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Flexing Knowledge | Tendon Health Decoded with Dr. Gerard D’Onofrio

Episode 100, duration 2 hrs 00 mins
Episode 100

Flexing Knowledge | Tendon Health Decoded with Dr. Gerard D’Onofrio

Let’s take a look into the fascinating world of tendon health with Dr. Gerard D’Onofrio in this latest episode of the Dr. Gabrielle Lyon Show. Join us as we explore the crucial role of tendons in overall mobility and discuss the various factors impacting tendon functionality. Learn about the basics of how tendons work in harmony with muscles to support movement and what makes them vulnerable to injuries. Discover the significant influence of nutrients such as hydrolyzed collagen, leucine, and omega-3 fatty acids on tendon health, alongside the effects of hormonal changes and medications like fluoroquinolones and corticosteroids. This episode not only sheds light on critical components of physical health but also offers practical advice for enhancing tendon resilience through diet, supplementation, and mindful medication management.

Dr. Gerard D'Onofrio, a specialist in nonoperative treatment of sports and spine injuries. Dr. D'Onofrio excels in diagnosing the root causes of pain and uses advanced imaging techniques like musculoskeletal ultrasound and fluoroscopy to guide his conservative treatment plans. His expertise includes creating personalized therapy programs and performing guided injections and minimally invasive procedures aimed at pain relief and function enhancement.

Whether you're a fitness enthusiast, dealing with tendon issues, or simply interested in maintaining optimal health, this episode is full of insights that will help you strengthen your body's connective tissues and improve your overall well-being.

This episode is brought to you by Timeline, CozyEarth, MUD/WTR, InsideTracker, and 1stPhorm.

Flexing Knowledge - Tendon Health Decoded with Dr. Gerard D’Onofrio

In this episode we discuss:
– The crucial role of tendons in overall mobility
– The various factors impacting tendon functionality.
– The basics of how tendons work in harmony with muscles to support movement
– What makes them vulnerable to injuries

00:00:00 – Introduction to Dr. Gerard D’Onofrio’s Expertise in Muscle and Tendon Health

00:08:19 – Understanding the Role of Hormones in Tendon Health and Longevity

00:16:10 – The Interplay Between Muscles, Tendons, and Hormones for Optimal Function

00:24:15 – Exploring Non-Operative Approaches to Pain and Functional Improvement

00:32:16 – How Physical Medicine and Rehabilitation Enhance Quality of Life

00:40:09 – The Impact of Fasting and Nutrition on Muscle and Tendon Health

00:47:57 – Strategies for Preventing and Treating Tendon Injuries

00:55:54 – The Importance of Biomechanics in Physical Medicine and Sports Performance

01:03:42 – Corticosteroids and Their Effects on Tendon Repair and Healing

01:11:47 – Nutritional Supplements and Their Role in Tendon Recovery

01:20:09 – The Relationship Between Hormones and Tendon Health

01:28:08 – Exercise Recommendations for Cancer Patients and V2 Max Training

01:36:50 – Kettlebell Training and Its Benefits for Stability and Strength

01:44:49 – Dr. D’Onofrio’s Approach to Diagnosing and Treating Pain

01:52:35 – Preventive Strategies and the Concept of Anti-fragility in Medicine

 

Gerard D’Onofrio

Welcome to the Dr. Gabrielle Lion Show. Today, I am honored to sit down with my friend and colleague, Dr. Gerard D’Onofrio. He was chief resident at Columbia and Cornell, and did a fellowship in spine and sports at HSS, which is the Hospital for Special Surgery. He is a physical medicine and rehab doctor, and in this episode, are you ready for it? We talk about what you are missing if you only focus on muscle health, how tendons are the key to longevity, and the role of hormones in tendon health. We talk about this and so much more. As always, I produce this content for free. Please take a moment to share it, subscribe, rate it, like it, you know the drill. If you are not part of our community, head to my website, dr.gabriellelyonn.com, and join us because remember, we are forever strong together.

Dr. Gerard D’Onofrio, thank you so much for joining me. I am very excited to have this conversation. You and I have known each other for many years now. You are extraordinary. You are a physiatrist. You’re gonna explain to the listener what that is. And I’d love for you to talk about, a little bit about what you’re doing and how you got here. – Fantastic, so thanks for having me on. So physiatrist is a specialist of physical medicine and rehabilitation. So I did my residency in physical medicine and rehabilitation. And you can think about that as a combination of a few specialties. So it’s a bit of neurology, a bit of orthopedics, a bit of internal medicine. We take care of patients along the entire spectrum of disability and ability. So throughout the course of my medical training, I’ve taken care of patients with stroke, hemiparesis and hemiplegia, spinal cord injury patients, worked a fair bit at the VA, taking care of our veterans.

