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“We tend to see people with tendinopathy that are more sedentary. So they’re not typically the athletic populations and they’ll still develop tendinopathy. So common areas would be the gluteal tendons, the rotator cuff, the lateral elbow.”
“I think we can get very sidetracked on pain mechanisms. And this isn’t just for tendinopathy. I think we can sometimes end up treating the pain mechanism rather than the patient.”
“Ultimately, the pain mechanism means very little to me if I don’t know what to do about it.”
“Earlier on, I would have been trying to categorize people into nociceptive versus nociplastic, central sensitization, this kind of stuff. But I just didn’t feel that it was really enhancing anything I did clinically. It was still coming back to their story and what things I can change.”
“When someone says, you know, when they point to pain in their Achilles tendon or they point to pain in their low back, you know, we’re dealing with similar neurobiological mechanisms. Now, at an individual level, that’s going to vary.”
“If you’re dealing with a very athletic population and there’s a very clear load increase and they develop an Achilles tendinopathy, we can be fairly sure that that’s predominantly driven by something in the tendon, in the tissue. There’s something that the tendon isn’t happy about.”
“Structure is a difficult thing to change. If we assume that the structure is the driving factor in terms of their pain, then we probably need to be more specific in terms of our loading protocols if the aim is to influence the tendon structure.”
“So it’s basically people that are generally fit, active, healthy. They may have a larger buffer, meaning that they can get away with a little bit more before that tendon says, you know, I’m not happy. Whereas in other groups where they may have more complex risk factors. you know, we might discuss the role of kind of metabolic endocrine, you know, more systemic risk factors for tendinopathy in that group. Then a very subtle change in load may drive that tendon response and drive the pain. So you can look at that both ways. You can say, well, it still was the load that resulted in the tendon change, but the load was often so small that normal changes in daily life, that daily life require means that this could potentially happen again, or it’s likely to happen. So in that situation, I’d be very keen on addressing or at least acknowledging these other factors in addition to any exercise intervention that I might give the patient specifically to enhance the health or function of the tendon.”
“As we age, there’s probably more scope to develop some of these systemic risk factors.”
“The tendon health has to be considered in the broader context of overall health.”
Metabolic factors: “The well-documented ones would tend to be things like diabetes, obesity, hypertension, and high cholesterol. So I suppose collectively term the metabolic syndrome. And these conditions often coexist with one another. they often have shared mechanisms as to why they increase the risk of tendinopathy.”
“We see in the Achilles, we see it in the surgical literature around rotator cuff repairs, post-surgery that, people with things like diabetes have poorer healing responses. And of course, even outside the tendon, we see this, you know, just the healing of people with these comorbidities is poorer than if they didn’t have these conditions.”
“Diabetes, hypertension, obesity, and I suppose another mechanism by which some of these factors might influence the tendon is that they’re generally pro-inflammatory.”
“So the metabolic syndrome is associated with an increase in the low grade inflammation or systemic low grade inflammation. So these are driving pro-inflammatory changes that are long-term probably not very healthy for the, again, the structural integrity of the tendon. But even moving away from the tendon, we know that these risk factors are also risk factors for pain in general.”
“We see hormonal changes can be linked to tendinopathy. We see an increased rate of tendinopathy, for example, postmenopause or perimenopause. And this is where we typically see things like lateral hip pain, lateral gluteal tendinopathy type presentations.”
“I rarely see something like lateral hip tendinopathy in particular in the context of single site pain. So, know, when you ask these people around pain and other sites of their body, it’s quite common that they will report things like low back pain or shoulder pain or knee osteoarthritis, for example.”
“If you look at the research on osteoarthritis at the moment, we see very strong parallels with tendinopathy, particularly in relation to the metabolic health side of things. So we’re suddenly realizing that there’s commonalities across these various diagnosis and you know, that there might be specific things to each of the diagnosis, but there’s a lot of things that are shared across them.”
“When you’re dealing with somebody, particularly with sudden onset or fluoroquinolone induced tendinopathy, it tends to be a lot more aggressive and a lot more sudden from the ones I’ve seen and unfortunately can lead to the very serious side of the spectrum.”
“It’s a very important topic of discussion, is the potential for autoimmune driven insertional tendinopathy, or what you’ll see termed as enthesitis in the research. And enthesitis is a hallmark feature of certain types of autoimmune conditions, particularly the group of conditions that we refer to as the spondyloarthropathy.”
