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Tendinopathy, inhibition and force output

David: Hey, Pat, how are you?

Pat: Good thanks, Dave

David: That's good. Thanks for joining me on the podcast today. It's great to have you here. I'm looking forward to talking all about tendinopathy. You've spent a lot of time researching tendinopathy, and there's been lots of really interesting developments in the tendinopathy space over the last few years.

You know, when we're looking at patients that come in with a patellar tendinopathy and you test their quadriceps, you may be using a leg extension test or something to isolate it, they're gonna test weaker, you're going to get that lower maximal force production.

And so I wanna dive into the causes that someone might have that reduced force output when they've got a tendinopathy, what we can actually do to help improve that force production, and then how do we effectively treat tendinopathies.

Looking forward to diving into that with you.

Pat: It'll be great. Really excited to, talk through all things tendinopathy.

Measuring inhibition

David: A bit of background. I mean, we've been looking at this tendinopathy space and in particular the inhibition, 2016, Dr. Ebonie Rio found that there was that altered motor drive between your brain and your quads, in a patellar tendinopathy, and presented the theory around corticospinal inhibition.

And so we've been using, your externally paced tendon neuroplastic training, your TNT, using that metronome to sort of address some of that inhibition that was going on in that corticospinal tract. Sounds like there's actually a little bit more to this inhibition story than, we've known about before.

So how do we actually know for a start off that there is inhibition going on, that we don't just have, say, quads weakness that's causing that reduced force output?

Pat: That's a very good question just in terms of how this might manifest in the clinic. The main clues would be weakness, or reduced force output at the upper end that doesn't quite fit the person in front of you. If Perhaps they've been, in that gym setting for a while or engaging in the activity that should be resulting in quite a high level of force output, and they're just not, seeing that, adaptation that they should.

That's one big clue. We see it manifest in other ways, and, this is perhaps a little bit less, robust in terms of its confirmation in the research setting. But, we see, a alteration to the quality of movement as well.

As opposed to a, contraction, say it's knee extension, that's nice and smooth. We see it's, got that reduced quality. It's quite jittery, um, fasciculation we might describe it as. So that, that's another way it can manifest. But predominantly in, patellar tendinopathy, it's that cap, that inability to really achieve the higher ends of, force output.

What's interesting is we can quantify this to a degree by comparing people with patellar tendinopathy to those without, and we've seen that there is a reasonable deficit there. In my own research, in the lab here at, at Monash with Pete Malliaras and co., we found that athletes with patellar tendinopathy, so volleyball, basketball athletes, they sit around on average point seven or high point sevens, call it point eight, knee extension strength for kilograms of output per kilograms of weight.

Where their healthy comparators, so athletes taken from the same settings, volleyball, basketball athletes, they're achieving over their body weight. So a screen could be something as simple as if they're active young, should otherwise be exerting quite good force in that patellar tendinopathy cohort, looking at that relative output of force in kilos, compared to their, body weight in kilos.

That was with an isometric, so perhaps with a dynamometer might be the way to go there.

David: Yeah, for sure. And so they're gonna test weaker and you, even when you compare them to the opposite side or normals without tendinopathy.

But how do you know it's an in- inhibition case, they're not just weak?

Pat: Well, I guess there is an argument to be made there that it could be a degree of, weakness. But these people, these, athletes, at least I'll speak to the athlete population, they are generally already in that gym setting. They are generally already, ticking the boxes that should be, enhancing their strength. So it's just a lack of, I guess the strength that should be there or the, gains that they should be making aren't being achieved. So something's not quite fitting, is the best way I could describe it.

David: Yeah, for sure. Also looked at some studies there where I think you were doing some neuromuscular electrical stimulation, in conjunction with the contractions. Did you find that that made a difference in different groups, or how did that sort of impact it?

Pat: Yeah.

So, It was a fairly high-intensity electrical stimulation we use there over the femoral nerve, which, supplies the, quadriceps. we get them doing a max contraction, and then we stimulate with that electrical stimulation, and we look at can we achieve more force, i.e., Their voluntary drive, is that reduced?

David: It's not the sort of thing you're gonna be providing strong electrical stimulation in the clinic, but basically, if you had those patients that had decreased force output and you gave them a bit more electrical stimulation at the quads or over the femoral nerve, then you got higher force output

Pat: Exactly that. Yeah. we have a few measures when we look at inhibition. We've got a, a fairly robust protocol that we've worked up over a bit of time, and some very clever people in the lab, much more clever than me, have, chipped away at that and built, that up.

But yeah, with that particular protocol, it's really interesting and it really-- resonates with the, the participants in the lab when we have them sitting there in the chair doing the isometric knee extension force.

They're contracting as hard as they can. We apply the stimulation, and then there's a jump in their force beyond what they can produce voluntarily by themselves. So that's telling us that they're not fully engaging their motor units and not able to access the potential of, their infrastructure, of their, muscle.

So yeah, really fascinating and, it paints a picture for the patient or the participant in that setting, for the deficit , being present and also helps us build a case then because we, have some interventional studies at the moment. So it's easy easy to motivate when you say, " Would you look at this? Maybe we can gain a bit more of that. That's, within reach."

So it's a nice motivator.

David: Definitely. How does that compare when you've got a patient that doesn't have patellar tendinopathy? Do they have any change in their force output when you add that neuromuscular electrical stimulation?

Pat: Yeah. so this is where research gets quite interesting. So in my own PhD, we showed mild reduction in people with patellar tendinopathy compared to those without. It wasn't statistically significant, but there was a prior study, the work of Stephan Davi from over in the US a few years prior, and he did demonstrate there was a significant difference.

We are working at the moment on a, a review, and when you pool all the data together, it seems to be that there is a, bit of a reduction relative to our healthy cohorts.

So The patellar tendinopathy group they'd have a ten percent deficit. When they try to access their, knee extension maximal strength, as opposed to achieving, let's say a hundred kilos for the sake of being nice and simplistic, they'd be hitting that, 90 mark. Where your healthy cohort, there is a deficit, say five kilos if it were a hundred kilos, otherwise achieved.

