“Early 2000s, I developed a paratenon disorder from having tight fitting boots on my foot. So wet suit boots, doing some water sports, doing lots of walking in it and it rubbed and made my paratenon horrendous. And then probably six months, a year later developed a true sort of tendon disorder.”
“Every tendon in the body, they’ve either got a synovial sheath ⁓ or they’ve got a paratenon generally, so you can develop irritation of the sheath around it. So obviously we see them in wrist and hands. You get de Quervin’s tenosynovitis, so quite a common one, and that’s due to synovial sheath. The paratenon is just the same, it’s not got the synovial membrane, that’s all.”
“Occasionally in a younger athlete, so we’re talking often sort of teens or early 20s, where they’ve gone on a training camp and been exposed to a dramatic increase in training loads, they’re the sort of person who may just get true sheath disorder other than having sort of tight fitting strapping or boots that might be in the step. But it’s something to squash it and create that friction is what normally happens.”
“If you’ve got a true tendon disorder, we know one of the risk factors is calf muscle weakness. And obviously then a lot of our rehab would focus on calf muscle strengthening. But for these guys with a paratenon disorder, it’s probably not related to calf muscle strength. So we don’t really want to focus rehab around this progression of trying to strengthen the person. We probably just need to focus on simply settling it down, taking away whatever the aggravating sort of stimulus was and then basically just reloading them up and if they’ve developed a bit of adhesions between the sheath and the actual tendon itself, which can happen in some cases, then you might want to do something that tries to free up the tendon. So that might be stretches, it might be isometric contractions, so the tendon slides in the sheath, it might be doing isotonic movements that are full sort of range of motion to free up these adhesions. You can literally hear crepitus in the worst cases. It sounds like Velcro being pulled apart with the worst scenarios that you get of this. But yeah, then few and far between thankfully and normally sit together with a true pathology inside the tendon.”
“Really the problem with a lot of the old evidence is when you’ve got your tendon they didn’t actually cut open the sheath and look inside the Achilles to try and find your plantaris. They looked around it and couldn’t find it but it’s often I would say normally embedded inside your paratenon. In my clinical world, I don’t scan many tendons and find the plantaris sits outside the Achilles. It normally merges with it and is within the sheath.”
Plantaris rehab: “Look, the person’s always had the plantaris in that same spot all their life. Why has it become symptomatic now? If it’s only been there for six months or whatever time frame we’re talking about, it’s likely to settle just like any other tendinopathy is. And the other challenge is how much of that medial-sided symptoms and medial-sided pathology is actually linked to your plantaris rubbing or how much of it is linked to the medial bundle, which is the soleuus section getting more stress and developing tendinopathy. And that’s a whole debate.”
“So if you’ve got your tendon and you’re looking at it end on end, the ventral surface, the deep surface will be the soleus. But then as you rotate further towards your insertion, the tendon actually twists and turns. And what happens is that the sort of ventral surface will rotate more towards that medial section, which is again the soleal section.”
“If it’s the deep surface of the tendon, we can probably assume that that might be more soleal bundle, in which case, we might want to see how the person responds to doing straight leg versus bent knee loading exercises. You often find it will be a bit more provocative on the bent knee in that instance because it loads that bundle a little bit more than it would do in the straight leg position where it will work both bundles. There’s some confusion then about what it does to your muscles and people assume that because it’s soleus we must do bent leg rehab. We don’t need to. The soleus muscle itself will work when you’re straight leg as well and it just inhibits gastroc when we go to the bent leg position.”
“That’s typically what I observe and you’ll sometimes be able to see on the scan that you’ve got the plantaris is visible, you then have a normal bit of tendon tissue next to the plantaris and then you have the bundle change and that’s quite common that we may visualize that in which case I’d be saying it’s not about the compression of plantaris, we’ve got a normal section of tendon in between, this is a section within that medial pillar.”