And then I’ve also been on the sidelines of professional sports teams as a assistant team physician for the NETs organization and the Red Bulls organization. So I’ve seen human movement, disability, dysfunction, pain, these things. And a physiatrist is a non-operative specialist. So we go through a variety of non-operative ways to help patients with their pain, function, et cetera, and basically improve quality of life. – It’s amazing because it actually takes human movement into medicine. – Yes. – Why? Why did you choose this specialty? And by the way, you’re a very fit guy.

But it’s an unusual specialty, I would say. – Yeah. So I started to learn about the specialty as I was thinking about going to med school.

And prior to medical school, I was a personal trainer. And so what I used to do is, during the summers of college, I studied up for my personal training certifications. I used to be a personal trainer. And I loved every second of it. You get so much experience watching how people move. And you get to see what it looks like when somebody has a dysfunctional movement pattern, when they’re being loaded correctly. And you really see what happens when you load a system. And that’s what this all comes down to. So we’re loading somebody’s biomechanics. Either those biomechanics are functional, and they’re going to improve. They’re gonna put on muscle. They’re gonna gain speed. They’re gonna gain functionality.

Or you’re gonna have dysfunction that leads to pain and disability, whether it be something like back pain or tendinopathies, which we’ll speak more about. But as a personal trainer, I wanted to go into a field where exercise was a really important component. So we pride ourselves as physiatrists as having very close relationships with physical therapists and writing detailed physical therapy prescriptions. So we really are uncovering in the office, what are the biomechanical determinants of pain? So let’s take, for instance, your shoulder hurts. But your shoulder might be more the end product of dysfunctional movement at your shoulder blade. So uncovering with a good physical exam and using things like X-rays, MRIs, CAT scans on the spot ultrasound, and of course taking a very thorough history. You could put together what is really the dysfunctional biomechanical diagnosis, and then at the tissue level, what’s occurring. So my residency training in physical medicine and rehabilitation preceded my sports medicine training. And all of this has led to me having a great appreciation for the musculoskeletal system, how it works.

And we were connected several years ago because I saw that you were talking a great deal about muscle-centric medicine and a lot of the endocrine determinants of muscle, the importance of muscle as we age. And looking at this holistically, if you were to think about how, say, a nephrologist goes into their training, like Shane, neurology, they look at the macrostructural approach, they look at the microfunctioning approach. So like, how does the organ actually look in the body? What is it made of? And then what does it do? So I’ve been voraciously consuming your work and I’ve read your book and I’ve found great appreciation in it because it’s looking at, I’m looking at the musculoskeletal function from locomotion, walking, lifting things, athletic endeavors, throwing, kicking, et cetera. But we’re also, I love that you brought to the table and to the scientific conversation, what is the actual biochemical aspect of that? Now we’re looking at the organ much more from the entire spectrum of what it is. – And quite frankly, you and I have, again, been talking for years, so it’s really nice to be able to sit down and have a conversation. Of course, this is the beginning of, you and I are working on some projects behind the scenes.

You bring in a very important perspective. It is wonderful to think about the health of skeletal muscle from a metabolic standpoint, from its impact on fasting insulin, fasting glucose, triglycerides, and that’s impact on, say dementia or cardiovascular disease.

The question becomes, how do we get to these, what I would consider inflection points. Inflection points of aging or inflection points of disability. I love how you said you look at individuals and take care of them through disability and ability. – Yeah.

– I really appreciate your perspective on skeletal muscle as its organ system, which is exactly what physiatry does, but I also think that you have a very unique perspective that brings in very closely the biomechanical aspect that I don’t think is actually super common in physical medicine and rehab. We talk about it as physical medicine and rehab, but your perspective is certainly becoming, and you use this tagline in your Instagram, antifragile. – Yeah.

– Which there are a number of topics that I’d love to discuss on this podcast, which include and are not limited to the things that limit our ability to progress, like tendon issues. – Yes. – Like back pain, hip pain, things that ultimately limit the quality of life for individuals, and then other things beyond, like should we be stretching?

