to this point, I think even before a phone call, so much of the Achilles, when there's a tendon opathy or Achilles issue, we always are pointing the finger at the solias and people make the argument of like the amount of body weight loads. It has to support and then it makes up a huge volume of the calf muscle bulk. But yeah, what have you, where did you arrive at reading through all this stuff with the solias? Like, should is this, were you finding that maybe the solias is not so much to blame in these people with Achilles had an op there or what, what did you see? Yeah, I think that one thing that I've learned with research is that we can't generalize. We have to be specific to what was measured. And there are obviously a lot of mechanisms and types of contractions that we didn't test. But going to the first study where we looked at the cortical mechanisms, we found that it's so to measure the cortical mechanism is we use this machine called TMS or transcrying in magnetic stimulation. So we stimulate the motor cortex area associated to the leg muscles. Specifically, the cuff muscles. And we give a magnetic stimulation. They will measure the motor-voxed potential with the EMG. And what we found is because it's so hard to pinpoint each of the three muscle separate because the motor cortex area associated to the leg is deep in the motor cortex, we tested the triceps area as a whole. So we found that in runners with engine up feed, they had increased inhibition. So if you have more inhibition, you have less input arriving at the muscle. And we found that associated with depth-setting in plant-flexion endurance. So we used a single airase test and we found bilateral endurance, depth-setting endurance, sorry, in evening in your lecture presentation. So people with Achillesian jumping one side, we found depth-setting endurance on both sides compared to controls. And there was no differences in peak as a metric force. We test the as a metric force is normally with any straight. That's what we used because you're using all the three muscles of the triceps array. And it's maximum capacity with the knee straight. So that's what we used. So it was interesting that we found that there was something happening. There was a increasing inhibition. And then we decided to go more specifically. So going from the brain through the spinal cord to the muscle, we have the motor neurons. And the structure that we looked at, it's called Mori unit. And it's also called, it's known as the final pathway. So it's the final pathway from the nervous system to the muscle. So that connection through the motor neuron to the muscle. So a Mori unit is an individual Mori neuron and the bundle of muscle fibers that that Mori neuron innovates. And the way that the central nervous system modulates force is in two ways. You can think of as a imagine you have a car they're trying to pull and you have two people pulling this car and it just can't move it. So the two people being more units, the nervous system will have two strategies either increase the the firing rate or the the frequency of the action potentials of those model units or to recruit more units. So we have more people doing the work and producing more force. So looking at the Mori unit firing rates gives us an idea of the neural drive of how much that nervous system is driving that muscle to to contract. So that's what we did in the second study. We looked at increments of force and how that modulation was changing with increasing force because you expect to have a higher firing rate. And again, we looked at the soleus immediate gastric and the lateral gastric and in this time with more detail. And we found that the lateral gastric didn't change the firing rate as the dog increased. But we saw an increasing firing rate in both the media gastric and the soleus and in both groups. And that was the you know, the second study showing that the soleus that there was something wrong within your drive, but it was more specific to the lateral gastric. There was another study that was in hours from cruziere that there was about force sharing strategies. So that's a very interesting paper. And I think it's very, very relevant because the the triceps array is a synergist for plant deflection, right? So they work in synergy with the three muscles. And what we know, you know, these days on the newer strategies is that the nervous system has like a partial independent control of each muscle. So we can fine tune and adjust the amount of stimuli to each muscle, to adjust for joint stability and control and to distribution of muscle force. And what they studied from cruziere found was that in people with aculos and genopathy, they had 28 percent lower contribution of the lateral gastric in force production. And there was a nice study, they used EMG and and force plates. And they did a bamychanical modeling of force estimation to each muscle. And they found that the reduction of the lateral gastric. And there was there was interesting to see, you know, the support in the findings. And we wanted to try and understand if there was something that we're missing, right? Because the this paper of the of south on you said found that the solias were the muscle with deficits. So we looked at another another type of of circuits circuits in the specifically to the solias. One of them is called persistence inward currents. And it's a type of modern neural excitability. So the the PICs is is a mechanism of amplification of synaptic input. So it amplifies the amount of input arriving at the muscle. And one of the interesting things with PICs is that they have very sensitive to inhibition. So if you have the cortical inhibition that we talked about that we found on our first study arriving at the solias, you would see a reduced PIC because the inhibition inhibits reduces that PIC activity. So we looked at the PICs and we looked at other types of modulatory drive, the neuromodulation such as acceleration and the firing rates of the more units as well. And we we found that and we looked at the solias of the gap of the people with eculous and job thing without and again there was no difference in any of the measurements that we did in the solias. So as far as we're we studied around solias physiology and the nervous system playing a role in in solias force production. Not only our study but our other studies as well the looks at that. It doesn't seem to be we can't find anything that justifies the solias being with an altered capacity to produce force. As I said like there could be other types of contractions that we didn't measure like explosive contractions that it may be even during running or other things that we didn't actually test. But with the things that we tested that piece to be no difference between the people with and without eculous and job pain in solias physiology, neurophysiology should say. For me maybe people listening to so that study you came the satanial study on the solias like kind of yeah looking at what the solias limitations with eculous and what's what did he test? What did he find in that study that made people start thinking solias is something we need to look at? Yeah so they tested the azimetric peak torque with the knee straight to knee bend and the assumption was that because the the gas strokes they work less with any bend they found differences in torque on both positions right between groups. So the assumption was that if the depth that's in force were in the gas strokes you wouldn't see it as a bend knee because it would be less active. The gas stroke being the depth that's being in the solias means that you can see on both knee straight to knee bend that was their assumption. But I think that the issue with that and I should rephrase it. I think that there's a possibly limited view on that because it's not just about mechanics you know like when you bend your knee you have less tender strength because the tendon of the gas strokes less you know gets less stretched. You have reduced your drive to the gas stroke knee me and it might be that you have some compensation of the other muscles it could be that the compensation is not great and maybe that's why you see the deficits on both knee positions. So it could be that you know the solias in that specific separate group that he tested had a greater deficit. Again it was the the foundation of my PhD was it was these studies trying to identify the deficits in solias and the idea is not to say that he did something wrong was to say that there might be something else that we need to be looking at instead of just focusing on the solias as the main driver of what you listen drop thing as as we have been for a long time. This okay so you're looking at these individual three individual