Episode 128 – Tendon Pain Update (with Jill Cook)
Episode Transcript
Summary:
Whitney interviews tendon expert Dr. Jill Cook, who discusses the current understanding of tendinopathy as a degenerative condition, emphasizing the importance of proper loading in rehabilitation.
Interestingly, she makes compelling arguments against some fairly ingrained treatment protocols for these conditions. She explains why she advises against traditional treatments like friction massage and stretching, why anti-inflammatory medications are ineffective, and highlights the risks of certain drugs on tendon health.
Throughout the conversation, Dr. Cook provides evidence-based insights for all manual therapists on treating tendinopathies effectively.
Key Topics:
- Shift from thinking of tendinopathies as inflammatory conditions to degenerative conditions
- Factors that contribute to pain in tendinopathies
- Clinical signs and symptoms of tendinopathy
- The role of loading and compression in tendon pathology
- Treatment strategies for tendinopathies, including friction massage and anti-inflammatory medications
- Medically-induced tendinopathies, such as those caused by fluoroquinolone antibiotics
- The role of active movement and soft tissue treatments in tendinopathy rehabilitation
Whitney Lowe:
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And welcome to the Thinking Practitioner Podcast. Today we are honored to have a very special guest, Dr. Jill Cook. Dr. Cook is an internationally recognized researcher and expert in tendon pathology with decades of experience studying the mechanics, treatment, and rehabilitation of tendon injuries. She’s a professor at La Trobe University in Melbourne, Australia, and her work has had a profound impact on how we understand various aspects of tendon pathology, injury management across a range of disciplines including sports medicine, physiotherapy, manual therapy. And we are thrilled to have her here today to talk about some tendon pathology insights. So welcome, Dr. Cook, to The Thinking Practitioner.
Jill Cook:
Thanks for inviting me.
Whitney Lowe:
All right. I’d like to start off if you can just maybe give us a little bit of additional background there, information on your primary research interests and the scope of your current work that you’re doing.
Jill Cook:
Okay. So we’ve been investigating tendon injuries for 30 years now. We started off in the bad old days of the inflammatory perspective and we rested tendons and clinically… Which I’ve always worked as well as doing research. Clinically, we found that was just a waste of time, and so we started to do other things like loading tendons and trying to find the right way to manage them clinically. And then we put it over into research to see if we could find evidence to support that loading a tendon and rehabilitating them actively was a better option.
Whitney Lowe:
This has been a pretty significant change, this whole idea of moving from inflammatory aspects. Can you tell a little bit about that whole process, the sequential process of us thinking mostly in terms of tendonitis as an inflammatory thing and now how that’s changed?
Jill Cook:
Yeah. It really started to change in the late eighties, early nineties where everybody who failed to get better went to surgery. And so they started to take tissue samples and what they found was just profound degenerative changes rather than inflammatory changes. And then it really truly took off in a study we did… Oh my goodness, I’m trying to remember what year it was, 2004 I think, where we took patella tendon from people having ACL reconstructions and were able to look at the tendons that weren’t degenerative. And what we found was there was quite a sequence of changes, that it was the cell that changed first. Then there was an increase in proteoglycans and that drove the collagen change.
And so that was started to be the continuum model, which I think we published in 2009. It’s certainly been updated since then, but that was the first sense we had that inflammation wasn’t a key driver. Now it keeps coming back. It’s sort of like there’d be some myth or something, but it just keeps being revisited. But it really doesn’t matter how many times you look at it. Inflammation doesn’t drive pathology and it doesn’t drive pain. And so as clinicians trying to treat it as an inflammatory thing doesn’t help us.
Whitney Lowe:
Yeah. I get this question a lot and I’m curious to hear your perspective on this. If it’s not an inflammatory problem, what is really the driver of pain in those tendinopathies? Do the degenerative changes themselves cause pain? Or what is the pain process?
Jill Cook:
Not the first to ask the question and not the first person to say, we don’t know. What we do know, the degenerative process doesn’t drive the pain because there are thousands of people out there with profoundly degenerative tendon that have never had pain. So this classic study, sorry, in 1991 by Cannes and Yosa showed that people who rupture always have profound degeneration, but are 66% of them weren’t symptomatic prior to rupture. So when somebody steps off the curb and ruptures their Achilles tendon and someone says, shame you ruptured your normal tendon,” it wasn’t normal. It was profoundly degenerative. They’re just asymptomatic. So we know that degeneration doesn’t drive pain, but the nociceptive driver is unknown. We know that pretty much degenerative tendon doesn’t have an increase in nerves, but as to what does drive the pain is very unclear.