So about double the deficit, which is quite interesting. It's force that they, can't generate that could otherwise in an athletic population be really useful to them for performance.

David: Definitely, yeah.

Why look beyond the tendon?

David: So, When we're looking at differences in their force production, why then are we interested in the spinal cord in particular, looking at the different spinal tracts? Can't we just give them some sort of exercises to load the patellar tendon? Or, why do we need to sort of go further?

Pat: It's a very good question, and it's something that I've mulled over for, some time, and it's a, topic of, discussion in our lab.

The current projects we're working on, we're, we're working towards trying to come up with a more targeted rehabilitation, program.

So we've landed on a-an approach with patellar tendinopathy that if you search backwards across years, the way we got there was largely driven by a little bit of happenchance if I, I can be a little bit cheeky.

David: Yeah.

Pat: The, original Alfredson protocol, the eccentrics, as as a result of, Alfredson having Achilles tendinopathy and being down the line in the public system and wanting to get the surgery, which at that point in time was the way to go, and thinking, "Well, if I make this worse, I'll bump myself up the list or at least get a rupture of my tendon, and that will bump me up the list." And doing his eccentrics and improving. So there was a little bit of chance involved in that. But then the iterations since have been built on that. So this idea that if we put strain through the tendon, we'll get some adaptation, or if we make the person a bit stronger, that's going to be a good thing. There there has been some finessing at different stages, but there's been a bit of stumbling forward in a sense. So we thought why not try to explore what the actual mechanisms are underlying the deficits in the first place or the impairments for function?

What's also driving pain? Can we understand that any better?

And then can we use intervention that have been established in the literature elsewhere to try to target those more directly? This is where the nervous system comes into it in a, bit more relevance.

Corticospinal vs reticulospinal pathways

Pat: So the corticospinal pathway is the primary pathway generating force, and it's absolutely critical to force production.

We, don't have force without the corticospinal pathway. Kicks off at the motor cortex where we've got these corticospinal neurons and they run from the M1 from the motor cortex all the way down the spinal cord to the level they synapse onto the peripheral nerve. They either fire or they don't.

They'll carry that signal down. If they fire, they carry it down. All going well, they synapse onto the peripheral nerve. It carries it to the muscle. You get a contraction. There are a couple points that can be manipulated or altered in terms of generating the signal in the first place or carrying it across and this is where that cortical inhibition came up or that's where it's relevant.

So at the very top of the chain, we've got some neurons that input onto the motor cortex and they're going to dictate whether or not those corticospinal neurons fire or not in the first place.

So if cortical inhibition is higher, we've got some neurotransmitter activity up there that's making it harder for the neurons to fire.

So, if that's higher, less, less signal going down, less force.

David: So that's where it's originating. It's, it's all happening up there in the motor cortex. It's then like sending those signals down that corticospinal tract to the peripheral nerves. So up at that motor cortex, there's some inputs to that, that could also cause it to have reduced output?

Pat: Yep, absolutely. And then the other site that can be altered is that synapse between the end of the nerve in the spinal cord and where it synapses onto the peripheral nerve. So where we have a synapse, there is opportunity for other neurons to have input. So that's where we can have inhibition, so we call that spinal inhibition. So that's another site that, we see in different pathologic populations, that there is an increase inhibition and that spinal cord can't communicate with the peripheral nerve, and as a result of that, get this force output. So that pathway is super critical, and we can pull that apart, and we can look at the different elements that matter and might impact force output. And that's where it gets a bit more complicated because there is another pathway to add into the mix which, hasn't necessarily got the attention it probably deserves across the years, and that's just because we've struggled to measure it in a robust manner. But we've got some techniques now that allow us to look at it in a bit more depth. So that's the reticulospinal pathway. So this pathway, think of it like the dimmer switch that can be tuned up, to enhance the sound coming out of the pathway. Or I can even run you through a different analogy if you want.

David: Yep ok. Hit us with it.

Pat: Yep. I call it the garden hose analogy. So if we look at drive from the brain to the muscle as the garden hose where you've got the tap, you've got water pressure sitting there at the tap, so that would be our motor drive, and the tap itself.

So if it's open, the water's gonna flow through. Our cortical inhibition is, fine. It's not, um, affecting drive. If we close that tap, that's like the cortical inhibition being tuned up and then making it harder for the water to flow through the hose. So if the tap's open, water's going to flow through the hose. Ordinarily, if there's no kinks in the hose, it will get to the end of the line and come out the sprinkler, and there's your motor output. What we've discovered in patellar tendinopathy is that the tap is open or at least open in a sense that it's not impacting on force output. So cortical inhibition doesn't seem so relevant to force output, but there's a kink in the hose.

So that kink in the hose, it's folded over on itself, it's stopping water flow, and that's something downstream, and that's our, spinal inhibition. So we've worked out that it's a bit further down the chain. It appears that that drive is being affected, and critically, we've been able to link that inhibition, to force output, lower maximal strength output.

So, we've been able to make some important links there. The other pathway I mentioned, the reticulospinal pathway, so call that the supplementary pathway of sorts. The really nifty thing there is it directly modifies force output by targeting spinal inhibition. So it works via a, um, bit of a reflexive loop, at the spinal level. It can enhance force output by, sort of counteracting spinal inhibition. So we can help cancel out that spinal inhibition to restore force output. So there's some really, really neat interventional changes. Not necessarily complex changes, but certainly changes that we could make that might modify, the result of our rehabilitation if we were to sort of tap into that system.

David: All right, let's kind of dive into a few of those things there because there's some complex stuff going on. So we've got the corticospinal tract, we've got the cortex, motor cortex sending signals down this corticospinal tract, and then we've got the synapses onto our peripheral nerves.

That's in sending the signals out and we're getting, say, a quads contraction in this case. Then we've got our, this reticulospinal tract that's almost like a secondary pathway, we'll just say. And so where does that originate and where does it go to?

Pat: There still is some cortical input onto it, but it's brainstem mediated. Given that it's brainstem mediated, our cortically targeted intervention might be slightly less impactful on it. uh, Runs bilaterally and it, inputs onto our gamma motor neuron.