“The tendon fascicles are continuous all the way from the muscle that it’s sort of originated from. So what you get when you do the bent leg is you get more of a slide, more movement, more excursion of the sub tendons… there’s studies that use ultrasound to track individual fibres of the tendon. They show that the deep surface in those instances will move more. So it’s a way of loading it more arguably.”
“I’ll sometimes do training courses around the world and people are still talking about using theraband like a yellow one, a red one and you’re kilos of force versus the multiples of body weight that we get when you’re doing a heel raise.”
Soleus: “It’s not a postural muscle like we maybe got told at university when we did our training. It’s a key locomotive muscle and is inherent to our propulsion and force through the Achilles. Therefore, it should be a big part of our rehab.”
Soleus: “For most steps when you’re jogging, you’re probably looking at about 7-8 times body weight at most speeds in steady state running. If you then accelerate, the soleus will get about 10 times body weight for acceleration phases in the studies that looked at that. it’s huge. Gastroc on the other hand is about three times body weight for the steady state running. And then it goes up to about six times body weight in the accelerator phase. So that’s like a track athlete coming out of blocks on the track.’
“It’s a case of soleus eclipses, all of the lower limb muscles, except when you hit maybe a sprint, but even then there’s a bit of debate around that because the accelerator study shows that the soleus eclipses, hams, glutes, quads, everything is right up there. So really what we’ve got to think of is that that’s our distal strategy. That’s what works maximally pretty much every step, but to go fast, we then increase cadence and that comes from the proximal and that’s why we see proximal muscle injuries when we’re sprinting normally, so hammies and quads maybe hit flexor rarely but it’s that switch.”
“Just from an athletic perspective, we know that calf strength directly corresponds to your sprint speed. So whether you’re looking at 10 meter sprint distance or time or 30 meter calf strength is a direct link to that performance.”
Running vs. Calf Raises: “We’re talking two different elements. So when we’re talking about the sort of internal load, we’ve got to understand its internal loads. So that eight times, 10 times body weight is an internal force production. And that depends on the lever arm and the axis of movement. So if we are looking at measuring that externally, so we use an isometric strength test in a flex knee position, you’ve got your foot on the floor, the axis is through your metatarsal heads and then you’ve obviously got your calcaneum at the back and your achilles coming down. you can work out a typical sort of lever arm for that. If you hit twice body weight as an external force production on that test, the internal force will be between seven and 12 times body weight, depending on how big your foot is basically. So that equates to the typical internal physiological load. So externally, twice bodyweight is our target. Internally, that will be then somewhere in the region of our typical demands. And we’ve got a large amount of data to substantiate that.”
“So we’ve got a large rugby orientated study, 350 players. BACs, are the guys that are like your runners you have in NFL, they’re the equivalent of the guys that are doing all the running around and on the wings. They’ll hit twice bodyweight as their average force if we look at a whole load of players, their whole squad. If we look at the forwards, they’re the ones doing all the heavy hitting and in a scrum, in a rugby perspective, they’ll be lower. They’ll be about 1.8, 1.85 times body weight. Interestingly, they’re the ones that get most calf and most Achilles injuries like. And they still have to move their body weight around on field. So they should be stronger to cope with the internal demands, but they’re not.”
2x bodyweight isometric test: “The internal force then will be in the realm of eight, seven, up to 12 times body weight, depending on their lever calculations which will vary. that’s it. Really if you’re talking to somebody in the gym and you want to lift they should be lifting one and half times body weight as a minimum in order to actually be hitting a threshold that’s around 80 % of their maximal voluntary contraction. That’s the key here. So that would be my body weight, me standing and then additional half body weight in our Smith machine or on a squat rack or whatever we’re talking about. It gets different when you look at leg presses or seated calf work because the lever arms are different. So you might only be lifting 100 kg or whatever that is in pounds, 225 pounds, 250 pounds, but it’s a case of the lever arm calculation will make it harder maybe on the tendon and the actual calf work. So you have to do a bit thinking around it.”