And a number of other things, but let’s start with one of the things that I think that we both see in clinical practice are issues with tendons. And why are tendons important? What are they? How do we think about them in a global sense? – Sure, so muscle is contractile tissue. Muscle is made of actinomaus and filaments. You have this incredible cross-linking phenomenon that’s mediated by our energy molecule ATP.

And we contract muscle and ultimately to move bone, but muscle doesn’t attach directly to bone. It attaches to bone through tendons. And collagen is our most abundant protein in the body, and no surprise, tendons, that tendinous attachment from muscle to bone is predominantly made of collagen. So tendons are, by definition, they are non-contractile tissue. They’re almost like if you think about a short bungee. So they exist in a relaxed state called the crimp state, and when the muscle contracts, it pulls on that tendon, takes the slack out, and then it winds up attaching to the bone to move the bone. And tendons have this incredible quality called viscoelasticity, which is a cool word. – Everyone is gonna be quizzed on this later. – There you go, so viscoelasticity, it means that the mechanical behavior of that structure changes the degree of strain that you put on it. So at low strain rates, tendons dissipate energy. At high strain rates, they really put down the force. And so you can think about as you’re walking, you might be putting some tension through your Achilles tendon by definition, but you’re not putting as much tension through it as you are when you’re running, and it’s like a really tight spring. So the mechanical behavior of it does change.

The tendons are sort of an organizational level. Muscles have, they contractile elements, you have muscle fascicles, and fascicles, for those who are listening, are bundles of proteins. So you have the structures, you have a larger structure, and then you also have within that, these composition of these microstructures of fascicles. And fascicles are a fascinating thing because they are present in muscle, tendon, and nerve. And the reason for that is because we’re not uni-planar individuals. We don’t just function in one plane. We function in forward and backwards, left and right, and also we rotate. And so muscles and tendons, as they’re trying to move a bone, they need to have specific elements stressed, not the entire system stress simultaneously, but the fascicles actually allow for tendons to be strained specifically. So you could think about like a pitcher. So a pitcher, the job of a rotator cuff, this is a cool point that I really like, the job of a rotator cuff is actually to stabilize the ball on the socket. We think about rotator cuff strengthening exercise. You’ll see a lot of people with bands and cables and strengthening up the rotator cuff, and it does that, it does rotate the arm, hence its name. But the shoulder is an inherently very mobile joint. It’s comprised of four different joints actually. It starts over here at the sternocovicular joint, you have your AC joint, and then you have your true glenohymeral joint, and you have the scapula shoulder blade that rests on the back of the rib cage. So there’s a lot of mobility in it, which is why on average, unless you’re a rock head, you can raise your arm higher in the air than you can your leg. So similar ball and socket joint with the hip, but more stability there.

Job of the rotator cuff is to stabilize the head of the ball and socket joint. It’s almost like thinking about a golf ball on a tee. So as you raise your arm into a pitching motion, all of your rotator cuff muscles are active, but different fascicles are actually more stressed during different phases of that. So that’s one of the fascinating elements of this. It’s a really cool mechanical adaptive thing that we’ve evolved to have. And we have it in all of those mobile structures of the musculoskeletal system. We have it in muscle, we have it in tendon, and we also have it in nerves to allow us to be more athletic in multi-planar motion. So it’s very cool. And collagen itself is, most of tendon dry weight is type one collagen. And then you have lesser components of type three, type 11, you have other types as well. And when a tendon starts to become diseased or overloaded, that can change. It’s actually part of the process of developing tendinopathy.

– Let’s talk about tendons. Would it be fair to say that you couldn’t have a healthy muscle without having a healthy tendon? Or vice versa? – Yes, so it is fair to say. And it’s fair to say because we have general principles. We use this word homeostasis to describe how everything is regulated.

Healthy muscle to exhibit its mechanical effect of moving bone effectively needs a healthy tendon. You can develop your muscle. It’s actually, muscle will develop more quickly than tendon adaptation occurs. – Muscle will develop more quickly than the tendon adaptation. And is that why designing a really good training program is essential to avoid injury? Because essentially the people listening are thinking, well, why do we care about tendons? Nothing will take you out of the game faster than a ACL tear, than an Achilles rupture, than a tendonopathy, which then becomes chronic.