So as opposed to our main peripheral nerve, which supplies the muscle, which is the alpha motor neuron, it inputs onto the gamma motor neuron, which helps to pre-tension the muscle. So via a, call it a sensory loop, it enhances excitability at that spinal level. So for us to achieve maximal force output, it actually, this reticulospinal pathway has to be active and excited. Without it, we're not going to get the same level of excitability, and that's across the board irrespective of pathology. So it's really critical to max strength output.

We're starting to learn now that a lot of the adaptation to strength training is due to this pathway and enhancing its excitability. So the corticospinal pathway might be important to output in the first place, and when we're enhancing things, often it's more so that reticulospinal pathway is being, improved upon, made a bit more effective, and that's where we, we see people, might get that top-end strength and so maximal strength and even power output.

Pain and spinal inhibition

David: Okay. So it's important for that maximal force output. It's starting at the brainstem, it's then traveling down and impacting spinal inhibition. So when you're talking about, say, spinal inhibition, is that happening down at those synapses between, the, um, corticospinal tract where it's meeting the peripheral nerves.

Is that where you're thinking about spinal inhibition happening?

Pat: Yes. Yeah, yeah. So localised to that, that synapse between the, end of the spinal cord so far as that corticospinal neuron to respective region runs and the adjacent peripheral nerve. So it acts on that, that synapse.

David: Right. So, so we've got a few things coming into that, synapse. We've got that corticospinal tract and we've got that reticulospinal tract all coming in and meeting onto that, or synapsing with those peripheral nerves, a bit like, you know, some feeder roads all coming into the, the major highway or whatever to the quads. Is that right?

Pat: Yeah, exactly. and we have to consider what is the source of this spinal inhibition. So this feeder road that comes in and produces the inhibition that makes it harder for the corticospinal neuron to communicate with the peripheral nerve. and with some of the work that, we've run here, we've been able to link our ascending nociceptive input. So our, nociception coming from the, tendon, activates a neuron at that spinal level, and it then, will inhibit or make it more challenging for that corticospinal neuron to communicate with the peripheral nerve.

it's very similar, if I can draw parallels to arthrogenic muscle inhibition. A lot of clinicians will have heard of arthrogenic muscle inhibition, and it's a very popular concept in ACLR, um, patellofemoral pain as well. It's well established. So it very much is that same mechanism where as the sensory information comes up, it will, at that spinal level, excite a inhibitory interneuron, so a, a nerve there at the spinal level that's going to then make it more challenging for that synapse between the corticospinal pathway and the peripheral nerve.

David: If you look at that arthrogenic muscle inhibition type, pattern, you've got pain at the knee, then you get this inhibition going on. The body goes, "Oh, we probably don't want to use this knee so much and these quads, so let's inhibit those muscles." so then you've got this nociception going on, feeding this loop where you get inhibition of those muscles at that spinal level. And so this works in a similar way. So from a tendinopathy point of view, you're getting that nociception that's activating those inhibitory interneurons, and then that's causing-- it's turning down that signal then in that little bit of a feedback loop to the quads.

Pat: Yeah, precisely. and the, thing I'd really highlight there is that this is in patellar tendinopathy, so I won't extrapolate that to, uh, other tendinopathies. but in patellar tendinopathy, that's, our working, theory at, this stage that's based on, our work in the lab and the work of some others that we've been able to get to this point where, call it quadriceps muscle inhibition, if you will, if arthrogenic is a bit jarring, uh, when it's coming from the tendon rather than the, the joint surface.

But, it seems to be very similar to these other conditions. And I think it's, sensible to a degree that it, makes a lot of sense that if we've got this ascending nociceptive input and concurrent motor signal coming down, one's going to make it more challenging for the other. Pain is going to make it more challenging for motor output. That's a very sensible design of the body. But, this point, we had thought that it was more so that cortical inhibition that was responsible for altered force output. So it's a bit of a bit of a discovery. It's a bit of a, a leap forward for us in that it highlights some different options that we could consider for intervention to try to restore maximal force output.

David: Yeah. And, and I do want to get into that with you. I just want to explore this a little bit more because we've got this corticospinal tract that's, sending signals down. We've got the reticulospinal tract, and so we've got, two different pathways coming down, they can vary in how much each of those is inhibited.

And so how do you actually go about telling? I mean, when you're, you're looking at research, obviously you can't do this at the clinic you can't look at these tracts and go, "Oh, yeah, we've got this much inhibition of your corticospinal tract." But when you're looking at these in the lab, how do you go, we've got inhibition of the corticospinal tract versus the inhibition of the reticulospinal tract?

Pat: It's a very good question, and I'll be completely upfront. We, probably haven't got quite so far as having, the tests there. A, shout-out to a, a mentor in Danilo de Oliveira Silva, who I've chatted with at length. We've got these really hardcore laboratory measures that aren't overly or they aren't applicable to the clinical setting. He's very big on establishing these links between existing tests in the clinical setting and our laboratory tests. So we are working away on it. You'll be the first to know as soon as we've got something a little bit more concrete where we could put that to the test and work out, yeah, what pathway, is responsible, but we haven't, quite got there just yet. I guess what I would say is while there will be heterogeneity across the, the populations with patellar tendinopathy we have e-enough data now to start to form some, decent understanding and, I guess acceptance of what some probable drivers for impairments might be. At this stage, it all seems to be pointing towards that spinal inhibition, which would be a deficit in the cortico-spinal pathway. I guess the other thing you could consider as well is the trial and error of rehabilitation approaches and, different rehabilitation approaches will target those different systems. one might be preferable based on the likely deficits, but in failing that, you can absolutely trial the other, and if you get a good response, then that might be your indicator.

David: Yeah. So you've

mentioned there before that there's some excitability sometimes in that reticulospinal tract. So how do you measure whether there's inhibition or excitability in those tracts?

Pat: In the lab we use, transcranial magnetic stimulation. We use the electrical stimulation we mentioned before, and the new addition, we're looking at some, high density EMG.

which is where we can measure each of those components we've covered so far and their relevant contribution to force output. So in a research sense, we can measure inhibition of the various components quite well. Or alternatively the upregulation of certain components, quite well and we're at a point now with our protocol, I mentioned before some very clever people in the lab, have helped to, move our protocol forward to a point where we can be very comprehensive so we can capture most of those components between brain and muscle, and that's something that hasn't been done overly well historically.