muscles and the the drive so I guess maybe before I ask this question that analogy you had of like pulling the car and you could you could add more people or you could make them I guess pull harder like increase firing rate right um those deficits you didn't find you only saw those deficits in lateral gas stroke you didn't see those deficits in medial and solias. No and these are people with a killer standing up with the there was two groups one with a keyless and jump fee and one without they're both running running groups most runners and there was another interesting study that tested um firing rates as well but with higher intensity contractions and they didn't find anything in the media of gas stroke and solias and they didn't find a low reduction or a low activity of the lateral gas stroke they found that it had higher contraction densities the lateral gas stroke goes working harder so again I'm not saying the lateral gas stroke is working less with saying that there's something wrong with it um so imagine that this modulation is outed any it's impacting it um you know the control of the muscles um there's these um with synergist muscles and in with our understanding of of the common drive and this um I don't like the word motor control too much because I think it takes it gets taken out of context a lot and um when I'm trying to you know get very niche exercises to fix something it's not the idea behind it but you know in terms of how the muscles the nervousness and controls movement and our understanding in your physiology improving um we can see that this uh people with um specific um coordination strategies um as I said with the those specific deficits in lateral gas stroke for example uh there was a study that found that for the for the triceps array and for the quadriceps people with the specific signatures with what they called uh in a movement tended to reproduce the same recruitment pattern in other activities so I think what we're trying to say is that this altered neurodrive that we're seeing in asometric contractions um maybe seeing other types of exercise like running for example um one of the interesting things that um that I observed I was questioned a little bit about how the how the the lateral gastrodeficit would come about right as they as a primary um issue with tangenopathy and um we we exactly don't know that and that's normal we try to answer with with our studies but one of the hypothesis is that the soleus is a muscle with a um huge endurance capacity right it's a fatigue-resistant muscle running is an endurance exercise um with these independent coordination strategies the muscle they will fatigue quicker would not be the one that is like a high resistant to fatigue muscle like the soleus would be either lateral gastric meter gastric but this fatigue inducing exercise like running probably wouldn't be enough for you to stop running because again a few our my lateral gastroc is tired it's your whole tricep sorry to this enforce so one when one muscle gets less active as I said the nervous system has this capacity to readjust the input um and we don't know to to what extent but to um maintain the same force because as I said like we didn't find deficits in in peak force but they were deficits in your drive so it could be that there's compensation like one muscle increasing to compensate deficits of another muscle and this is where we are starting to to to to find interesting things uh uh research in tangenopathy then we want to keep exploring to try and understand what happens when does it happen and how we can change that I think that's the that's the main thing and whether we can change or not yeah okay um he said a lot of things there the the fatigue thing um I think when we had our phone call you were kind of you were talking about that how when we talk about rehabbing and to kill his tendon it's like we need heavy loads and the environment says it kind of says we need to do that but how do you even even like with your work how do we say that yeah you have this deficit this this motor drive problem with the lateral gas truck but it's like yeah what is what's going on when you're running do you have any speculations of like what's what do you think happens with the other because your contraction types or isometrics right that's what you tested is isometrics yeah and then I guess it probably has some carryover but it's like what do you yeah how do you start to test what's happening when someone's running at like mile one or mile ten or mile twenty you know what what what I don't know me can you speculate what do you think is happening it's as I said it's very hard to expand our findings to other types of contractions um one of the limitations with the high density and g which is the system that we use to look at the moderators is that um to look at so the way that the the system and the algorithm finds and and decompose that into uh modern aspiring rates is that it gets a Royal MG and this high density MG electrode matrix has up to 96 electrodes we use 64 now now study so you imagine you have 64 monopoly MG electrodes and then you can get them bipolar connecting to one another because it's one big matrix with all those electrodes um so we have a lot of EMG data and and these decomposition methods that exist they identify the action potentials and they say okay so this is one modern urine this is another modern urine and then you separate that into individual model model units or modern urans and um and then you're looking at the uh the the identify the modern units for you to do the analysis but the way that the head in SMG works is if you do dynamic contraction you change your muscle length and the dipole is of of the muscles as well so that the the sample of modern industry getting they're going to change in um location so we're going to get a lot of noise and and probably no good quality data to work with so we're still limited to asymmetric at the at the moment um one of the interesting things with running and obviously as I said I'm we're not can't we can't get our results and say that that's applied to runny but um runny it works the muscles in a quasi-agreometric contraction so the muscles are in a sub-maximal intensity contraction and they're not in a you know real um as a um as a tonic contraction uh model so it's a more isometric and the tendons are springing and stretching more than anything so it's not that far from what we're doing um but obviously we don't take in consideration with those specific studies that we did the the tendon behavior that would be you know um very different with running than what we do with um with the asymmetric stuff on that a momentary um okay the EMG um that maybe I've most of the you know I mean it's in like the high-fertrophy world and I'm a little bit in that and there's been some like criticism of like um anyways surface EMG I just immediately think from like the most surface level understanding is like the gastrox are superficial and the soleus is deep so is there any issues when you're trying to see the EMG with the soleus because it is so deep or yeah what's what's going on there yeah um there there's that that's a very good point uh note that there isn't um for for two reasons one the location that we put it uh the electrodes um just below the muscle bulk of the gastrox and uh where the cuisines and the seats at that level is just soleus so you can you can clearly get the data from the soleus there there's there many studies that've done that that way um this high-density EMG data and and tests have been extensively validated and they are as reliable as intramusso EMG so we do not compare that with surface EMG with the RMS analysis and surface EMG amplitude so we normally see in other type of studies these are not the same types of data so it is electromyography but with the data that we get out of the electromyography is the the related to the modern unit not actual EMG activation amplitude of anomalicity in those strength and conditioning exercise science research uh so this is more specific to neurophysiology and uh there's that's even been used in um stroke, modern urinsies um you know to look at aging so it's it's a very um strong and accurate representation of neurodrive um okay the uh you said earlier this this ebony real the ebony real stuff maybe that was what started the whole cortical inhibition thing and intended opte with the patellar tendon and you're going and looking at the three different uh calf muscles did did she look at the cuis individually was she able to do that or was it just the cuisines are inhibited period yeah if i'm not mistaken i think she looked at the rectus from where i instead of the cords as a whole um it is the same deal with