Could you have a,

I suppose a better question is which goes first? – Yeah, so this is something known as the athletic accommodation timeline. So when you start, let’s say you’re not a runner, or I could speak from a position of truth. I’m not a runner. So I– – Me neither. – So let’s say I start running. The first thing that occurs in the first six weeks is I learn how to run better. And basically that’s called neurokinetic response. So starting all the way up in your brain at your motor cortex and going all the way through your nerves as they go through your spinal cord and go through your peripheral nerves and into the muscle, you learn how to coordinate your motion. You basically learn how to use your muscles for more efficient motion. So if you were to test my ability to run in the first day, it’s not gonna be as good. I’m gonna be much more gassed. I’m gonna go deep into those energy zones. I’m gonna really kind of stress to do the activity, but I get better at it with time.

Then in muscle tissue, after the first couple weeks, you start to get psychoplasmic hypertrophy. So your muscles start to bring in some products to help them function. Now, the body perceives, it seems, putting down collagen, putting down protein. From one aspect, we have a substrate-driven issue, which I think you’ve elaborated on the importance of leucine, the importance of protein intake.

Then the other aspect is you need a continuous stimulus to convince your body to say, “We need to put down some new framework here.” So then you start laying down some muscle. By the time your tendons and ligaments start to adapt to the athletic endeavor you’re engaging in, you’re almost looking at six to nine months. – And that is much more of a significant timeline than it would take for a muscle to adapt. And by the way, tendon turnover is very slow. – It is. So as opposed to muscles, which have a very rich blood supply and a rich nerve supply, tendons do not have a rich blood supply. They’re relatively avascular compared to muscle. So they’re not going to turn over as fast. About 90% of a tendon is more or less static. And then you have maybe five to 10% that’s the variable element that changes with time. So this is one of the important principles that I think gets missed. We hear about this concept of progressive overload. Well, you’re not just progressive overloading your muscle. You’re progressively overloading your tendons. You’re progressively overloading your joint capsules, your ligaments, et cetera. So this is when I sort of harken back on my personal training principles. I say, well, where is the periodization? Where are we dropping back? Where’s the deloading? Where’s, are we working towards a goal in two to three months? And then are we scaling back and maybe changing and kind of starting back from a point just ahead of where we started before?

You can’t just progressively overload until you find yourself into injury. And that’s something I very commonly find. One of your quotes I’ll steal from you is, you can’t change what you don’t track. And it’s too true. And some people are very nuanced. They know their bodies really well. They’ve been training for 20, 30 years. They may not need to track as much, but if you’re a beginner or even an intermediate and you need to think about, I wanna train, I have a long-term goal. Well, your short-term goal should be proceed without pain, without dysfunction, and really just knock down the goals that are in front of me as opposed to train until I get an injury and change the training types, for instance, or give it up altogether. And that’s so, so important. I see that in my office all the time. I ask, what does your training program look like? Well, I do, they’ll tell me a split. I do back and bays on Mondays. I do shoulders and tries on Tuesdays. – Chest on Monday, universal chest day. – There you go. I do, yeah, sorry. Yeah, probably chest on Monday. – Matt, Matt only does chest on Monday. – Matt has a good chest.

– Lots of pushups. – Lots of pushups. And they’ll tell me a training split per body part, but what about the global period? Like, how are we actually looking at the overload of these tissues over two to three months? And what is the expectation? Is the expectation that you’re going to progressively overload until you’re the world’s strongest person, or are you gonna have to scale back? – When you think about injury, where do you see them? And again, you are a clinician. You are seeing a lot of patients every day from a very early hour. I’ll call you in the morning, we’ll have some great idea, and you’ll already be there reading. – That’s right. – Very early.

What are some of the most common things that you see as it relates to tendon injury? And I really like how you discuss this progressive overload. Is there something that we can do now that potentially can change the way that we move so that we don’t have to deal with these injuries that seem to really inhibit our capacity to live, right? Like you said, sometimes individuals will say, well, I used to do bench rest, but now I can’t because I have, I don’t know, tennis elbow. – Sure, sure. – And it’s not the muscle that the problem, it’s the tendon. – It is, that’s right.

You will infrequently, and to some degree frequently, depends on what you’re seeing, but you will see muscle strains.

And muscle strains can be on a graded scale, but the more frequent thing that I see in my practice is tendinopathy. And the most common tendinopathies I see are rotator cuff tendinopathy, specifically one muscle in the rotator cuff named the supraspinatus, and the Latin terminology means that’s above the spine of the scapula, so it’s one of the higher ones.