So at this stage, we can, with a bit more certainty, say, " This component contributes more," or, "This component isn't affected." So it's been a very exciting time in the lab.

Power vs control

David: Yeah, it was pretty interesting to read the articles and you've got someone sitting in a leg extension machine then you're positioning transcranial magnets over the motor cortex, sending a brief pulse of magnetic force down and then measuring with EMG at distally, say at the quads, that sort of thing, while they're performing different levels of contractions. I was like, This is some pretty cool stuff going on here to, uh, send these magnetic pulses and then measure at the other end how much of that amplitude of pulse is coming through."

Pat: It's a interesting one when you're talking to prospective participants and trying to explain it in a way that you don't scare them. It is very, very safe. It's been used for a lot of time. But yeah, electromagnetic pulse, and we search for the, area over the motor cortex that directly corresponds with the corticospinal neurons that would carry that signal down the pathway to the quads.

I'm very lucky to be surrounded by some, clever people that, have developed some protocols and taught myself and it's not lost on me that it's a very interesting tool and, gives us some very interesting insights as well for what might be driving motor deficits in tendinopathy in particular.

David: From the studies, it, seemed like there's a difference in speed. Like you mentioned before, you've got the, the alpha pathways, when you're looking at corticospinal tract, then you've got the alternative pathways in that reticulospinal tract. Those were gamma neurons. Is there a difference in speed of those signals that's, getting down to that spinal level when you're going with the different pathways?

Pat: There is, and that's something that we use actually to measure the excitability of either respective pathway, in one context. but the, corticospinal pathway, because it's monosynaptic, it's got that one synapse, the end of the, corticospinal neuron onto that alpha motor neuron, it's a bit quicker.

So we see from brain to quad, it's about ten milliseconds, while the, reticulospinal pathway is a little bit slower. It's got an extra, synapse. So, it's a polysynaptic pathway because we've got cortical neurons that then input onto the brain stem, so that's an extra bit of delay for that synapse to occur. What is really, really interesting is despite that speed of, transduction down towards the muscle, we see that it's the reticulospinal pathway that is particularly critical to power and peak force output. So it's used to a degree, the pre-tensioning of the muscle, spindle in particular. So it just means that there is a greater level of sensory feedback, to that spinal level to optimise excitability of the alpha motor neuron. It puts back onto the alpha motor neuron. So it sort of optimises the engagement there of that alpha motor neuron. So the reticulospinal pathway, unless it's fired up, we'll find that our peak outputs are actually, diluted a bit and a bit lower.

David: So we've got, the slightly slower reticulospinal tract, we've got the faster corticospinal tract, the reticulospinal is a little bit slower because it's got that bit of a join it's a road with a stop sign or a give way or something halfway through, you got to slow down.

So you get there a bit slower But you get there in the end, and both of those can be inhibited. Is one more involved in different tasks when you look at the corticospinal tract versus the reticulospinal tract? Do they have a different role?

Pat: They definitely do. The reticulospinal pathway, we associate more so with that, peak output. So maximal strength, power output. Given that it is a brainstem pathway, so you don't have that same level of cognitive, or the same level of, cerebral involvement necessarily. It's meant to be a bit more autonomous, so it's really important to locomotion, bilateral tasks. it's also more important from a reflexive perspective or reactive, I should say reactive, not reflexive. So if you were to trip and you put your leg out to catch yourself, that's a reticulospinal pathway doing its role, in acting to allow you to produce that power very quickly, autonomously to stop yourself.

You don't necessarily think about it too much. In contrast, the corticospinal pathway is a lot more about positioning and control. So, we see it as being a lot more important to the upper limb. If you're thinking about the upper limb where we, move the arm to position the hand to pick something up that control is very, densely innervated and resultant from the corticospinal pathway. While we see a lot denser innervation to the lower limb with the reticulospinal pathway, just in that it's particularly, critical to the types of tasks that we, perform with the lower limb, locomotion, jumping, running, all these sorts of things.

David: Yep, that makes sense. So when you're looking at, say, your corticospinal tract, it might be more involved in those fine motor tasks or like the control, balance, motor control, that sort of stuff, and then your reticulospinal is more involved in like those faster or more powerful sort of movements.

Pat: Yeah, I think that's a really nice way to describe it. .

Metronome-paced vs self-paced training

David: I think it'd be good to, move from, the science in the lab to

some of the clinical implications for people. So

a patient comes in, they've got a patellar tendinopathy in this case, and you're saying, "Okay, we, suspect based on the research that you've got some inhibition in the corticospinal tract, the reticulospinal tract.".

So we've got this inhibition from top down. You know, we've got nociception coming up, and maybe that's impacting it. We've now got lower force output. So how do we actually go about addressing some of this inhibition?

Pat: I think it all, stems from a thorough assessment in the first place to identify that individual's impairments. We have likely functional deficits. So when you're saying functional in that context, it's max strength? is it, your, output that's more aligned with your general strength, muscular endurance, power, all these sorts of things. So we can assess them, we can profile the individual in front of us and that gives us some good clues and then we can lean into what we know about the nervous system, the the motor neurophysiology, and try to bridge that with clinical practice, and a nice solid S and C principles to land on an approach that's going to help that patient. So I'll use the patellar tendinopathy example. We anticipate that based on the literature, it's most likely that they're going to have a maximal knee extension deficit, that would be the most probable deficit. We can assess their max strength, but it's also worthwhile - looking at power, muscular endurance. These are the components that are absolutely going to be essential to that person being able to do the things in life that are important to them, be that sporting or, otherwise. From a a max strength perspective, you can then work out, is that impaired compared, for example, to normative data?