Whitney Lowe:
So what has changed in terms of clinically recognizing tendinopathy? What are the main things… Our main listeners are massage and manual therapists, so they’re doing a lot of hands-on work. But what would be the main factors to recognize specific tendon pathology outside of the history of information that people give us about the nature of that problem?
Jill Cook:
Yeah, look, the definition of tendinopathy, and of course we’ve moved away from tendonitis, is pain and dysfunction in the tendon. Now the thing that you see in people with tendinopathy is pain with a high load. So high load in a tendon being energy storage and release loads. So if slow loads don’t hurt tendons and low loads don’t hurt tendons, but it’s the change of direction, the sprinting, the jumping, that’s the load that gives you tendon pain… So that’s the first thing. It’s got to be present with these very high tendon loads. The second thing is it’s got to be localized. And so pain that’s diffuse is likely to be something else. And in some tendons it can be tendon pain and something else. In some tendons, it has to be something else. So classic anterior knee pain is either a tendon or it’s patellofemoral pain. It’s not half and half. So diffuse pain gives us a clue something else is going on. And then we see profound… Depends how long we’ve had it of course, we see muscle dysfunction and kinetic chain dysfunction.
Now what happens with tendon pain is that when you load it it hurts. And so you very quickly learn not to load it. So your brain inhibits movement and inhibits load. It’s very different from a lot of other musculoskeletal problems, say patellofemoral pain where sometimes it hurts and sometimes it doesn’t. And so your brain doesn’t have quite the desire to damp down movement. So we see quite a lot of dysfunction in the muscle tendon unit and dysfunction through the kinetic chain.
Whitney Lowe:
And is that mostly… That’s, as you’re saying, a pain avoidance response predominantly in there? Yeah.
Jill Cook:
Yes, absolutely. If it hurts every single time. So if you had a pin and you pricked yourself and it hurt every single time, how many times would you do that-
Whitney Lowe:
That’s right, yeah.
Jill Cook:
Before you stop doing it? Whereas if you did it once and it hurt and then the next three times it didn’t hurt, you wouldn’t quite have the same response. And that’s the key driver of tendinopathy dysfunction is you just learn not to load. You change direction in a different way, you jump in a different way. You use every strategy you can to reduce the load on the tendon.
Whitney Lowe:
In some particular tendons, especially like the Achilles tendon, we see significant thickening that seems to be associated with many of the pathological conditions, but lots of other tendons, thinking like chronic overuse in epicondylitis or something like that doesn’t seem to be the same degree of thickening. What is happening with tendon thickening?
Jill Cook:
Okay, so a couple of things. First, the area of degeneration is going to be bigger because it’s not all lined collagen, it’s not normal tendon structure, has a lot more water in it, a lot more proteoglycans, a lot more cells, some extravascularity if you believe some things. And so that’s thicker. But Sean Docking did this fabulous study in 2015 where he looked at how much degeneration was in both the Achilles and the patella tendon, and then he looked at how much normal tissue was in a degenerative Achilles and/or patella tendon, and he found that there was plenty of normal tissue, and in fact, there was more normal tissue in an degenerative tendon than it was in a normal tendon, i.e, the tendon doesn’t leave you incapable of tolerating loads. So the thickening comes from both the degeneration and of course the increase in normal tissue.
Now that doesn’t happen in every tendon, and we’ve never ever worked out that there are some tendons that just elongate, don’t thicken, just elongate and let go. So tib post being a classic, long head biceps in the arm being a classic, they don’t seem to have this response. It may be due to the tenosynovium that they have. Who knows? We actually don’t know why that happens. It may be due even just to the load that they experience. So Achilles and patella tendon would experience the greatest load the body for sure. So it may be just that. So it almost is every tendon has its own response in some way.
Whitney Lowe:
Yeah. If we look at…. You’ve spoken a good bit about loading these tendons as a means of effective rehabilitation. If you’re loading those tendons that have let’s say a damaged collagen matrix and the structure is sort of degenerated in there, does that degeneration repair? What’s happening during the loading process to improve the function of those tendons?