And then I’ll see a lot of Achilles tendinopathy, a good bit of patellar tendinopathy. – Which is neat, right? – Yes, that’s right. So, and then gluteal tendinopathy. And that’s one that really impacts a lot of people over the age of 50, and is very much present when someone’s walking. So if you think about the importance of walking as it relates to not just calorie expenditure, quality of life, locomotion, one of the most common things I see is something called greater trochanteric pain syndrome, otherwise abbreviated as GTPS.

Some people know it by a similar term, which is bursitis. Okay, so when somebody has a bursitis, and a lot of times you’ll get the clinical diagnosis of bursitis, you can get either a traumatic bursitis or a bursitis because you have an adjacent tendon that has a low grade of inflammation. More commonly I see the adjacent tendon that has a low grade of inflammation. Bursa sacs, they exist in the body to allow tissues to glide on each other. So we commonly see the greater trochanteric bursa, which is in the sides of the hip. That may be a little bit inflamed because the gluteal tendons from the gluteus medius, which is on the side of the hip, and the gluteus minimus will be inflamed because they’re not connected to a muscle, rather they’re connected to a muscle that’s not doing its job. – And are there movements that we should all be able to do, or is this an impairment in our ability to be able to move appropriately? – Yeah, so some of it is the basic sports medicine principle of you have a load-bearing tissue, you have exceeded the load-bearing capacity of that tissue, and that tissue is now in a state of disrepair. That is the hallmark of tendinopathy.

Whereas tendin tear, the collagen fibers actually separate. Tendinopathy is characterized by a state of chronic disrepair. White blood cells are in the area, you start to aggregate things like fat molecules, you start to have the collagen type change a little bit, and your body actually grows little nerve rootlets into the area to sense pain more readily. – Oh, that’s not good. – That is not good, and it’s actually, it’s an interesting phenomenon because it is also preserved, this same thing just like fascicles or in other places, the same thing occurs in interprotebral discs in the back. You have a collagenous structure without a rich blood, you have a nerve supply at baseline, but the more frequently that you injure it, it actually, there’s good scientific evidence to suggest that there’s little nerve roots that will grow into the area and make you experience pain more readily, basically telling you to stop it. – To stop. – Stop, shut it down for a while. So I think one of the things that you don’t ask me about, what could we all be doing? Take stock of what’s bothering you, listen to your body. If you are, you’re training shoulders and you’re doing a set of military presses, but that night you notice that you’re waking up and the side of your shoulder is hurting in the middle of the night, that’s a sign that one of your tendons is a little bit of pain and might have the beginnings of tendinopathy. Re-examine how you’re doing a military press, maybe sub that movement out for the time being. Don’t ignore those things. There are good pains and there are bad pains. Good muscle soreness, I think anybody who trains, you know it. You feel good, you get the endorphin release,

for instance, providing a stimulus to the tissue and it’s clearing that the byproducts of exercise over a couple days and you feel better. Bad soreness and a tendon, you typically have, you’re either compressing the tendon too much during activity, you feel like a snapping sensation when you’re going through a military press,

when you’re walking on those sides, your hips hurt a little bit more, or you go for a run and you notice that your Achilles tendon actually feels painful to touch and is a little bit bigger. Listen to that, decrease the training volume and then think about always pairing what you’re doing in your exertional work with what I call capacity work. So this is a framework I always bring to patients.

One thing you can learn from studying and working with professional athletes is that they take care of themselves very well. In addition to having fantastic genetics and athletic ability, you know, they also take care of themselves in a way that we don’t. So we don’t, for instance, spend a lot of time doing what I call restorative work, boring exercises, isometrics, or really taking time and saying, all right, well, I’m not gonna train today or I’m gonna train differently today because this structure’s inflamed and it’s a problem, I’m not just gonna take a couple of Advil and see if I can train through it. I’m gonna listen to my body and say it needs to heal, I’m not giving it adequate time, and I’m going to a percentage of my time to that. I like to use the 80-20 principle with us. So 80% of your time, exertional work, go for it. You wanna do your cardio-respiratory work, you wanna do your strength training, your power training, whatever it might be, somewhere around 20%, you should think about the injuries you’ve had in the past, you should think about the stuff you’re dealing with in the present, and you should be building capacities in those tissues. If you have to work with a physical therapist to learn how to do that appropriately, that’s fine. But you also, there’s a lot of great content online about how to restore normal mobility in joints, how to strengthen up your tendons. So that’s something I readily engage in, and I encourage my patients to readily engage in it as well. Spend a certain amount of your time increasing your capacity to then go exert yourself. Don’t have the entirety of your program, just be exerting yourself. Because the sum total of your human movement is not just the gym, it’s life. – That’s right. – So it’s the degree to which you are sitting, it’s the physical and psychological stressors that you’re putting on your body throughout the course of the day. It’s your ability to sleep well, and repair well, and get enough protein in, and get adequate nutrient intake.