I mentioned before that, measure of, knee extension maximal isometric strength in healthy, athletes being one kilogram of force per kilogram of, of weight. If they're hitting those marks, they're probably not in a bad spot. If they're below that, then that might be something worth targeting and, noting that that would be beneficial to them. So if you've got a, a good understanding of the person in front of you and, I guess what their impairments are, it's no different to any patient. We then lean into our, um, I guess the, the science and try to come up with an intervention that's going to be most likely to produce improvement for them. If it is max strength that's reduced, and it is someone with patellar tendinopathy, the, the evidence tells us that it is more likely the spinal inhibition that's affected, that's going to be part of the picture in terms of them being weaker in that output. What we can do there is through what we know about the reticulospinal pathway and its input onto that spinal level and targeting and counteracting the spinal inhibition, we can try to, um, channel change there.

Jonas, one of the PhD students who graduated here last year, he... compared metronome-paced training. This was for the biceps, mind you, but three weeks of metronome-based elbow flexion training, to, self-paced training and concurrently looked at nervous system change. So he looked at the corticospinal pathway and the reticulospinal pathway, and what he found was that the metronome-paced training The people got stronger generally. This was with, your pretty typical, four by six to eight, I think it was reps. They got stronger, but the corticospinal pathway was what was adapted with the metronome-based training. So very much in line with what we know and believe about, the corticospinal pathway, that if you use external-based cues, it becomes a bit more like a motor control task, and there's neuroplasticity that results. So those people got stronger, and that was great. The self-paced training, no change to the corticospinal pathway. They got stronger, their power also improved, and the reticulospinal pathway got more excitable. So we've got different levers we can pull, and that's a very small tweak to make to your rehab. Could be the exact same exercise dosage in terms of you're still looking at your top end, yeah, your four by six, for example, strength training, knee extension work for patellar tendinopathy, but have it be self-paced rather than metronome-paced, and that will tap into the reticulospinal pathway as opposed to the corticospinal pathway, and that should result in a more optimal outcome if that were the deficit, the spinal inhibition. In contrast to that, and I, I'm, really mindful of when I say this, this is that patellar tendinopathy, um, example. In other tendinopathies, that may not work so well. So achilles tendinopathy, Gabriel Fernandes, brilliant Physio researcher and lecturer up at Southern Cross Uni in Queensland. he looked at cortical inhibition in Achilles tendinopathy, and cortical inhibition is more relevant there.

Cortical inhibition in Achilles tendinopathy seems to be more of a problem. So the metronome, don't throw it out just yet. It might be useful in Achilles tendinopathy as far as we know at this point in time. But in patellar tendinopathy self-paced training might be the way forward in terms of tackling, um, these deficits and really trying to target the underlying deficits that are most important.

What is self-paced training?

David: So they had compared the four weeks of self-paced training to four weeks of metronome-based training. With the metronome-based they had changes or improvements in the corticospinal tract, excitability, and then when they performed self-paced, that they had improvements in the reticulospinal tract.

Did that, result in any sort of measurable differences in strength, or were there any, overall differences at the end besides excitability of the different tracts?

Pat: So both groups increased their maximal strength, so that's good. I guess the context there is they were healthy, so there wasn't necessarily a deficit existing that could be tackled to promote greater benefit.

I guess the key difference there was the power benefit. So the self-paced training, they increased max strength and power, where the metronome-based training, they only improved on the maximal strength. It, links back into what the individual in front of us, their deficits are, and, I guess our, our knowledge of these conditions from a motor neurophysiology perspective and what's actually driving the reductions in strength in the first place. We can use that knowledge to help shape our intervention based on the, the different cohorts we might come across.

David: So they both had improvements in strength, four weeks is not a very long time, and it's, you know, the biceps, but they had improvements in power after four weeks with the self- paced training. So what's self-paced training?

What's that mean?

Pat: It sounds simple, but you're just removing the external pacing at the point of doing the, exercise. But you can give a bit of cuing beforehand, give a bit of a demonstration for a rough pace. But allowing the patient to then perform the reps at the pace that they feel comfortable with is that hopefully mimics to some degree what you showed them beforehand. You're taking away that external cue, the component that's going to make it more of a motor learning task essentially.

David: They often use, say, three seconds up and four seconds down with your metronome-based training. Whereas self-paced, you're saying, okay, just, perform your reps, at whatever speed feels comfortable for you.

Pat: Yep, at first when you hear that, you think, " Well, what about some of the other variables that matter " so time under tension, for example.

David: That's what I was wondering about, yeah.

Pat: When you then, look at the strength and conditioning literature, the ACSM's recent position stand , some of the variables... are important, don't get me wrong. But some variables they identified as not being important to outcome, and time under tension was one, which really surprised me. So it's more about, when it comes to max strength in particular, it's about performing the movement at the relevant intensity. For how long that occurs for doesn't matter, so long as there is a, minimum amount of reps, but it's not about how long those reps last for. It's about the intent and the intensity that you're working at.

David: And I guess even looking at those specificity principles, your externally paced metronome-based stuff, so you've got a slower, based rep. You've got three seconds up, four seconds down. You're quite a slow rep, whereas maybe self-paced is quicker. So I guess you got, if you've got quicker reps, you're gonna expect an improvement in your power, which is more your, force divided by time.

So you're gonna expect improvements in that, those sort of factors. So I guess that fits with those specificity principles as well. But then what you're looking to, do, you're tying that together and saying, "Okay, they also had improvements or increases in excitability in that reticulospinal tract," and sort of associating those two things together.

Pat: It was a really interesting paper, and fascinating results. And, it's a case of was it the, speed that they moved at or is it the change to the drive through those pathways that we chatted through and the, the resultant, change to power and could be a bit of one and a bit of the other. but super, super fascinating. And then circling back to looking at the person in front of you and, what they need to improve, and what the likely deficits are as well in these conditions as well matters there.

But we've got a few levers we can pull there. And at the very outset, earlier you asked about, well, how can we know what system is or which pathway might be affected? And to a degree we go with the likely deficits first and the known impairments for, function. So if it's max strength, we suspect spinal inhibition, you might try your self-paced work first, but that's not to say the, metronome-based work wouldn't work.

That might just be failing self-paced. Maybe we try the metronome.