the trusps array like it's so the the multicultural area is tiny the uh the coyote is the size of your head and you have it's like a figure eight coyote so the center of the figure eight is way in each position to simulate so you have um some in some setups you have um a uh neuro navigation system so you visualizing what is stimulating and um and and some use other muscles as a um criteria to adjust your position so the way we did was we had a soleus metogastrochalatrogastroch with a normal EMG just to get the the amplitude response and we had another EMG on the tbr's anterior uh just to see if we're getting high tbr's anterior activity means that we're going dorsiflexion or plantiflexion so it was one of the things that we used to make sure you're in the correct position um i'm i can't mill it up my head what Ebony used as to control the the position either i don't know if they had the neuro navigation but i think that they just focused on the uh EMG on the litte ratus for more i some of them second um now there are other studies on other tendons of the body and this this cortical inhibition or is it really just like patellar and Achilles i think it's just patellar and Achilles um upper limb it's not they're hard to do but the tendons are hard to you know to to then file like it can stimulate the like the biceps or the the deltoid really easily but you wouldn't be able to get the data and to be selective with the Brutericaf um there's not much stuff done in heap as far as i know yeah with with TMS so i think it's just the Achilles and and the quads and the patellar um okay this lateral so when we were talking uh last week um i was i was speculating myself on like okay why does this lateral gastroc seeing this inhibition and i mean you've probably done the same for yourself um but this sub tendon twist so i was kind of talking about is it because this lateral gastroc twist and that's like the deepest insertion on the calcaneus but yeah is there any credit to that or is the twist just like two variable between people i think it's it's it's hard to say um it is variable i think they're classifying to three different types to be most common and one being more rare uh we normally have the the solias is the the duper layer and the gastrox as the most proficient layer um of the of the free tendon but i'm i'm not sure if the it might be that we get it at a point that we identify in the um you know phenotypes of of sub tendon um twist and and in those that will be more likely to have tend to up to your north but i don't know if we're quite there yet i think there's too a lot to understand of what it actually means if it's just an anatomical variation of that's gonna be predisposing people with two don't know and that that study you did was okay you said an optimistic mid portion it was people with mid portion twist the first one was yes um or did the yeah the first one was the two first ones the two first ones the two that we talked about uh were with mid portion and then the latter one that we haven't talked about yet which is the foot position we included in session as well um okay um this i've had a i've had a number of people on with like Achilles calf and there's this whole thing like soleus is is i don't know what the percentage is but like 50 50s i mean and that's this probably variable too but 50 percent slow to which and then 50 fast and then the gastrox is more fast to which than slow to which um have is that anything that has any any value to look at in all these things we're just we're just talking about in terms of the the neurophysiology is there any difference with like more of a slow to which muscle there's more of a fast switch muscle well there is for running like if we're talking about as we talked about last week um runny's in the during sport and you know you if you have a muscle like the soleus had there has a higher percentage of slow to each fibres higher resistant uh fechi resistant muscle it's i i see it is a very very hard to see that that muscle will be the most effective uh because it's the strongest in in the the punter flexors uh is a high resistant to fatigue and runny's in during sport um whereas the lateral gastrochne media gastroc have less of that you know slow fibre twitch and will be more likely to fatigue before than the soleus um one of the things that we talked about last week as well that i find it interesting is that um you know i'm i'm running this survey and i i think it's a good opportunity for me to share my survey i'm running this survey on um clinicians understanding on a chelousian job fee and there's you know a few um a few questions about uh whether um you know how you understand your uh your pathophysiology or your your your diagnostics and you know your treatment and you know how each type of treatment differs and you know um and all that and it is something that that's been growing in research these days which is a co-design so you um interview you know your consumer you know and get your consumer feedback so i did that i interviewed some people um and you know experts that treated and stole runners with ten job fee or athletes with ten job fee and in in during this interview one of the the people that i was talking to um as i asked you know do you normally see uh you know a lower endurance capacity and in the calf of those people um because everyone talks about uh you know heavy slow resistance training or uh plyometrics and um so it's all tendon-based you know obviously understand that you know it's a ten job fee problem uh so the load needs to be focused on the tendon when we want tendon adaptation um but as we talked about the neurodrive and all that and the distribution of strain if the muscle is not contracting like if you're passive if you're just sitting you know watching tally you know there's no strain going on the tendon because you need that muscle contraction right so to to get that force distributed and across so while they're running you have that contraction some maximum intensity for you know prolonged period of time and um and depth setting endurance is something that we've been seeing a lot in in this population so i asked this person uh you know do you normally see that because it is a very ex-experience clinician and and they said um yeah they did see that but they and i asked how they addressed that in the clinic and they say well i don't because they get that from running so what i don't understand is if they're getting that from running you know the endurance component shouldn't they not have endurance depth sets if they're getting that from running so i feel that you know a lot of the interventions that are done for ac ulysses and job the hour tendon based like you want to improve function or structure and then on the other hand we say we don't care about structure you know like treat the donut not the whole um so i think that you know different treatments focus on different things but we might be failing to address those literal things that we're talking about like the this specific depth sets of the lateral gastroc or the endurance depth sets that we have seen this population i was i was watching your podcast with um the the crossfit guy forgot his name yeah brant for kowski brant and he was saying he was a high level athlete and he never did a calf raise you know it's exactly what i'm talking about like you you're gonna be you know runner and you don't train your calf raises and as we know and as you train conditioning uh you know running doesn't work the muscle the same way as a calf raise you know even your body weight single leg calf raise will work you know two fatigue we're working a different way than running you can run for two hours you can't do more than 40 calf raises when the single leg you're gonna get fatigued so the muscle work in a different uh energy from mana and the the environment that you know that you're working on might benefit your muscle in a different way the same way as you do it have the loading and getting your stronger bulk your muscle and uh that will get you you know more force produced and that will help with endurance as well because your muscle getting stronger but it's not that specifically endurance so um i think there's like a few things that we you know the research is really hard to translate into clinical practice but one of the things that we are seeing is depth sets endurance and i don't know how much that's being addressed in in in clinic i don't see specific endurance exercises in a lot of the guidelines um i don't see that being specifically said they just say uh you know any type of contraction in type of exercise but do clinicians consider endurance or are we always considering tendin structure which you know endurance wouldn't