“That’s where we get confused is when we talk about what we might use as colloquial terms for strain versus actually a biomechanical term for strain and that’s sometimes lost in translation between talking with research groups, talking with clinicians, talking with an athlete. We use the terms sometimes interchangeably so it’s just to be very clear what we’re all about. So I tend to try and use load and use body weight force because it’s easy for people to interpret rather than tendon elongation which we can’t measure unless you’re in the lab. So I avoid strain normally for that reason.”
“So the biggest fault I come across with tendon rehab and calf muscle rehab is overly focused on the plantar grade up to plantar flexion. You’re talking about half the force capacity of a dorsiflex calf position. Injuries occur in an eccentric phase into dorsiflexion. They do not occur from plantar grade up to plantar flex positions. Even when we look at triple extension in sport, it’s a recoil. It is not a force generation position. So my real bugbear, I guess, when it comes to rehab is that we spend all this time from floor, plantar grade up to focus on developing inner range strength. Inner range has no relevance to sporting performance unless you’re a gymnast or ballet dancer. It’s not relevant for field-based sports. We need to develop huge forces in dorsiflex positions. You look at all the Achilles ruptures in the NBA in the last year. If we look at the seven that occurred then and you look at the slow-mo footage of them, they are all about a dorsiflexing position with the knee extending, with the hip in extension, the position we should be training our athletes in to make sure they’re robust in positions of relevance. All of our calf injury videos that we’ve looked at are all the same mechanism and our Achilles tendinopathy, that’s the biggest Achilles stress, that’s where the degradation occurs, that’s the position we should focus on. And like we said it’s about 50 % more. So for example if you can hit one times body weight when you’re in a neutral position you’re probably getting one and a half times body weight in a full dorsiflex position.”
“I can’t stress it enough, it’s literally the clubs I go into and work with and they’ve been doing rehab and they’ve sort of banging their head against a wall. It’s always this same story and it’s because of some of the isometric push that people have been putting out both in America and in Australia around isometrics and rehab and they’re all focusing on this up position because it’s easy for us clinically to visualize a deficit because people are weak there, they can’t hit the top and we go, they need to the top. They don’t need to hit the top. It’s a way of proving they’re weak. If you don’t have all the strength kit to test them, but we need to then go to the positions that are functionally and performance linked, which are the dorsiflex positions.”
Restoring full plantarflexion post rupture: “Yeah, I’m not bothered by it. So literally my counsel when I’m doing a consult in pro sport will be that this is largely irrelevant unless we’re ballet or gymnastics.”
Injured Achilles tendons: “The deficits primarily exist in neutral to dorsiflexion.”
Lacking strength in plantar range post-rupture: “I don’t fret it. I’ll say well look it’s a way of proving you’re weak… I know other experts would talk to you about and they’ll use that position, it’s just not relevant. The only time I will use Plantaflex loading is post rupture in the early phase. So maybe three weeks, four weeks from rupture, you’ve had a surgical repair.”
Focusing on plantar range: “People have confused the ease of spotting a muscle weakness with where we should work for performance. That’s not the case and it’s a misconception as often happens in the physio world and physical therapy world.”
Restoring full plantar range: “You’ll probably never get it back. You’re chasing something that is a real struggle. I say you probably never get it back. If you’ve got a ballet dancer you must get it back. It’s critical… we do use peak height that they’ve achieved as part of a metric for research but as I said clinically I’m not chasing that, I’m chasing the force in this lower part.”
“Concentric, eccentric will bring in energy storage in the tendon, and actually you get a lot more recoil. And obviously we know when we look at any muscle, the eccentric force you can generate is often double what you can get concentrically. What that means for rehab is if we do a concentric phase we’d probably use both legs and get you to lift the weight that’s really hard to lift on both legs and then you can probably lower the weight down on one leg. Now that’s the way of actually getting the dosage for the eccentric phase correct because if you’re using what you can concentrically lift and then eccentrically lower it’s too easy. You’re working well below your sort of MVC of 70 or 80 which is we probably want to be high up there for tendon adaptation and neuromuscular adaptation.”