David: Yeah. They're not mutually exclusive, are they? And looking at impairments that would help you identify that they need to work on their max strength. So I mean, that's pretty an obvious one to test and you look at that, with your tests.

But then when you look at, say, your corticospinal tract, some of the indications in the clinic that indicate that the corticospinal tract's impaired are your cogwheeling or like some of those, control issues maybe , when they're lowering it down, it's not that smooth lowering or coming up through your isotonics,

Pat: It's a clinical phenomena that a lot of people I've spoken to have commented on, and at the moment I'm, running a trial. And apologies if you can hear some, some noise in the background.

That's a bit of a, a similar trial running across the corridor.

Yeah, it's all happening here at the moment at Monash. but yeah, this, fasciculation that, lack of steadiness in, contraction, and we're trying to really pick apart what, could be driving that. And it's, gotta have a relevance to pathology as well in that if you don't have a, smooth motion, and if we extend that to function, if we're running, say, people with Achilles tendinopathy, this can be common as well. That's going to impact on the degree of strain going through the tendon at any one point in time. If the muscle's, not smooth in its contractile, it's, you know, it's fasciculating, it's on, off, on, off, some of that force is then going to be displaced onto the tendon, you would argue.

So, it's absolutely relevant. Could be cortical inhibition that, like Gabriel Fernandes his work, he's, certainly identified that cortical inhibition is, higher. he also has, done some really interesting work where he's looked at the activation patterns of the calf. So he's even been able to extend on that and look at, of the triceps surae, is one of those muscles more affected and how that might play out.

So, there's definitely a bit to explore further there, but looking at the quality of movement, we might be able to relate that to cortical inhibition. But some more work to confirm that.

How to reduce nociceptive drive

David: Okay. And then we're looking at, self-paced training to try and address that reticulospinal tract. Any other ways you can try and address it or, you know, get that more excited or less inhibition coming from that reticulospinal tract?

Pat: I mentioned as well the similarities or parallels between the drivers for this spinal inhibition being that nociceptive information coming up, between what we're seeing in patellar tendinopathy and arthrogenic muscle inhibition. So we can lean a bit more into the literature there, in these other conditions where that's been established earlier in the piece. can we try to either enhance the excitability of drive from brain to muscle via the reticulospinal pathway with the self-paced training? Or alternatively, is there something we can do to try to reduce that nociceptive signaling in the first place? So that's where, while we aren't necessarily letting pain dictate the terms when it comes to our rehab, we're conscious of pain, and we're trying to find a stability in that pain as well.

So pain with exercise, for example, pain in movement. but certain interventions might be effective for that. And I would have, been shocked if a few years ago, and this is just where we've got to with this research, if I had said to yourself that TENS might be something worth considering. But the AMI literature, it's really, really fascinating, and actually... the, the evidence behind TENS being, effective for reducing some of that nociceptive signaling seems to be a little bit in that. Um, equally, that Yeah. I, I would've been shocked a few years ago 'cause I was adamant that it wasn't necessarily a, an intervention of, interest. but if you're looking at reducing pain, as simple as that is, of course, but if you can reduce some of that, pain in the first place, there should be a concurrent increase in force output because you've got less of that signaling going up, activating that interneuron. So, we're exploring this space.

We're early in the piece, but certainly there's a few levers we could pull there. One being enhanced drive down, the other being, reduce the nociceptive signaling going up.

David: Interesting. So you're looking at TENS to reduce the nociception that's then, inhibiting it at that spinal synapse. So, anything that you found that's, working to address that, local inhibition or the spinal inhibition?

Pat: Yeah. And again, it's simply, leveraging off the existing literature for those other conditions. And, As I mentioned, TENS, but you'd be also considering other adjuncts that could reduce pain or, act to lessen that, nociceptive signaling. icing, for example, is re-really popular. And again, that's something if you'd asked me a few years ago, would I be recommending ice for patellar tendinopathy? Probably not. But, this is a bit speculative, and it is leaning on the literature elsewhere. But, I think if we can borrow from the interventions that are used for arthrogenic muscle inhibition and have been shown to be fairly effective, reduce that signaling up, that's going to be something that would be beneficial for sure.

David: So you're not using it as an intervention by itself. You're not going, "All right, you've got this patellar tendinopathy, go whack some TENS on it." But you're using it to reduce that local nociception, you're then getting them to perform their exercise program just after TENS or whatever.

Pat: Exactly. it's part of the picture and, in reality, it's going to be a case of, we can excite the, reticulospinal pathway or we can reduce the nociceptive signaling, but we've still got to then maximise the adaptation that we can then access as a result of that.

So it's then got this opportunity via, these interventions that continue to use our solid S&C principles to target the known impairments for the person in front of us, and again, it all comes back to what are the, impairments that we've identified. Have we, um, identified that it's max strength, muscular endurance?

Is it something else? and and trying to improve upon that to get them closer to their goals, whatever they should be.

How to target the reticulospinal pathway

David: Yeah. Okay. We're looking good ways there to start to address the reticulospinal tract. Anything else exercise-wise, self-paced training, anything else that really targets that, reticulospinal tract?

Pat: It's about, the higher ends of the continuum, intensity-wise that is, and speed-wise, exercise. So trying to get as close as we can to those maximal strength principles, will tap into that, pathway in addition to the, self-paced component. so, we see this play out with patellar tendinopathy rehab, if we look at a heavy slow resistance training, for example, that's what you're four by eight typically.

We're getting close to that mark, but you'd say that's in that grey area between your true max strength and your general strength. So it's a little bit more you can do in that space to enhance the response in the reticulospinal pathway even more so. Be that getting down to six reps, four reps even, so working really hard, proximity to failure, not necessarily failure, that's going to help. Additionally, our, higher velocity of work as well. so that's more tapping into your, power type training. Pain being a factor, of course, and I've chatted with a few clinicians about this, and they've said to me, "Yeah, great in theory, get them doing some, split squat jumps or jump squats or something like that, their pain will love that." But at the right point in time, we can tap into that. So if you're starting first with maybe the, reps and sets are a little bit higher, but you've got that intent to progress them down to a point where their reps are lower, the intensity is higher, and then as pain becomes a bit more stable, that's where you can then, start to engage in more of that, power type training, with an intent to move quickly is the emphasis there to tap into that system.