do anything for it you know because it's low load um yeah what do you what do you think needs to on the training side what do you think are you at that point of of of having a suggestion for like how do we how do we build that endurance i think that one of the easy ways is you know it's with anything in physio for example like if you attesting a patient for a balanced issue and you're doing a single leg balance and you see that they can't hold for ten seconds you could stop the bat right so um one way that i think it's easy to do and it's being used more and more as a single leg cuff raise um i like to do it off the floor instead of um off a board or inclined board or a step or something because it's easier for patients to do if they don't have a board or you know some people might use a 10 degree board or a 45 degree board so which which one would the patient get so it's hard to compare progression or to compare with your other patients so i would normally do it off off the floor especially because that can be used over with insertional tension up there as well because you've already that compression the emphasis um and just as many as you can um the i think that the overall consensus is that we have a metronome trip and trope so patients are hurrying up to you know to do it quickly and um i think understanding the criteria right like i think that um exercise or sports science does that very well with protocols and guidelines and understanding um fatigue specifically i remember when you know my first fatigue test there has been pilots and you know people just say you got a screen that you know and they is and you stock the test not them and so it's because they will give up like such burning they just stop and they haven't reached fatigue yet they just didn't want to continue so sometimes you just got to push them through obviously if it's not provoking a 10 then it's not causing an increasing pain if it's just that burn in the muscle just push it through as many as you can and it might be a first step and then you know you progress with loads on that after you reach a certain amount um i wouldn't compare with the other side because it's this being something that has been observed not only in Achilles but in patellar tension up as well that sometimes the deficits are bilateral and even in in your lateral presentations um so i think that's called for a normative data um for for athletes we have that and it's a very good study uh done from uh kin lozier for uh general population with the calf raises but we don't have that for athletes and uh i think that that might need to happen as well at some point uh so we can perhaps use as a normative data and um try and stretch by way of patients are and see if there's a way of understanding risk and um like a cutoff point for a minimum number of calf raises for those at risk of developing tension up the but it's just light light she is away yeah that's kind of what i did for the endurance is like we have that single single leg endurance test and i'm like let's just do that let's just do that a few times a week and we're going to be training endurance um i was going to say earlier on the the bilateral deficits yeah when you have like a patellar Achilles is like you could see or i guess let's just talk patellar you're going to see like that that that side much weaker but it's like then you have a healthy side that's stronger for you but if you probably look at normative data you're like they're both weaker um with this um cortical inhibition when you have people with unilateral tendopathy is it the same side to side do they have that cortical inhibition of the lateral gastroc on both legs even if they just have pain on one side that's a good question we didn't measure that um it's very time-consuming the protocol and we prioritized the the symptomatic side we looked at people with bilateral tendropathy and we focused on the most painful side but then we did a subanalysis of the single like calf raises just with those within your lateral presentations and with excluded of that analysis the bilateral presentations and the the deficit change risks were on both sides um i thought about the cortical inhibition there's a very good question yeah okay this i think earlier you were talking about that not that that um i guess peak was a peak force what was the thing you were talking about those like you're maybe you're not seeing you don't see that that change in peak force right with with some of these Achilles tendons um probably variable this lack of endurance is that pretty much across the board of people with Achilles tendinopathy you're going to see this these deficits in endurance looked at the deficit in peak force a lot more conflicting um and there was a a recent systematic review that even question whether those deficits exist or not um because of the how conflicting they were the deficit singing endurance a lot more perceived um that sathlon you pay perjede endurance as total work done so they did a data monitoring uh there's some studies from supernavel they used a single like arrays uh i used on on on my my studies a single like arrays as well uh and there's some other studies they used there as well so there's it's being more consistently observed um in in terms of the the deficit in peak force i can't say that there is a deficit sing in maximum capacity um but i think one of the issues as well is that a lot of the studies measured the um peak as a metric talk with any band so as we talked about like if you're just measuring the knee band you you're not working the full capacity because again you you're biasing solias you're looking at the solias capacity to produce force and and that might be one of the reasons why you know the the research is not more um certain to what's happening in terms of maximum capacity maximum force production or as a metric um it could be that once we only look at papers with the knee straight that we see something different than what is out there this days but at the at the moment i think there's so many different protocols and um ways of measuring that we's to sort of like looking at you know apples and oranges have a little bit um i kind of look at the seated or the bent knee or straight knee and i'm like the the bent i mean one of the problems is always controlling for variables of joint angles and what's what's helping and i'm like if you do the bent like it seems like there's no way to get around you you have to load the solias and you that is that sub tendon but when you get to the straight like it just seems like you could be using your knee you could be using your hip um is that one of the issues in the research of like if you're sure you're gonna do a straight leg half raise but how do we know we're really isolating the calves that's also a very good question Jake i think that um when you're doing dynamometry testing with the knee straight we have a strap just above the patellar so it's making the knee straight and we bring the participant as close as we can to uh on the on the force plate on the uh dynamometry plate so the only change that we see is from the ankle because your knee is in full extension your backs you know you holding here not pushing or pulling anything you just producing force in your ankle so it's a lot hard to cheat uh whereas with the knee bend is a lot easier to just do like a leg press you know movement when you when you're testing so i think the way i've i've tested i think it's a lot more variable with the knee bend um to use to compensate and use other muscles then with the knee straight because the knee straight to very well pretty much locked in and you can't really move the sides of the ankle um when you're doing a leg press in the uh in the gym obviously you're not going to have your knee locked and you know not doing anything but you can pretty much maintain it's like the stationary knee extension and you're just moving your ankle on the leg press uh you can do a standing calf raise on the on the machine on the Smith or when the you know that's standing calf raise machine and you know even if you're swinging your hips you're not really moving much so it's mainly your ankle movement there um and remember i talked to you about that on the on the on the chat last week i'm just gonna get the name here of the paper i've mentioned that to you last last week so it was a paper from kino shita in 2023 they compare um uh muscle volume of the immediate gastric lateral gastric solias and they compare the triceps area as a whole uh as like a whole hypertrophy uh over a period of time come remember they did eight or 12 weeks and they compare seated calf raise with a standing calf raise what they saw was that as we expected the uh hypertrophy of the