Deep dorsiflexion and insertional tendinopathy: “This is a misunderstanding of the research, think, although there’s some papers we probably need to flag. So the reason I say it’s misunderstanding is people have perceived that the devil, the thing we should avoid is dorsiflexion when we’ve got an insertional tendinopathy and people say it’s harmful. Look, we’re dealing with people who run, so field-based sports, court-based sports, whatever we’re talking about, walking even, you go into dorsiflex positions. We have to rehabilitate the person to cope with dorsiflex positions where they’ll get both a compressive load against the calcaneum from the tendon being squashed, but also the tensile load at the same time. It’s critical we have the person to cope with those two elements, tensile and compressive load. It might be in the irritable phase where the person is flared up easily. We isolate those loads and then work towards it. And when you’re looking at research studies that have then looked at doing dorsiflex positions versus just to plantar grade, they show that it’s better for the plantar grade. I get that, but you have to look at who they included. If this is a short term tendinopathy that’s been there for less than three months and is in acute flare, then they’re irritable often. And of course, what you’re doing is you’re modifying the rehab to their irritability level but in the longer phase ones where they’re still running they’re still performing on court we have to integrate those loads back so I think we have to be careful with what the research says and who’s in the study versus who we’re talking about when we’re managing people and that needs again a bit more thought around it so don’t avoid dorsiflexion it’s normal patients have unfortunately heard us speak heard podcasts around it read papers or read blogs and they think dorsiflexion is bad. They wear a wedge in their shoe, they wear high heel drop shoes and permanently try and avoid dorsiflexion and that’s why we actually need to swap their rehab. So it has a definite use but in the non-irritable phase of rehabilitation or non-irritable person.”
Seated deep dorsiflexion feeling better than standing deep dorsiflexion: “I mean absolutely possibly. It’s probably just about load. Doing the standing versus seated one, you’re probably just getting more load on it. If you’ve got the body weight for starters, I’m 100 kilos, so what’s that, 230 pounds. How do I replicate that in a seated position? I can’t put a barbell on my leg that’s that weight, and I’m always a bit facetious and say, you’re probably loading with equivalent of 70 pounds, 80 pounds on the leg, and you’re doing it in a barbell on that position and doing these lifts. It’s not the same force. When I teach a course I normally find the biggest person in the room and get them to sit on my knee and give them a hug and then lift them because you can lift a lot heavier weight than you perceive. I think that’s the problem. That might be why you see there’s a difference between the bent leg and the straight leg. My challenge to you would be to stand the person and do the same exercise and bend the leg and do it with the leg straight and see what you find then. Now you might find it is sore because you’re putting in sort of more strain as we talked about through that deep surface by bending the leg. So that might be what happens there. But yeah it depends so I don’t fret it too much but I always find what is the position that hurts the most and what I’m trying to do in rehab is clear the pain in that movement. So much like you’ve got a person with back pain you want to make flexion pain free because that’s what hurts them with this we want to make that heel raise in the straight leg position pain free.”
“And that’s the other bit that gets missed in rehab. People don’t try and clear the pain. They avoid doing that because it’s making them worse. Whereas I go, well, let’s do a lower dose. We use that to make you better.”
Psychological fear: “Some elite [athletes] will not be fearful. It just hurts them and we don’t necessarily need to expose them to much and it’s not so much exposure therapy, it’s then actually physiological load. It’s adding compression and tensile load in order to trigger a more positive adaptation but as with all tendons it has to be activity modification. I normally talk about Goldilocks and the Three Bears so it’s getting the Goldilocks zone where the porridge was just right, not too hot, not too cold. For this case it’s not too much load, not too much compression, it’s just the right amount in order to get the person better and it’s trial and error. You can only test it and see how they respond.”