Jill Cook:
Yeah, no, once you have a degenerative tendon, it doesn’t change. It’s there for life basically. And we know that through quite a few different studies now. And the reason for that is it’s not only bearing tissue, so it hasn’t got a line collagen, it hasn’t got normal cells or too much proteoglycan, so it doesn’t take load. The load goes through the normal part of the tendon. And so when we load a tendon, we probably strengthen mechanically, so the normal part of the tissue. The important thing to realize is once you are post puberty you don’t develop new tendon tissue pretty much. So all we can do is to improve the mechanical properties of the remaining good tendon and you just ignore the degenerative area. People go, “Oh my God, it’s degenerative and I have to worry about it.” It’s like, no, it’s there. It’s been there for a while. When someone presents with new tendon pain and you image it and there’s a gray area of degeneration, it hasn’t happened the night before. It’s happened years ago. It’s like every other musculoskeletal tissue. It happened years ago. You just found it. And then what we do is ascribe all our pain to that area when it’s been there for ages. It’s crazy.
Whitney Lowe:
Well, does that make that tendon more susceptible to further damage and potential, let’s say rupture at a later point if you’re only let’s say using a certain percentage of healthy fibers there and the others are degenerated?
Jill Cook:
Well, as we said, you actually form a lot of normal tissue somehow. And so a degenerative tendon has plenty of good tissue, certainly in the Achilles and the patellar tendon. The capacity to predict rupture is zero. So you can have a profoundly degenerative tendon and function exceptionally well. When we rupture is when the strength of the tissue is exceeded by the load we place on it. That’s pretty simple. Mostly if you have pain, you don’t load it because it hurts. The people who are at risk of rupture are the people who are asymptomatic because they actually don’t know they have a degenerative tendon.
And it’s those people that place an unusual load on their tendon that tend to rupture. The classic is the middle-aged tennis player who lunges for a ball at the net and their Achilles tendon ruptures. Now they’ve had a degenerative tendon for years, maybe never been symptomatic, but that one step. So they say, “But I’ve done it a million times.” That one step had a load in it that was too much for the tendon, and that’s when it’s ruptured. It’s just that balance between the two. And as I say, symptoms seem to protect you from rupture because you know can’t load it. But if you are asymptomatic, you have the potential. But can I tell you, if you are at risk of rupture? I can look at your tendon on imaging. It can be badly degenerative and you can function perfectly through life without any pain.
Whitney Lowe:
Yeah. One of the things that I found very interesting in a lot of your research that I would like to have you elaborate on is the idea of the intratendinous pressure and sort of the comparison between tensile loading of tendons and compressive loading of tendons that can both lead to pathology. It seems fascinating. We only sort of think about tensile loading in a lot of respects and don’t think about compression loading on those tendons.
Jill Cook:
And we are wrong basically because when we talk about tendinopathy, we think about a tendon and the answer is there’s only one in the body, and that’s the Achilles, mid-Achilles. Every other tendinopathy happens at the bone-tendon junction. Now there’s compression every single bone-tendon junction, and it’s compression in combination with tensile load that drives our pathology. And one of the key things in terms of rehabilitating these is to teach people to remove compressive loads. And that’s that’s when you try and load your tendon at length or you stretch your tendon, never stretch your tendon, where you force the tendon to come over the bony prominence prior to its insertion, greater trochanter being the classic example, and you compress the tendon against the greater trochanter, and that’s the compressive load. So we need to think about compression in every other tendons other than the mid-Achilles.
Whitney Lowe:
So you’re saying every other tendon, is that just because of the way they are architecturally, that they’re spanning across something that is likely to produce that with them?
Jill Cook:
I think the answer is the amount of load and the size of the tendon that seems to be the combination. And so something like long-headed biceps, it’s a classic example in the upper limb that ruptures and gets tendinopathy and ruptures and it has a tenosynovium that complicates things a little bit. But it functions very well. The time that it ruptures is when you do a lot of horizontal extension or extension of the shoulder where you compress it in the intersoccus group, whatever it’s called in the upper limb. I don’t do upper limb very often, inter-tubercular group. Is that right?
Whitney Lowe:
Yes.