David: Yeah. there's a difference , between those plyometrics, and, trying to move explosively with a, heavy load that's a different scenario. But it sounds like if you're going hard and fast, you, know, you're trying to get them to work hard with a higher intensity, that's gonna start to target those reticulospinal tract elements.

Pat: Yeah. And intent is a key word there. it may not be quick in, in actuality, but the intent is there, and that's the main thing.

How to target the corticospinal pathway

David: Yeah, fantastic. We've talked about some great ways there, and it seems like this is an emerging area that we're starting to look at. But if we've got some impairments in that corticospinal tract, or they've got some control issues, what are some of the ways that, clinicians might target that corticospinal tract?

We mentioned previously about the metronome-based stuff, but what else have we got?

Pat: Metronomes are most popular, but it, is anything that will shift the, locus of control, the focus of control externally, so it becomes more of a motor learning task. and I guess the, context here would be these types of options are going to most likely be more effective in your Achilles tendinopathy, where, I've mentioned a, couple of times that, that, cortical inhibitions is still considered a major player. Um, beyond just using the metronome, you can... there's a few different options I've seen used really well. So it could be, having the contraction mode be isotonic through full concentric, eccentric making the movement less predictable to the person in front of you.

There's some nice apps where you can actually have variations on what the contraction mode is. So it might be instead of going four seconds up, four seconds down, or three seconds down, it might be two seconds down, and then you get a cue to then go back in your opposite direction and mixing it up. In addition, there's some, interesting developments happening in our ability to maximise just the plastic response to exercise in and of itself. So that be, the resistance training, be that metronome or not, but what you could do beforehand even to try to have the adaptation of the, cortical inhibition be even greater, aerobic training before resistance training. HIIT training, so the higher intensity work seems to be really effective for this. I've got a PhD student at the moment exploring this and trying to really get down to the nuts and bolts of the best parameters for it. But, HIIT exercise, could be on a bike, for example. Lower limb seems to be important, but lower limb, HIIT training or just something with a higher intensity emphasis, getting, someone to do that for the, the 15 minutes or so, before then doing their metronome-based training, that, seems to be that it, it creates this window of plasticity that really enhances the adaptation of, the cortico-spinal pathway.

David: So aerobic exercise before doing your high-intensity stuff or your metronome-based stuff can help to enhance that corticospinal tract.

Pat: Yep,

Achilles vs patellar tendinopathy

David: Interesting. You mentioned there's some differences between the patella and the Achilles in which tracts are impaired.

So how is it gonna impact your rehab for Achilles versus your patellar tendinopathy.

Pat: This is a really, really important point. So we've often, fallen into the trap, and I've definitely fallen into the trap, in the clinical setting of using the same approach for the different tendinopathy presentations. For the lower limb in particular, that can be a bit of a lure to, treat the Achilles tendinopathy patient the same as the patellar tendinopathy. the likely impairments based on the literature are different. In Achilles tendinopathy, we're not so certain that it's maximal strength deficits, but more likely muscular endurance. So it, it would require a different stimulus or a different intervention to address those deficits. naturally, If, I can sort of explore that, deficit in muscular endurance that little bit further, it seems to be reasonably localised. There's a degree of uncertainty just because it's early again in that journey. But it seems to be localised to that lateral head of the gastroc, which is really interesting.

So, this is based on the work of Gabriel Fernandes and he did, some HD EMG, so beyond just your usual EMG, looking at down to the level of individual motor units, their firing rates, and how excitable they are at different contraction intensities. And the soleus, it's a workhorse. It just keeps going the whole way through.

You, I think he had... It might have been a, twenty and a thirty or a, ten and a thirty, percent max contraction. But the soleus, it just, does its thing independent of the other two, um, muscles of the triceps surae. The medial head, it contributes early to, sustained contractions. The lateral head, it sort of waits in the fold ready to go, and as the medial head starts to fatigue, the lateral head kicks in and takes over to help.

So that's what we usually see happen in healthy people. In Achilles tendinopathy, it seems that the lateral head doesn't come to help the medial head so much. So it switches on, but it doesn't switch on so well. So the working theory there is that cortical inhibition might be more directly related to the function of that lateral head of the, gastroc.

So, It's going to impact less so if it's just one of the three muscles, your maximal force, that won't be so much affected. It's going to affect your ability to produce sustained effort, so muscular endurance, which probably fits when you look at who's, got this condition. It's going to be more likely the, you know, runners are, are really affected by this, which is, in a way, a, muscular endurance, undertaking activity. When we're targeting with our rehab the, adaptation that we're after from a, function perspective, we should be really conscious of, you know, what we're trying to achieve and our clinical practice guidelines at the moment, they tell us load, as heavy as you can, as early as you can. But that doesn't sound like muscular endurance training to me, so at least from a traditional sense. So rather we need to think about, well, should we be using, a dosage that's more in line with muscular endurance, adaptation.

Looking at rep range, sets, the, that ACSM position stand confused a lot of people in that for muscular endurance, it sounded like the intensity and the volume didn't matter so much.

Endurance targets

Pat: But if we look at producing force in a meaningful way for muscular endurance of the plantar flexors for people with Achilles tendinopathy, that's heel raise exercise and we can look at should we be incorporating external weight to that or not, but we've got some normative targets, to, have in mind. And the work of Kim, Hébert-Losier she, has some really nice normative data if you wanna check out the paper at any point. But, I believe it's around the 30 repetitions body weight plantar flexion, heel raise exercise, single leg, should be our target, maybe a smidge below for females and a smidge above that 30 mark for males.

So, they're, healthy targets, and if we can train to, build the capacity to, in a single set, get to that point, that's going to be really, beneficial from what we know.

David: Yeah. Any other things we can use to target the corticospinal tract in particular, since that seems to be one of the ones that's impaired more in that Achilles tendinopathy population?

Pat: Yeah, so anything with that external cueing, so the metronome for sure. Let's, let's not throw out the, the metronome. It's, very easy to apply in the clinical setting, and it's very easy for a patient to then utilise at, their own training as well. So that's one of the real benefits.