lateral and the immediate gastric was great with the knee straight compared to knee knee bend but there was no difference in solias hypertrophy it was the same and the overall triceps are a hypertrophy was great uh with the knee straight so in terms of muscle adaptation the knee straight would work all three muscles more efficiently and you're gonna have more load and you're gonna you know have higher loads to to do your exercises um you have higher strength only attendant uh when you bend in the um you know even though you go into more dorsal flexion because your your true gastroxinal working and x-maximal capacity the strain through the tendons reduced so i i can see that in terms of tendons strain being a sometimes used as a uh starting point but you can also do a you know standing calf raise with no weight if that's your starting point because you don't want to load the tendon heavy right so i i don't see myself a specific reason for tendinople to do a seated calf raise um i would see it for a solias strain muscle strain you're trying to you know really make sure that you're taking the gastrox out of the equation equation so you don't overload and be provocative with higher load um in in in this sense um but in terms of tendon adaptation tendons strain and even in in you know working the the whole muscle i i really don't see a point of that you did calf raise really yeah yeah i kind of for me i'm i was like it comes with training calves i'm like we have to start with something straight leg and then if they want to add more if they have time we could do a seated one but um yeah i was gonna say the the high for that study with the hypertrophy when you when you have these people with the killer tendinopathy i mean i'm aware of it with patellar and i don't i don't need a study on patellar to tell me but i've seen enough people with patellar tendinopathy and their quad is tiny you can just see it with the naked eye where it's like okay that you're clearly inhibited there and we should bring that quad muscle up um and you could even see it side to side it's like way smaller that side we need to bring it up um with the calf i've always i've always struggled with this do you see this asrophy in the calves with this long term Achilles tendinopathy um it's there is one study i don't know if there's more that have seen that um there was one study that saw a read like a selective atrophy of the lateral gastroc um there was a cruiser study um from marion cruiser i can't remember the the ear um but she used the muscle volume as part of the calculation to estimate the first production and there was a uh a reduced volume of the lateral gastroc in the tendinopathy population in terms of whole triceps array we measured runners and you know a lot of the runners don't have like big developed calves uh you know like there's there's not very common unless you are uh you know you're doing your resistance training unless you're like a triathlete and you're doing some other types of of exercise but if you're just running and a lot of runners don't do resistance training i think things are changing um these days but there was a lot of um concern of getting bulk here and slower um i don't know how much you see of that of people being resisted with doing weight training um but that that's definitely something that we um going to be measuring the um i'm co-supervising a PhD student uh looking at a killer syndrome of the and um would potentially be looking at ultrasound and and muscle um volume and fascicle length and and adaptations as well in these vocalist because this definitely something interesting happening the um okay this makes me this makes me think of if you're not i mean based off your work this this we kind of are like blaming the soleus i guess you have people blaming the soleus for these killies sending up the what but i'm like okay if they're not having those deficits in the the motor drive to the soleus um maybe then the hypertrophy stays the same because and then maybe that maybe if that hypertrophy is or that atrophy is happening just in the lido or gastroc um a question for you on that maybe that's why i've had a hard time of like i don't see a clear muscle atrophy in achilles tendonopathy but i see a clear muscle atrophy in the quads because i can i can just see them um what is the percentage what is the bulk of the soleus do you know off the top of your head the bulk of the typical soleus um in terms of the muscle mass of the triceps sir but it's quite a bit isn't it quite a bit more than the gastrocs yeah yeah yeah soleus huge yeah yeah so maybe just thinking now i'm like maybe that's why i don't see this this atrophy because if the soleus is not inhibited and not getting weaker or not or whatever going through this bad cycle maybe the calves stay pretty big and like if that lateral gastroc shrinks maybe that's hard to see by the with the naked eye um yeah yeah uh okay we spent all this time talking on this and we haven't talked the the rehab or the training for for the lateral gastroc um the the little bit i know is like looking into the the bodybuilding world of like they'll do feedouts for like medial get this was like way back in the day they're like feed out for medial gastroc feed-in for lateral gastroc uh yeah in terms of the rehab and the training if if we can kind of accept that there might be something bad going on with the lateral gastroc what are we going to do in training and rehab to restore this yeah i think it's it's precisely that point they brought up like my the last study of my PhD was looking at the uh the effective foot position in the in the medial and lateral gastroc activation uh and that was based on two studies one was in looking at similar things with more units and uh EMG activity in healthy population and that with the foot position we were able to selectively induce that those changes in your drive that exactly as it talked about the foot position in increase the lateral gastroc the foot position out increase the medial gastroc um and there was a um study with like a training study done in Brazil in São Paulo uh i think with São Paulo might have been in São Paulo but it was in Brazil uh and what they did was a um training study for eight weeks and they measured the um the hypertrophy of the three muscles over this period of time and compared they did a leg press and co-plantiflexion on leg press uh resisted and increased the weight accordingly and as people got stronger over over those eight weeks and they found that the foot position in induced a lateral gastroc hypertrophy uh and the foot position out induced a medial gastroc hypertrophy so it's it's not only the acute changes that we saw in our study and that those other study that I've mentioned saw but there's a chronic effect as well so it's not only about changing the new drive and changing the EMG as a lot of people say I know but EMG doesn't mean anything in terms of muscle contraction but there is a training study showing that that actually changes the the the demand of the muscle and the muscle gets it works harder and adapts so the way that I see it is um we can't say do this for tangenopathy because you get better because we don't know uh I think the next steps will be doing some sort of um clinical trial and and do the you know foot position in and see how that affects um you know the physiological A's and the tendons A's and all those uh reported outcome measures that we have foot position of the uh you know pain during running and all that um but on the other hand I don't see the harm on doing that so one thing that might be good at um addressing this bestest in in the lateral gastric would be adding a planta flexion exercise with the foot in on top of your exercise routine uh and it might might be they see something and you know it might be that at some point when we do this this study this um rct that we actually can prove their works but and in the meantime um I don't think I don't see the harm of doing it and um the same way as we use as you said uh if you have time do your seated calf raise um some people will start with um I don't know uh doing hops and lunges um sorry hops and jumps and uh different types of plyometrics to work the tendon in a different way it might be there one day a week or two days a week you'd adding a couple of exercise with the foot in um and it might be you know the missing link we don't know uh but it's just definitely on the list on on things to do and and try and see how that randomisement for trial works on on that um changes in in function and and paying in these people but thank you for the job thing if I've done this on the on the seated calf um wondering what you think because this gas drop is not working well on the