Jill Cook:
And so that’s where it ruptures. It doesn’t rupture at where it attaches, it ruptures at the point of compression and tib-post is exactly the same ruptures at the point of compression, which is the medial malleolus. The insertion is another four or five centimeters away. And the tendon is massively long, but it ruptures at the point of compression. And so teaching people not to compress or keeping them out of compression, certainly in the early stages of rehab and putting tensile load on it without compression is a key thing that we do to manage tendons.
Whitney Lowe:
Yeah, we were having a discussion in the classroom the other day about tendinopathies mainly being localized to the extremities because you don’t hear about core musculature tendinopathies, the rectus spinae muscles, quadratus lumborum. Is that mainly due to the repetitive loads and the high fast loads? It’s also the architecture of the tendons, I’m assuming that has a lot to do with that. But are there such things as tendinopathies of core structural muscles along the spine for example?
Jill Cook:
I don’t know that they’ve ever been identified. I’m not going to say they’re not there, but mostly any tendon length, you sort of need tendon length to store and release energy in a tendon. To put those really high tendon loads, you need a bit of tendon length so that they in fact probably don’t have tendons that are really long enough to store and release energy.
And if you wanted to look at an extremity corollary, something like a adductor longus, yes, we do see tendinopathy in adductor longus, but it’s very, very complex and that’s because it has a muscular attachment to the bone as well. It’s not just a simple tendon attachment. The attachment is so complex there that the capacity to store and release energy in that tendon is probably relatively limited comparative to say something like the Achilles, which can do a massive amount of energy storage and release.
Whitney Lowe:
So I want to move and shift a little bit here and talk a little bit about treatment strategies because this is another thing that we hear a lot and I get a lot of questions about this that I’ve been dying to ask you for quite a long time. In our world, which is specifically massage and manual therapy, there’s been a lot of focus and work in our field for many years about friction massage as a treatment for tendinopathies. And in listening to a couple podcasts that you had done recently and some other work that I had seen on the web, it seemed like there was some movement away from that idea, that that was not necessarily seeming to be as effective. And I’d like to hear what are we currently thinking? What’s the most current research about things like friction massage being relevant or beneficial for addressing tendinopathies?
Jill Cook:
So I think it’s pretty simple. What are you trying to achieve? And the answer is you are not going to change the degenerative quality. You are not helping the normal part of the tendon. It doesn’t want to be friction, it wants to be left alone. You may have an effect on the no-susceptive driver somehow. So you sort of peripheral nerves that are in your peritendon area, which will be short-term last a couple of hours probably. And I don’t mind if people want a friction tendons. Certainly don’t friction a tenosynovitis or a tenovaginitis. That would be the worst thing you could do.
Whitney Lowe:
Can you explain why? Because that’s again something we hear pretty frequently. What’s the detriment to that?
Jill Cook:
Okay, so tenosynovitis is the easiest one to understand because there’s a synovial membrane, occurs when you move the tendon too much against the surrounding structure. So you create a friction between the tendon and the surrounding structure, and that concentrates in the peritendon. So it’s a friction-induced condition. Why would you friction it as a way of treating it? Because you get a reaction in the tenosynovium or the tenovagium, you get more water and more proteoglycans and you get cellular irritation and you just need to leave those damn things alone. Don’t take away the movement and don’t irritate them. And so frictioning something like that is just patently the wrong thing to do.
Whitney Lowe:
So let me ask about that because that’s… Again, a lot of our theoretical models about why we’re doing the things that we’re doing are not necessarily validated until research comes out later on. But the idea, I think for many years around tenosynovitis being that there were fibrous adhesions developing between the tendon and the surrounding synovial sheath that we could somehow rather break up those adhesions with friction massage. Is that not a realistic discussion then?
Jill Cook:
No. No. So you get fibrinogen deposited in there and fibrin, but that’s not a mature fibrous tissue. It’s there because it’s damn well irritated. If you continue to friction it, you could probably turn it into something that’s a little bit more fibrous and permanent, but if you leave it alone, it all settles back down. So it’s a very immature semi-fibrous] if you want to look at it. I don’t even like that term, but it would be cutting yourself and having some sort of response and scab and then frictioning it so that you continually irritate it. It’s never going to repair. You’re irritating it when it’s trying to settle it down. So it’s simple. Just take away the friction loads, take away movement from the tendon surrounding structures and it settles down, a couple of other things you can do as well, but that’s primary. So no, we don’t friction anything to do with carry tendon. It’s incorrect.