Insertional vs. Midportion Tendinopathy: “They all need the same approach is how I look at it. Some of our data has been very novel that we’ve identified about 20 % of people will have both. So insertional and mid-portion at the same time. That’s something that you won’t read in the literature and you won’t find in the papers, but it’s clinically what we observe when we look at large numbers of people. So how do you then do that? So I think you can rehab a mid-portion without going into dorsiflex positions if it’s normal person. By normal person I mean sort of literally like a work colleague down the corridor that’s not particularly sporty. As soon as you talk about elite sporting individuals the rehab is very different and we’ve got to ensure all positions become pain-free and need to become the later phase of rehabilitation. So I would always then utilise it in that later part.”
Achilles rehab: “The focus for us is to try to get the neuromuscular function better and the tendon to adapt. So that’s really what I’m trying to do from a rehab perspective. Actually, there’s three things. There’s the psychological bit as well. So fear of avoidant beliefs, catastrophizing, all of these other aspects are critical. Get the tendon structure and get neuromuscular function back. Neuromuscular function is my key. And I say that because we think it’s the chicken that lays the egg. This study that’s published already on army recruits, small number that develop symptoms, but they showed strength deficits prior to symptom development. Okay, so it suggests that chicken and the egg… And then when you look at strength properly, it’s not just the force they can generate. It’s actually a neuromuscular issue. So what we see in the lab when we were doing my PhD data is a tremor. So we see during an eccentric phase, you get this shake of the muscle. And most of you, if you do a slow eccentric lower, you’ll see this on your patient cohort, particularly if you go into the dorsiflex positions, and often more commonly when you put the person into a bent leg position, you’ll see the shake… But what it comes down to is it’s a fast twitch motor fibre not coordinating properly during the eccentric phase. That’s basically all it is. It happens at 8 to 12 vibrations hertz per second and it’s a fast twitch fibre. So we’re trying to rehab to improve the fast twitch coordination. That’s what we’re after. And you can do that using slow eccentrics bizarrely. The motor pattern you use for an eccentric contraction, whether you do it slow or fast, is the same motor pattern, it will transfer over to fast work and people have shown this with studies on heavy eccentric done slowly improving stretch shorten cycles dramatically. So it’s definitely the way to go so we’ll look at the neuromuscular aspect to get that rehabbed and then of course what we’re trying to do is adapt the tendon.”
“Now there’s two bits about adapting the tendon it can definitely adapt the donut and the whole theory is not what we see… even the ruptures with gross fibrosis adapt over a period of time. So this is really fibrous tissue that really does adapt. Both the cross section gets smaller over a long period of time and the diseased area, this organised tissue, those red bits on the UTC scanner getting smaller. So this is what’s happening when you do tendon rehab. And that happens for two things. It happens by loading the tendon, the stimulus for the tendon cells, which is part of what we do. But it also happens because we’ve got the muscle to function better and it’s now controlling the force through the tendon better and that allows it to recover. That’s our working hypothesis… So neuromuscular tendon adaptation and all the psyche stuff often comes by doing the two other things because you’re proving to the person it’s robust, it can cope and it doesn’t make them worse by doing the tasks. That actually worked really well to reduce lot of that fear and those thought processes when you do that well. Sometimes we’ll need to hit it specifically and we need to show them the tendon is strong, we need to show them that their muscle is functioning well and they can cope with these forces and demands. But that’s ultimately my sort of typical rehab. Whether that’s then in dorsiflex positions or not depends on who we’ve got and how irritable they are. But to do that we’ll use both bent leg and straight leg which was the original question. But we make sure that we look at if it’s a medial bundle, we’ll pronate the foot more commonly. We test them to see if it hurts when they pronate. If it does, that’s the thing we need to clear. If it’s the lateral bundle, we’ll often look at a supinated foot or a varus knee. And again, we can use those positions to then load them specifically.”