seated calf there pretty much be no point in doing different foot positions on uh well I mean maybe there's a difference for the soleus but at least for the gas drop uh how much how much worse is the gas drop working in a seated calf like uh if you can get us slow as 50% okay less yeah yeah yeah so that depends on the angle but about 50% less so the the foot in training is like with a straight leg straight leg yeah you'll be you'll be like we use the foot in position but it's sort of like you're rotating your hips inward like no your foot your foot is positioned inward but it's like it's your straight knee you're rotating your your whole leg inward and I feel that it's easier to do on either standing or um calf raise um then the leg press I think the leg press because of that compression after leg press might some people might feel uncomfortable on the hips doing it um but you know whatever works as long as the foot's position inward as much as you can it doesn't have to be 45 degree or 90 degree or whatever degree is just you know some people would have structural anatomic limitations but um as much as you can rotate it inward um and see how that changes for you in my you know it's with the whole as a metric thing you know initially some people work for some people doesn't work so for those that work it might be a good strategy to do um you know some people have clear small lateral gas strokes so they you know and it might be that there's just there anatomy um and there's nothing wrong with it but I don't know I think we haven't figured out yet who would benefit from it and whether this would add any extra benefit than just a regular exercise training but I guess that whatever position is comfortable and um as part of your training not as a replacement of the the rehab protocol that you're having place the what are you doing with when you're doing that foot in um as far as like the distribution of pressure is it like staying on the the first and fifth of the med heads or are you like going on to the pinky toe the outer med head what are you yeah what are you kind of queuing people trying to go towards the the big toe um because if you go out you sort of like using your your inverters inverters you know with ankle stability and all that so trying to make sure that you're pushing off and your your toes are on the ground they're not rolling out um yeah so just maintaining your whole uh toes on the ground as you push um to give you that foot stability not letting your ankle roll out okay have you looked at this in terms of like the bound mechanical gate cycle um how like the soleus is engaging kind of early on and then this more like later finishing is is the more gastroc um I might have that kind of the whatever I'm just trying to simplify it um yeah have you looked at that at all and you're like maybe these runners they're really good at this early stance phase of the soleus is really good but it's like maybe that finishing all those strides with the gastrocs it's like maybe they're not as good at that because you're having this lateral gastroc inhibitor head is this any thought you've had not particularly that way um we there's not much association with these stops of studies and the things that we do because it's as as I said before with with the neurophysiology stuff it's very hard to reproduce for people running you know it's a very complex movements running um so it I don't know how much we could control during running to say that that's being caused by exalyzed muscle um what we do see though is that um evening healthy population the lateral gastroc we know when you're doing rent contraction on the dynamometer and you control your your ramp up uh the recruitment of the lateral gastroc is later than the medial gastroc in the soleus and that's just how it is uh we haven't looked at if that recruitment threshold you know like the the level of the recruitment of lateral gastroc would change in people within geography or if the the recruitment between the muscles would change we haven't looked at that specifically um so that's definitely something again on the list of things do but um yeah it might be that the recruitment pattern changes you have a further delayed of the lateral gastroc uh versus or maybe a um earlier activation of the of the lateral gastroc or later after the soleus I don't know it's it's I know that physiologically in in healthy people it's soleus medial gastroc in late that you have your lateral gastroc coming in or coming on born uh but we don't know if that changes with tangiopathy oh and and again just to be clear uh because I know that you know it's very hard for people outside of neurophysiology to understand the different types of variables that we measure when we say recruitment threshold is based on the firing rates of the morning and it's when they start to fire during a controlled visual torque feedback control so it's very um controlled environment it's not the same as seeing mechanical delay that we see with torque and and surface EMG and it's not the same as seeing just the delay in on on the EMG activity of the surface EMG activity on muscle contraction that represents may represent something else and it might not be very easy to interpret and to correlate clinically so that's more complex to analyze then what I'm talking about it's what I'm talking about is going back to the firing rate the neurodrive and more detailed more unit analysis rather than raw EMG and this broad IG of the work you know and the many factors that could be influencing that EMG signal okay I don't know if I was clear Jake that was a big confusing I mean yeah it's a lot of big words that I don't I don't fully know but um you said something earlier on the the lateral gastro I kind of like having this inhibition but then it's almost like it is it like oh gets overexcited when the the demand is very high was that would you be saying something like that yes so um there's a pain let me yeah because I would say on I I felt like that was the same thing with Ebony with it's like the quads are inhibited but then they're also get like overexcited there's something along those lines and my my terms are probably off yeah different things that were measured she measured the the recruitment curve of the corticospano excitability so she found also increased corticospano excitability which is what you're talking about there increase excitation of the stimulus curve plot what I was talking about is this paper from contraris from in in 24 I think was and they measured different levels of contraction and they did on top of the main the the the intensities that we did they also did a 70% of maximal torque so the the way we do this we get the the pitch expense to do a maximum contraction right and NVC a maximal voluntary contraction and then we work with percentages of that force so if they did X amount of newtons we're going to say okay what's 20% of that then we do a you know a contraction with the top of the contraction being 20% or being 10% or being 70% and that 70% this paper found an increased firing rate or increased um neurodrive of the lateral gastric which could be a compensation for the earlier you know the the lack of contribution during sub maximal contractions then it just comes all in you know so but it's as I said so it's different papers showing different things it's hard to put it all together because there are different measures what we can see though as I said as a summary of those papers is that uh everywhere we look the gas lateral gastric is showing that there's something that's just not behaving as a control or someone without an job fee um would behave so the the uh neurodrive or the activity or the contribution of force production is different somehow um and as I said I think it's just something we need to explore further and um and and keep developing our thoughts and our knowledge around that it was two early stages on on these are very early um types of studies investigating these but they're very exciting at least I find a very exciting um okay something ebony had was that for the the motor cortex was the the metronome um because I'm they're talking about this getting the side of gas if if this is a problem training it that does um to win position um I'm kind of thinking what else can we do is that something you think could be could be helping out is that something that has an effect on on that the nervous system to help uh work that yeah yeah so one of the things that is being used quite a lot for um corcorcus at the bit uh excitability or corgonibition is the use of accidental visual audio feedback so the metronome is one of them uh it gets you to control your contraction rather than just doing randomly and you know becoming