“If someone has a strong history of insertional tendinopathy, especially when there’s no clear load inducing factor, then you’ve got to be suspicious of the possibility of an autoimmune spondyloarthropathy underlying this.”
“I’m asking somebody about skin conditions. I’m asking them about any family history of various inflammatory conditions, rheumatoid arthritis, psoriasis, psoriatic arthritis, a few other bits, other painful sites in their body, particularly joint pain, fingers, small joints of their hands and feet, any synovitis or any swelling that they’ve noticed, response to NSAID. So for example, if someone says, when I take my anti-inflammatory, I’m significantly better usually within 24 to 48 hours in the right context with the other factors in the story.”
“Clinical practice is often a game of probabilities and you’re always listening to the story. So if someone presents and they don’t have any of these strong risk factors, they don’t have psoriasis, they don’t have a history of low back stiffness in the morning, they don’t have other joint pains and they have a clear training increase in terms of volume or intensity that loads the Achilles tendon and they develop an Achilles tendinopathy. I think the balance of probabilities would state that this is less likely to be an inflammatory population.”
“If you read the RCTs on tendinopathy, particularly Achilles and Pateller, the vast majority of those studies are done on athletic populations. So they’re done on people that don’t have, or at least less likely to have these other risk factors, that the people with inflammatory arthritis are excluded. And that’s done for a good reason, because we want a more homogenous group. But the problem will arise is when we apply that research to the broader tendinopathy groups that do have all of these other risk factors, or it is an autoimmune process. We don’t have as strong evidence as they respond as favourably.”
“I don’t think it’s a bad option to at least apply some of those principles that we take from, I suppose, the athletic research on tendinopathy and how we know tendon adapts. But we have to be very clear that there’s an underlying systemic process involved in here.”
“When we ask things routinely, we take away the stigma that’s associated with it. So sometimes we add to the stigma by not asking them.”
“At the beginning of our conversation, I’ll have that conversation with patients that, these I need to understand you. And in order to understand you and help you, I need to know your general health stuff. I need to know what things might get in our way of getting you better. So when I frame it like that, firstly, it’s less intrusive and they just see it as, I’m here to understand them rather than I’m here to find things to blame on their pain.”
“It’s how you frame it rather than saying to them, you have this tendinopathy because you’re overweight. That’s not that’s not the right way to do it because you’re essentially blaming them for their own condition.”
“There’s also there’s also a duty of care in this. So if if someone has something that’s modifiable and it’s potentially changeable, then I do think we have a responsibility to raise those concerns, you know, by shying away from something that’s potentially detrimental to their health, you know, in some ways that’s ethically questionable as well. So, you know, it is a difficult conversation and there’s no right and wrong.”
“We probably have more influence on them than we think. When you look at the research on resistance training and metabolic health, it’s very favorable. So we can definitely play a part in that. You know, if you’re giving somebody a resistance based program that has these other risk factors and they’re from more sedentary population, you know, we can frame it in a way like this is good for your tendon, but it’s also good for your general health, you know, so there’s lots of benefits for doing this rather than you need to do this in this particular way because we need to get your tendons differ because that’s what the Achilles or the patellar research tells us in this athletic group.”
“Do we need to be loading people heavy, relatively heavy to their baseline strength to get tendon adaptation? We probably do if the outcome is the tendon. We probably do if the outcome is to get the structural change in the tendon, but probably not in many groups if the outcome is to get their pain down and get them functioning better and get them healthier and getting them their quality of life better.”
“Is this an athlete that needs to be able to repeatedly jump and hop and run the marathon? Or is this somebody that has gluteal tendinopathy that limits their ability to go on a two mile walk? That’s clearly different. One one is demanding a very spring like tendon and be able to function as a spring and, do all of the high level activities and the other is not so much from, the requirements are less. So if we’re too prescriptive with our programs, then we’re not going to meet the patient where they’re at.”
“If you look at the research on rotator cuff tendinopathy and you look at the various exercise interventions that work or at least look like they’re effective for this group, they’re quite different than the interventions that we would see in the lower limb for an Achilles. And why is that different? Is it because the rotator cuff is performing different roles versus say that’s something like an Achilles tendon or are we seeing a different group of people in terms of one is very typically athletic Achilles tendinopathy where there’s an increase in load versus a shoulder that’s more driven by these other systemic risk factors and the loading bit of the equation from a rehabilitation perspective.”
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