Whitney Lowe:
So this would be also relevant for those distal extremity tendons, wrists, and hand, fingers that have the synovial sheath around them as well?
Jill Cook:
Yeah. And it might be different. Say you have a laceration in and around your wrist or hand tendons and you’ve had a repair, it’s quite possible that you could get some adhesions between the synovial sheath and the tendon. It’s quite possible, but that’s a very different scenario to what we’re talking about here.
Whitney Lowe:
Something that was written… Well, this was a long time ago, maybe like mid to late eighties or something like that, when we were first starting to hear more about the non-inflammatory aspects of tendon pathologies had stated that something like friction massage, there was maybe one or two studies that had come out indicating that there was some potential benefit in encouraging fibroblast activity with pressure and movement from the tendons. Is that realistic? Is that happening at all?
Jill Cook:
No, no. Fibroblasts in a normal part of a tendon are very quiescent sort of cells. They don’t do very much. They can sit around without oxygen for days and not really do anything. They build a little bit of collagen and stuff. The ones in the area of pathology are extraordinarily active. They’re isolated. They don’t know what they’re doing. So they produce some collagen and then they break it down. They produce proteoglycans, they break it down, they’re motoring along at a great rate of knots. We know that the turnover in pathological tendon cells is much, much greater than a normal tendon cell. So again, we don’t want to be irritating things, just leave them alone. They’re sitting there in their own little panic room and building things and breaking them down and not responsive to anything, not responsive to load, not responsive to any sort of intervention in any sort of injection therapy. Just leave them in their panic room and let them be.
Whitney Lowe:
But there would be benefit in, for example, working on the muscles associated with those tendons.
Jill Cook:
Oh my goodness. This is the big, big factor. So what you need when you have a tendon that needs to store and release energy, which is the highest tendon load we’ve talked about, is a completely intact muscle with massive capacity and endurance. So the muscle’s the most important thing. So when you load a tendon in an energy storage and release way, you have a rapid eccentric muscle contraction, and then you set an isometric contraction and then the tendon operates as a spring of the stable muscle base, and so it stretches at the other end of the tendon. Now if your muscle is not strong or doesn’t have endurance, then you set a different base for each contraction and the tendon experiences a different load for each contraction. And so that puts… As soon as you have aberrant loads on a tendon, your potential pain increases quite dramatically. In fact, we know that it’s overload or changing load that creates tendon pain most of the time, all of the time almost. And so if your muscle is lacking capacity, lacking function, you are vulnerable to a tendinopathy. And this is exactly what we see. We see either people taking up a new activity where they don’t have the musculotendon strength to do it, and I think the primary changes is the inability of the muscle to set a tendon load that’s consistent and then the tendon fails.
Whitney Lowe:
Interesting. Yeah. So when we talk about ideal treatment strategies for us as massage and manual therapists and we’re doing work, and you’re saying that loading the tendon is a predominantly important part of that, is there an order to how we should do this? Should we do soft tissue work first and then load the tendon or vice versa? Or does it matter how those things are integrated together time-wise?
Jill Cook:
Okay, so you load the tendon, that’s your priority. Your soft tissue work for me is an adjunct, and as long as you are sure you are not doing something that might be negative for the tendon, I’m very happy that you continue to do that. And I see it as an ideal opportunity to educate the person about the condition rather than just a sort of passive treatment if you want to let them discuss their imaging, explain why their imaging is not important, explain what sort of load they need to do, find out what compressive loads they’re putting on it, explain that they can’t do that because that’s not going to be very good for them. So I see it as just a pause in time where you might be touching the person, which is good, and allowing them to come to your message, I guess that you are trying to make.
But the issue is is that we often do the hands-on touchy-feely stuff first, and then we give them a few exercises at the end of the treatment. It has to be the other way around. You have to review what they’ve done, review their response to their exercises, reset them, make sure you are right at the top of the peak. You’re loading the tendon as hard as you can without creating problems. Get that all right, and then spend the rest of your time doing education and whatever else you want. I think honestly, you could do anything in that as long as you are sure you weren’t making it worse. And that comes back to what we talked about previously.