automatic so you're putting thought and effort into it you control here um another thing that has a good effect on on reducing inhibition is essential contractions um and you might even explain why Alfredson's had you know good success with Achilles um but I think it's just part of that it part of that as well is um the the muscle specific you know as we talked about if if the lateral gas stroke is the muscle where the deficit the foot position in would be uh enough to increase that activation and as we've seen from the research training studies is enough to cause adaptation in that muscle with you know if you do it chronically with all the time so there are strategies for that uh and I think it's just including them uh as I said the the endurance calf raise I use with metronome um for pace you know to control the speed that they're doing um so it's easier to to um to reproduce and to compare the number of repetitions they've done today and that you know they're gonna be able to do in in in five weeks um but also in terms of um intracurricular inhibition would be a good factor because it stopping thinking and controlling and that engaging more of that voluntary control uh and and the drive to the muscle so they're the good strategies well I never heard about that with eccentric why is it with eccentric that it helps is because the loads are heavier or is it because what is it a very good question it's a very good question I can't remember it's up in my hand um the the mechanism behind the centric's uh I think the load being heavy is one of them but I can't can't really remember the top of my head the mechanism behind the centric but it's one of them yeah um okay so I I've done a podcast with uh car on sober nago is sober nago in uh Delaware and then I this was a long time ago but I recently did one with uh Rodrigo scatone and he was telling me they they're doing a lot of e-stem on the quads to get more tendon strain uh and they're gonna start doing it with the calves is that something like if you put the the e-stem on the lateral gastroc and you do your calf training is that a way to enhance this uh have effect on the nervous system would that have could could that have an effect or is that like I don't know too much about like e-stem but um or what the effect it has on the nervous system in the brain um yeah what are your thoughts there yeah so we we use that nerve stimulation or the neuromus stimulation with um you know that estrogenic muscle inhibition uh as to uh very classic post-op acl post-op knee surgery you know we all use it and and there's definitely good strategy uh that definitely increases the um the involuntary activation so that doesn't work passively it works in conjunction with exercise with resistance training so you're doing your exercises as normal and the nerve's team is just adding that extra layer it's just increasing that drives just making that muscle contract involuntarily you know that the so imagine you're doing 40% of your maximum contraction and the nerve's team is doing the extra you know 50 or or or or or the an extra 40 or something depending on the intensity so just engaging your muscle fibers more intensely um so that's what the the muscle team would be doing would be giving that extra input or the extra um peripheral component and over time with the the the feedback that we get from the muscle contracting with stimulate the neurodribe as well so that helps with that um critical inhibition by increasing that peripheral uh peripheral input that's not arriving at the muscle um okay uh okay last one I got for you here it's it's late for you over there um early here for me uh the you were talking I had a question on that and you kind of you kind of cleared it up for me so I want you to see if you can do that on the show here this whole subtendent twisting and there was there was that paper on the foot out position having more uh and you you you told me what it was because I kind of had it wrong but the foot out position had more of like this the sliding and gliding thing maybe between the subtendants or inside the tendons versus like the toe in position had more like to me like more of a stiffening up type thing um when we start talking about the subtendent twist or like the fascicle twist within the tendons what is yeah what's going on when the feet are out and the feet are in yeah I think that um there was as we talked about there was do a different papers um one of the papers measures the um the string of the tendon with the horizontal position so the foot being in or being out so the the foot position out would increase the the displacement of the lengthening of the uh latrogastro the medogastro sorry and reduce the latrogastroch and the other way around with the foot in it would increase the the lengthening of the latrogastroch and reduce the medogastroch which makes sense because increasing the the the lengthening increase in strain uh it goes it ties well together with the force uh capacity and the the contribution force um the other one that we talked about was the interfascals sliding and that's on the free tendon is not on the subtendent is where the Achilles tendon becomes the free tendon and it's the sliding off the deeper and the superficial layers that we talked about about the tendon twist and you have the more the deeper layers and the superficial layers and we have the interfascal sliding so the tendons are uh uh sliding gliding when we move um so the action things um okay yeah we've got to uh cover a lot of stuff here um i think it's it's funny at someone i posted i posted on instagram that i'm going to do a lateral gastroch tendon podcast with you and they were commenting how how niched down i am you know i'm gonna do an hour podcast on the lateral gastroch how crazy is that um yeah tell me what to know what's what what are the new things you're working on um yeah so as i said i have this PhD student that i'm co-supervising um i'm the same university that i did my PhD so she's continuing in a way of saying you know where where i stopped so she's looking at the different muscle contribution and activation during fatigue so as with as we found a lot of the endurance deficits in the cuff muscles we're stimulating fatigue and imagining the muscles throughout this process so we're going to have um one one one study that we just almost finished and we have another two studies they're going to be looking at different things fatigue related and how the each muscle contribution um changes with fatigue and you know and see if we can explain some of the things that we saw in terms of um with the participants rested and now if that's that can be observed more clearly off that exacerbates when they are you know with the muscles of fatigue um i am also organizing uh i have the survey that we talked about and i have a few projects on um on the draw that i'm i'm starting next year uh one of them is going to be with um single leg cuff raises and we're trying to see um how we can improve the protocol to make sure that it's going to be easier to test and um as i said like i i think that working in a way that becomes easier for patients uh is a good way to go especially with you know telehealth and some patients not having access um here in australia we have a lot of um you know regional communities and some of them um away from you know the the closest clinic uh there's a lot of telehealth there's a big uh startup telehealth after uh after COVID and drink COVID and after COVID and uh i think that you know developing this this test will be helpful for that as well so that's definitely on the on the list but i think that as a as of nation i think one of the interesting things that i want to look at is more explore more about about that relationship of each muscle in in in in in in runners with then job thing and try and see if there are more the nuances that we don't know yet and there are a lot of the questions that you brought up there are a lot of very good questions that we still trying to figure out a way of of answering that and and testing that so that's definitely on the on the next steps trying to answer all your questions take um i was gonna say earlier i'll put that survey in the notes i i did it myself the other day it took me like 10 minutes um great yeah so hopefully we get so get some more people to do that uh but yeah man tell tell everyone and we're to find you online yeah so my instagram is Gabe Tizio and so it's my uh twitter uh i'm a lecturer at Southern Cross University in Australia so if you go across the Indian uh put my name in you get my email and my details there so you know if you're watching this and want to do a PhD with me just get in touch all right man thanks for coming on yeah thanks Jake