You can just bring up, any of those apps with a metronome on it. Never pay for them. There's some good free ones out there. but yeah, having an external cue is the key there. you can, you can get quite creative with it, but so long as there is an external cue and it's more of a learning um, task, that'd be the main thing there.

David: It sounds like in your Achilles tendinopathy patients, they often have that endurance deficit, so you're, you're specifically targeting that with more of like your endurance-based rep ranges as well as your metronome and your skill-based stuff.

Isometrics and tendon stiffness

David: What about isometrics? I mean, that seems to be a big field that's pretty popular at the moment. We There's some science that seems to be more rat-based, and there seems to be some human-based stuff, and it's hard to you know, sometimes differentiate where the, actual clinical value lies in it.

So tell us a little bit about what's going on with isometrics at the moment and how this all relates.

Pat: Isometrics have, garnered a lot of attention in tendinopathy management. I think it all, it all boils down to what you're trying to achieve with them. They have been promoted for that analgesic response, getting a, reduction to pain. There's been considerable work in that space, across different ten- tendinopathy conditions to work out, well, can we bank on that response? And it, it seems like it's not a bankable response in terms of pain relief. Some people get relief, great, uh, but not everyone will. Some people get a bit worse, some get no change, but even then you you've got to consider, well, why would I use this, for, uh, pain reduction, great. Uh, you could use your isotonics, and they seem to be nearly as effective, if not, as effective. More so, isometrics, they can be really important from a, tendon thickness perspective. So we're still trying to understand the, absolute relevance of tendon stiffness to recovery, but there's some really interesting work that's been done first to quantify are tendons altered in their stiffness in the first place, and in Achilles tendinopathy, it looks like they've got more compliance, so they're, too stretchy, they're not stiff enough to give us that recoil. While in patellar tendinopathy, while it's based on a slightly different modality of assessment, it looks like, they might be too stiff. But, isometrics allow us to put a really nice amount of strain on the, tendon that might be really useful in terms of adapting that, tendon, to enhance the stiffness, so it's back in our... I call it the Goldilocks zone. You know, it's somewhere between where the patellar tendon is with pathology and the Achilles tendon is with pathology, where it's stiff enough that it can act as a rigid lever for the muscles to work, but not so, stiff that it, it doesn't have that elastic recoil, capacity. And that's where, as opposed to the, five by forty-five seconds, you really need to be bringing that number down quite a considerable lot further, um, to get the strain that we would ideally need to have that adaptation occur. There's some numbers that are floated around, but, we want closer to, twenty seconds, duration contraction.

Some will go lower. I know my good mentor, Pete Malliaras, he likes even shorter than that, if tolerated well, And they definitely have their place, so I think we, probably need to stop putting the boot into isometrics because they, do have their place in rehab. They're tolerated reasonably well in being non-provocative, but they can help to, get us towards getting back into that Goldilocks zone for the stiffness of the tendon and its ability to, operate well for us in a, functional capacity.

Where the research is heading

David: Excellent. All right, we've covered a fair bit there, and it seems like this is a pretty recent development. You've been involved in a, a lot of the research recently over the last few years that's really helped to, expose this reticulospinal tract and helped to give it some time in the spotlight.

It's a nice target that we can start to incorporate into our rehab. And it sounds like it's not always just throw away the metronome. We use that when that's indicated, but we're starting to understand how the reticulospinal tract can be important.

So it sounds like we're in the early days. We haven't quite got to the point yet where we're comparing the different methods of, treatment or ways of approaching these tracts in more of a, like a longer term research point of view, like what's giving the, better outcomes over a longer period of time.

But we're looking at more from that, neurophysiological point of view and, the specific deficits or the tracts that we wanna target. Is that where you'd say the research is at the moment?

Pat: It is. It is. And, and that's why, I really, really think it's important that it all starts with a good assessment. With really understanding that person in front of you, what their impairments are, and if you've got an understanding of their impairments, and we know the, neurophysiological deficits, respective to the conditions, then that gives us a, a good starting point at least, and we can always alter our approach from there. But it gives us a starting point that's more likely to give us the best outcome. And, hopefully, the things I'm telling you a few years down the, line as we learn a bit more about this system don't change dramatically, and we were somewhat sensible in that interpretation of it all.

David: Excellent. Any other recommendations for clinicians out there that are interested in incorporating more of this into their treatment?

Pat: I, I think just, trying to, not be overawed by some of the, the complexity of it. I mentioned a few mentors already that, speak to these topics really well. You know, Pete Malliaras, anything he's involved with is always really sensible and got that nice level of, questioning to it.

He finds that, nice space between being, not too certain, but, able to draw upon the research and its, strength. I think as well, just look out for opportunities as well to, incorporate some of these, these strategies and play around with them in the clinical setting, because it's all good and well for me to say self-paced training, but the person in front of you, that might not be, um, something that, that works for them.

Maybe, the metronome is really nice for them to moderate their reps, and they find that's a really beneficial approach. So, um, otherwise, there are some, training opportunities for sure where, You know, I'm, I'm working with Pete. We're doing a few courses, so feel free to pop into some of our courses that we're running, where we're going to try to bridge some of this neurophysiology and try to make it sensible and clinically applicable as well.

So, yeah, keep an, keep an eye out for that. Later this year, actually, in Melbourne.

David: That's great. thanks very much for coming on the podcast and sharing all that with us, Patrick. It's been brilliant reading your research, and then it's great to have you on, be able to chat about it, and hopefully expose clinicians to some, other ways of thinking about inhibition in this tendinopathy space and ways to address it.

Where can people find out more about what you've got going on?

Pat: Yeah. so just keep, an eye out for, um, I guess our papers as they come out, but you can also find me at, the Tendinopathy Circuit Breaker on Instagram. That seems to be where, I post a lot of, this content and try to make it as clinically, applicable as well and try to break it down and otherwise, yeah, I'm h-here at Monash and part of

David: Thanks again, Patrick, appreciate it, and we'll look forward to reading more of your research as it's coming out . So thanks, mate.

Pat: Thank you very much.