Whitney Lowe:
Yeah. So assuming there is some kind of Goldilocks zone of loading then for the tendon, we get this question a lot from people who already developed, let’s say repetitive stress disorder of some kind or some type of apparent tendinopathy. How do you load that when it’s already damaged? You just go just under the level of pain tolerance for them? Or what’s sort of like the magical approach to doing that loading when it’s already damaged?
Jill Cook:
Well, remember, damage doesn’t mean anything. So let’s take that out of our lexicon when it’s painful. So what we know from tendinopathy is it’s the high load stuff that creates our pain. So it’s the energy storage and release and the compression, so we can load them slowly out of compression at really, really high loads very early. And this is the mistake we make with a lot of tendinopathy is we don’t load them enough because we are frightened. We don’t know how to load. We don’t know what sort of loads to use, but you can’t have an out of 10 number for pain. But you need to know that you can do slow heavy loads out of compression with almost every tendinopathy and not get yourself into trouble. The exception would be somebody with primarily a tenosynovitis or a tenovaginitis, where you wouldn’t load them at all, you take load off those and let them settle and then look to the reasons why they’ve got the problem in the first place.
Whitney Lowe:
Yeah, there still seems to be a kind of, I guess, rampant use of the word tendonitis, which tends to also drive the prescription of anti-inflammatory medications for a lot of these kinds of things. My understanding is for decades we’ve recognized and realized that that’s potentially problematic for a lot of these things. Has anything changed in some of the newer research about that, or do we still recognize that as a potential problem with many of the anti-inflammatory medications?
Jill Cook:
There’s been repeated randomized control trials that show that non-steroidal anti-inflammatories do not help tendinopathy. It’s a recipe response. It can change pain a little bit. It’s not changing anything about the load or the compression or the inefficiency of the musculotendinous unit. That’s the stuff you have to change. But you can prescribe anti-inflammatories. What we do know is that corticosteroids work really well in the short term for tendinopathy, and that’s not because of an anti-inflammatory effect, because it’s a anti-cell proliferate, anti-cell activator. So it just calms all those hysterical cells in the panic room down, that seems somehow to be part of the pain process. We don’t know how, but we do get a change with corticosteroids, but we can’t use them extensively because they’re not great in the long term and they haven’t been associated with tendon rupture, et cetera. Whether that’s causal or correlation is hard to know, but you’re best staying away from them. The only caveat I would say in that is you’re five days out from an Olympic final and you’ve got a tendinopathy, then yeah, sure, go for it. That would be it.
Whitney Lowe:
Yeah. What is sort of the current thinking or research on the relationship between medication-induced tendinopathy, like the fluoroquinolone antibiotics and things like that? Are there other categories of things that we have found also to be problematic?
Jill Cook:
Yeah, fluoroquinolones are a massive issue. There’s nothing that we have to offer these people. They do not respond to a loading regime. They do not respond to a resting regime. They don’t respond to anything basically, if you have it really badly. Most people get better over time, but there are a group that are really resistant and can be years out and still have problems. If you look at the research mostly in rats and stuff like that, fluoroquinolone-induced tendinopathy, it’s all over the place. We don’t have a target to treat. We get epigenetic changes, we get cell changes, we get collagen changes, we get all sorts of things happen in the tendon, but recognising the driver of that fluoroquinolone-induced tendinopathy, tendon pathology, tendinopathy is very unclear. So simple, stay away from them. And it would be very clear if athletes have some sort of infection, unless they’re dying, don’t use them because you run the risk of finishing an athletic career with them.
Whitney Lowe:
Wow. Yeah. And is that then also true for the average person who’s not necessarily a competitive athlete, that they also run the risk of further tendon problems that they weren’t even aware of as a result of-
Jill Cook:
Yes. Absolutely. Absolutely. It’s a relatively low risk but it’s quite… So I think it’s about 10 people per hundred thousand scripts that get a tendinopathy out of taking fluoroquinolones. And there’s that balance that you have an infection that needs them, you take them. Better to have a tendinopathy than die an infection. So it’s always that sort of balance, but if you have an option, then stay away from it. But just highlighting that it’s a relatively uncommon complication, but it is a nasty one actually.
Whitney Lowe:
Yeah. Are there any other broad categories of medications that we’ve seen having those kinds medically-induced tendinopathies?