“What I really hate is a pristine gym-based rehabilitation program that doesn’t use, often I’ve termed it dirty, on field positions. So these players, when they’re out on court or in sport, they will go into very extreme positions of rotation of the foot and the tibia and the hip that will load different fascicles in the tendon or different muscle bundles and that’s how our rehab should be. The players often or athletes know something else and they avoid it and this is what causes us the problem with return to play that they’ve been avoiding this position for a long period of time, not telling the clinicians that are dealing with them and you’ll spot it when you check all these positions, find one that hurts, make that better, they’ll perform a lot better than out on field because they’re not subconsciously avoiding it, ending up doing it then when they can’t focus on how they move and flaring up after the game which is typically how it goes.”
“My current thinking is if you’ve got poor neuromuscular function, we don’t know how you really define that. We often use force as the measure at the moment, the strength. But if you’ve got poor neuromuscular function, we think you’re more at risk of developing a plantar flexor injury. And that could be tendon rupture, could be tendinopathy, could be a calf muscle injury, all of those things. There’s a fourth one, which is ACL injuries, we’d add to it as well. So your soleus particularly will pull your tibia posteriorly about 30 % of your capacity of your hamstrings… But basically in the work we’ve already got, we’ve shown big deficits in the calf function post knee surgery, post knee injury that does not resolve when people return to play. So we’ve got elite rugby players been rehabbed for a meniscus injury or ACL repair or even footballers and then you find that they start to get Achilles and calf stuff. You measure the calf, it’s way down and that’s been part of it and we’ve identified this in guys prior to the onset of the calf and Achilles now as well. So they’re the big bits we want to look at.”
Achilles ruptures: “I don’t think people are looking at it in the right way… I think you need a perfect storm. And currently where I put my money at the moment… Neuromuscular function, important. These people have done a step back normally when you look at all the rupture mechanisms. ⁓ There’s nothing fancy about that step back. They’ve done it hundred times maybe in that same game, ⁓ but not done it. So something misfires at that point, a bit like an ACL injury where you get the quads and hams misfiring and you end up with the ⁓ anterior translation. So part of it’s a misfire and that’s probably down to then poor neuromuscular coordination in the first place, fatigue, all those other bits that are part of it. You probably need the tendon structure to be abnormal. So, and I say probable because we’ve got data that suggests maybe not. There’s a lovely study that’s been done, again I can share the reference with you, the doctor biopsies post rupture. Years ago the work all suggested that people had gross pathology prior to the rupture occurring. Much more significant than tendonopathy normally is. There’s a new study from, I think it’s Korea, could be China and they basically found about 80%, it’s a bit less than 80%, of people had gross pathology prior to a rupture when they’re taking a biopsy at the point of a surgical repair. But that means 20 % didn’t have that. And that then gets interesting. And we’ve got 16 ruptures. We’ve actually had UTC scans within a few weeks of the rupture happening. And what we found is 14 of them were predictable based on the imaging. So the really gross deterioration in tendon structure. Two weren’t. Two of them had absolutely pristine tendons. And we went back and checked these after the ruptures had happened, obviously. And that makes it interesting then. But what we’ve retrospectively identified is that the tendon cross-sectional area, the amount of healthy tissue, is super small below the normal levels, especially when you then add in that these are very explosive. They’re both athletes, both very explosive athletes. So huge force generators for the sports they were doing and their weight and that makes it a bit more interesting in them.”
“So it may be possible if we stuck with the NBA as the example that those injuries occurred in perfectly pristine tendons that were very small cross sectional areas. But having said that, they were all in a simple step back, a normal task, and I suspect they were all grossly degenerative before. But that’s my suspicion. I don’t have data. I don’t work with those squads and stuff. But that’s where I think it sits. So if we’re trying to prevent ruptures, for me, you’ve got to look at all of those elements of tendons: structure, muscle, neuromuscular performance and strength and trying to spot the perfect storm happening.”
“If you ever get to go in and look at a rupture being repaired, they’re not this transverse rupture that we have in our heads they’re more like a spiral fracture. The tendons gone in different sections or actually a better example would be a frayed rope we’ve got our bit of rope we’ve got areas that frayed and we’ve got intact perfectly normal rope as well that’s what we get with a tendon and then all the force goes on the healthy bit and then it goes twang.”