Podcast Summary

Key Points:

  1. Gabriel Fernandez's research challenges the traditional focus on the soleus muscle in Achilles tendinopathy, suggesting the lateral gastrocnemius may play a more significant role.
  2. Neurophysiological studies using TMS and high-density EMG found increased cortical inhibition and altered motor unit firing rates in the lateral gastrocnemius, but not in the soleus or medial gastrocnemius, in runners with Achilles tendinopathy.
  3. The findings indicate a potential issue with neural drive and muscle coordination strategies within the triceps surae, rather than a primary deficit in soleus force production capacity.

Summary:

Gabriel Fernandez, a physiotherapist and researcher, conducted a PhD study investigating neurophysiological mechanisms in runners with Achilles tendinopathy. Contrary to previous research that blamed strength deficits in the soleus muscle, his work points to altered neural control of the lateral gastrocnemius. The first study used transcranial magnetic stimulation (TMS) and found increased cortical inhibition in the triceps surae area, associated with reduced plantar flexion endurance.

A subsequent study using high-density electromyography to analyze motor unit firing rates revealed that the lateral gastrocnemius did not appropriately increase its firing rate with higher force demands, unlike the soleus and medial gastrocnemius. Further investigation into specific spinal circuits for the soleus showed no differences between groups. Fernandez hypothesizes that running, as an endurance activity, might lead to fatigue in the less fatigue-resistant gastrocnemii, prompting neural compensation strategies that could alter force-sharing within the calf muscle synergy.

The research suggests a shift in perspective is needed, moving beyond solely targeting the soleus in rehabilitation to consider the coordination and neural drive of all triceps surae muscles, particularly the lateral gastrocnemius.

FAQs

Gabriel Fernandez is a physiotherapist originally from Brazil, now living in Australia, with 16 years of experience working with sports, including Olympic athletes and everyday runners.

His PhD research focused on neurophysiological mechanisms affecting the soleus muscle in individuals with Achilles tendinopathy, using techniques like transcranial magnetic stimulation and high-density EMG to study cortical inhibition and motor unit firing rates.

The research found that the lateral gastrocnemius showed altered neural drive, such as not increasing firing rates with force increments, suggesting it may play a role in Achilles tendinopathy, contrary to the common focus on the soleus.

The nervous system modulates force by either increasing the firing rate of motor units or recruiting more motor units, similar to adding more people to pull a car or making them pull harder.

The findings are based on isometric contractions, and dynamic activities like running involve changing muscle lengths and tendon behavior, which current high-density EMG methods cannot accurately measure due to noise and technical constraints.

High-density EMG electrodes placed below the gastrocnemius bulk can capture soleus data effectively, as this method is validated and comparable to intramuscular EMG, unlike traditional surface EMG amplitude analysis.

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