Jill Cook:
Not many. There’s a little bit of evidence around statins, but probably through changing muscles. So rhabdomyolysis is a consequence of statins that will change the load on the tendon. But frank evidence of tendons-related statins is really poor. People talk about it, but I don’t think the evidence is there. Any other medications, the anti-acne ones seem to be associated with tendinopathy. The… What are they called? Starts with R, name has escaped me, the roaccutanes and things like that. So there was a study recently looking at tendon ruptures in young gymnasts, and that was one of the risk factors being African-American having very high loads and using acne-based medications.
Whitney Lowe:
Yeah, interesting. One of the other things I was curious about, when we talk about load and soft tissue treatments and things like that, there’s a lot of soft tissue treatments like what are frequently called active release or active engagement techniques where there’s active movement while there is soft tissue manipulation being performed, is that potentially beneficial for addressing tendinopathies through a movement capacity more than just a passive treatment?
Jill Cook:
No.
Whitney Lowe:
It’s not enough load or what’s the-
Jill Cook:
Yeah, you’ve got to load them. You’ve got to put some load through the musculotendinous ut, go down the gym and do some leg extensions and some leg press. It’s going to be much more useful. If you get some muscle soreness, maybe, yeah, sure. Go for it. So it’s an adjunct treatment, but it comes back to exactly what we said is it’s got to have the right loading environment first. And if you don’t do that, then everything else is a complete waste of time. You can add things to it, but you’ve got to do the loading first.
Whitney Lowe:
So the loading is really essential at the outset type of thing?
Jill Cook:
At the outset through the recovery process and after the person has recovered, you never give up loading the muscle tendon unit while you are trying to accept load through that in your daily activities or sport. So we make people go to the gym regularly when we’re rehabbing them, not everyone, of course, older people, perhaps not. And then… But maintain a musculotendinous load outside of your activities for the rest of your life basically.
Whitney Lowe:
And when we talk about the treatment process as well, one of the other things that we were talking about here is the soft tissue work that we might be doing in conjunction with the other manual therapy loading. We can easily back off when somebody says that hurts too much when you’re doing this. So would the same thing be true with their loading that they might be doing on their own at the gym or something like that, is it a good idea to tell somebody don’t go past the point of pain? Because some people might be saying like, “Well, I’ll just push through the pain,” or what’s the relationship between that sort of cap on it with pain?
Jill Cook:
Yeah, look, if they’re getting pain with loading, you’re doing something wrong, your load is wrong. Okay, you haven’t prescribed your load correctly, you’re pushing them into too much compression, they’re doing it too fast. It would be really rare that you would flare up a tendon by doing too heavy a load because the muscle’s going to fail before the tendon.
And so it’s you that needs to change. You need to go back and reassess what you are asking that person to do and get your load prescription right, because if you get the load prescription right, then you are not going to experience pain during exercise. The time that you will is when you are transitioning back from your slow heavy loading through into your anti storage and release load. So once you start people jumping and running and changing direction, then you have to be a bit careful because you can’t go from zero to hero in a session. You might allow them to do 10 jumps the first time and then 12 second and that sort of stuff. So it’s about quantity prescription there rather than anything else. So that’s a time where your prescription becomes really important. But in the early phases, you almost can’t get it wrong. You load the muscle tendon unit slowly and heavy and they get benefits out of it and rarely create problems if you are smart about how you prescribe it.
Whitney Lowe:
In our treatment processes, there’s a lot of… We hear a lot about people talking about the need to release or let go or soften people’s iliotibial bands because there’s this idea that they’re overly tight. My thing is I’ve always said, well, it’s a tendon. It’s supposed to be feeling that way. So is there any capability of stretching a tissue like that or is there any purpose in trying to stretch something like that?
Jill Cook:
Let’s go back to tendons first. Don’t stretch tendons because you create compression at the bone tendon junction. That’s the first thing.
Whitney Lowe:
Can you just briefly elaborate on that for our listeners about how does tension of a tendon pulling at the attachment site create compression forces?
Jill Cook:
Okay, so tendons always come over a bony prominence and attach in a hollow. So there’s a bony prominence there to give you a mechanical advantage and to work as a can. So it takes pressure off the insertion. Okay. You stretch that tendon, you just compress here. So this is where the tendon fails, doesn’t fail here where it inserts into the bone, it fails at the point of compression proximal to the insertion. As we talked about both the biceps and the tib post, the classic examples of if you stretch tib post, for example, you can press it at the medial malleolus that’s where it’s going to fail. Okay. So that’s why you don’t stretch tendons. There’s a fabulous article by Fairclough something like that in JSAMS Journal of Science and Medicine in Sport where they did a dissection of the iliotibial band.