“There’s a nice big study in the armed forces in the States that has shown that ⁓ people of black heritage, Afro-Caribbean heritage, were more likely to suffer Achilles, patella and quad ruptures. And we don’t know why. But that’s really where I’m sort of going at the moment is there’s maybe a genetic difference in cross-section area in some cohorts, but this is probably again individual and it’s probably not about necessarily a race per se. It’s just individual and some genetic elements on collagen genes. So again, there’s collagen 5 1a, collagen 5 gene that links with the ACL injuries, it links to Achilles ruptures and Achilles tendinopathy. But all of the studies have unfortunately just been white Caucasian cohorts. They’re not on mixed sorts of heritage groups or on people of black or Asian heritage. And that’s partly what you have to do with genetic studies is control and that’s why it’s been done, but we need that to be done across larger cohorts. But that’s definitely a factor in its understanding why. So something genetic, but who knows what.”
“So the background to this is like our local hospital down the road did a drugs audit, all hospitals do this regularly, they did a drugs audit and asked them to send it through. We were interested in setting up a study around fluoroquinol. So ciprofloxine being the typical drug that’s used and they’ve done 5,000 prescriptions in a given week on fluoroquinolones and then you go, come on then we’re surely going to see loads of ruptures. So there’s no consequence of that level of prescription in an area that has one ER so all of those ruptures would have come through if they were going to rupture which starts to then beg the question.”
“Clinically, how I look at this is if you’ve got a really degenerative tendon and you’re given the Levo, the high risk one, and you’re older and your tendon is really poor structurally, then there might be a risk there. But if your tendon is healthy and you’re given this drug, you’re probably not going to a problem.”
Bad effects from fluoroquinolones: “I mean, clinically, we’ve seen that and I used to think fluoros caused it until we started to look at it a bit more and ask the question. But you have seen people that have had a flare when they’ve been put on the fluoros, but then have they had a flare because they’ve had a systemic illness, an infection that’s created inflammation. If you’ve got the flu or a cold bug and you’ve got pre-existing knee pain, your knee will hurt you more. That’s what happens. So if you’ve got pre-existing tendon issues and you’re then ill, is that just what you feel and that get with it. There is a large debate about a neural aspect of this as well. there’s sort of, again, data that’s mostly association studies suggesting widespread musculoskeletal problems with fluoroquinolones due to toxicity levels. And it may be that some people don’t process the drug. It may be it increases your risk of neural stuff and other aspects. And that’s something we need to be really cognizant about.”
Metabolic issues: “I use a wear and repair imbalance which is what all of the tendon models talk about that exist in the world. It’s basically stress on the tissue and then your recovery afterwards that influence whether you develop pathology and it’s just the metabolic conditions influence your recovery. So that’s your ability to repair afterwards. Diabetic or if you’ve got high adiposity and that creates this systemic inflammation. That influences your general background inflammation and your healing rates because your immune system is busy. So that’s really the key here is that this may slow down recovery but equally that the tendon cells are often so switched off because the person does so little exercise and activity to prime them that actually they might be easier to prime and they might need to do so much less than an athletic person needs to do to lift that muscle strength and the metabolic activity in the tendon upwards that actually it might be quicker as well. So we’ve got to consider it from both sides but I look at the metabolic ones as critical. The mechanism is the same but their background capacity is lower than the athletic person so what their tendon can cope with the where that the activity levels is less for them and that’s really probably what we’re talking about.”
“One great example of this was an athlete who had ongoing tendon problems and had surgery and all sorts of stuff and ended up with persistent pain three, four, five years later and wanted to chop his leg off because it was that bad, it was gout. When we got the blood test done he had gout, it had been missed previously, put him on adipurinol to alter his uric acid levels and symptomatically wonderfully better. So there’s stuff like that where we need to think about metabolic stuff, particularly in non-responders or atypical responders.”
Contact: https://le.ac.uk/people/seth-o-neill
Twitter: https://x.com/Seth0Neill