Whitney Lowe:
Yeah, it’s an article. Yeah.
Jill Cook:
Yeah, it’s completely continuous with all of the connective tissue through the quadra and through the hamstrings. You’re never going to stretch the damn thing. It’s crazy. It’s not an issue. Why are we trying to stretch that? Your biggest effect would be looking at TFL. If you wanted to really do something, yeah, maybe. But I don’t understand why we’re so focused on it. I don’t understand what condition it creates. Very occasionally you get an insertional issue or a compressive issue at the knee, but we… Yeah, way too much.
Whitney Lowe:
Yeah, maybe it’s just a reason to sell a bunch of foam rollers or something like that.
Jill Cook:
Yeah. Someone will be making money out of it, for sure.
Whitney Lowe:
That’s right. Yeah. Well, lastly, again, I want to thank you so much for your time, but I would like to know, just looking forward, what areas of tendon pathology research you’re most excited about and do you see anything new or interesting coming down the pike for us?
Jill Cook:
Oh gee. I’m semi-retired so I’m not looking very hard at a lot of things. We’ve done a study looking at hormone replacement therapy as an adjunct treatment to gluteal tendinopathy. We’d love to take that a little bit further in other tendinopathies and sort of working around that. Just about to finish the trial in proximal hamstring tendons. So that will be available relatively soon. We’re talking research time, 12 months, probably. A little bit of work on pathology. That’s interesting because that’s my area that I love a lot, so just bits and pieces, but nothing massive because I’m not running a research team anymore having PhD students.
Whitney Lowe:
Yeah, well certainly those of us out in the manual therapy world are very much appreciative of all the work that you have done over the years and produced some outstanding work for us to continue refining what we’re doing clinically with everybody. So thank you again so much for all of the contributions you’ve made and for taking some time to share those with us here.
Jill Cook:
Yeah, thank you so much for asking me, and I hope it helps a few people.
Whitney Lowe:
Okay, that’s great. Well, thanks so much for joining us and we’ll see you in our next episode.
Jill Cook:
All right, thanks Whitney. Bye.
Whitney Lowe:
Okay, Bye-bye. And The Thinking Practitioner podcast is supported by ABMP, the Associated Bodywork and Massage Professionals. ABMP membership gives professional practitioners like you a package including individual liability insurance, free continuing education, and quick reference apps, online scheduling and payments with PocketSuite and much more. ABMP’s CE courses, podcasts, and Massage and bodywork Magazine always feature expert voices and new perspectives in the field such as those from Til and myself. Thinking Practitioner listeners can save by joining ABMP at abmp.com/thinking.
So thanks again to all of our listeners and to our sponsors. You can stop by our sites for the video, show notes and any other transcripts and specials over there. You can find that over on my site at academyofclinicalmassage.com and over on Til’s site at advanced-trainings.com. If you have comments, questions, or things that you’d like to hear us talk about, just record a quick voice memo or send us an old E, regular old email, and you can send that to us at info@ thethinkingpractitioner.com. You can look for us on social media under our names over at Til Luchau or Til and under Whitney Lowe for myself. And where can… Scratch that. Let’s this whole thing again.
And thanks to all of our listeners and to our sponsors, you can stop by our sites for the video, show notes, transcripts, and any extras. You can find that over on my site at academyofclinicalmassage.com and over on Til’s site at advanced-trainings.com. If you have any comments, questions, or things you’d like to hear us talk about, just send us a quick email over to [email protected] and you can look for us on social media. You can find Til over Under his name, Til Luchau and under my name, Whitney Lowe, as well over on social media. If you would take a moment out to rate us on Apple Podcasts as it does help people find the show. And you can hear us wherever you happen to listen to your favorite podcast player. Please do share the word, tell a friend, and we’ll look forward to seeing you in the next episode.
- Dr. Jill Cook: [email protected]
- Fairclough J, Hayashi K, Toumi H, et al. The functional anatomy of the iliotibial band during flexion and extension of the knee: implications for understanding iliotibial band syndrome. J Anat. 2006;208(3):309-316. doi:JOA531 [pii] 10.1111/j.1469-7580.2006.00531.x