We think about it in terms of the gym, because for a lot of us, the gym becomes our sport. And it becomes something that we really look forward to, we kind of rise and fall on our performance within it, and it can hurt a lot to think about, well, I can’t engage in my workout. My workout’s my release, I need my workout. My foundation for my day. But spend some time doing the hard stuff in the background, and you’ll be rewarded for it. Don’t wait until you get a really bad injury, until you learn how to rehabilitate them. – And then just, because I think that as you age, it becomes more challenging to recover.

I was looking at some of the research on tendons, and thinking about how can I relate this to something that I know about, which is skeletal muscle. That when you are very active, and you are young, you’re improving these satellite cells, you’re able to prime the body to be able to put on muscle later on in life. The literature that I was reading about on tendons was that the activity in youth is really critical for the thickening and the ability for these tendons to form, I don’t want to say in a meaningful way, but in a way that will withstand a lifetime of activity.

Which I want to ask you about, what do we know about training up tendons in youth, and then is there a natural decline? With skeletal muscle, there is somewhat of a natural decline to skeletal muscle because of increasing anabolic resistance. Again, there’s some controversy in this space, whether it’s because of inactivity, or a natural process of aging. But where, if we were to think about a concept that we know a lot about, which is skeletal muscle, and maybe the listeners know more than I do about tendons, which is why I wanted to have you on, so that you can teach us all about tendons and injury and approaches to training. But what is the progression from tendons from youth to aging? – Yeah, so in your teens and your 20s, you build up the college and content of your tendons, you build up the area. So we’ve talked about cross-sectional area, which is basically the thickness of the tendons. And with time, you do have a little bit of resistance to modifications in your tendons. So we find that in the aging athletes, you tend to develop this low-grade tendinopathy or tendinopathy-like features where you have, you’re aggregating these other cell products, like the fat content or calcium content. And it also tendons lose some of their stiffness with age. – And we want tendons to be stiff? – You do. So tendons are supposed to be stiff by design. You want a good spring to be mechanically efficient. – You want a good spring to be mechanically efficient. Think about running, bounding, hopping, et cetera. You want your muscle contraction to be highly efficient and go towards bone. There’s this really interesting principle called Young’s modulus. And Young’s modulus is basically a calculation based upon the stress-strain curve of a tendon.

So your Young’s modulus should increase with training, which basically is the efficiency of the tendon to do work and some resistance to injury. Every tendon, in theory, could be injured at its maximum, just like a muscle could be. You go try to pick up a car, your bicep might tear. – No, I could totally do it. – There you go. There’s some days I think I can do it too.

But the tendon does appear to have a decrease in that Young’s modulus, a decrease in the ability of its mechanical efficiency as we age. You also will see some degree of decreased cross-sectional area of tendons, and you’ll also notice some decreased collagen content as we age. But these are all modifiable, but to the same extent as muscle, less modifiable. So building up good tendon tissue does not mean you want the largest tendon. You want the mechanically most structured tendon. And this is an important note, larger doesn’t always mean better because tendonopathies actually are characterized by larger tendons. They aggregate water, they aggregate these things called proteoglycans, so the tendon does get bigger.

We want the same way some elite power lifters aren’t necessarily the most muscled individuals, but they’re some of the strongest individuals. You have to think about, well, how are they the strongest individuals? They’re the strongest individuals because they’re mechanically very efficient. They know how to move neurokinetically. They know how to position their bodies. They do have muscle strength, but they don’t necessarily have the largest muscles. A bodybuilder will have larger muscles on average than a power lifter. In the case of tendons, the collagen,

we hear about DNA as a double helix, and it’s a very fascinating thing to learn about. Collagen is a triple helix. So you actually have these cross-linking of molecules in the collagen, and that allows the collagen fibrils within tendon to link more effectively, to move more effectively. So a lot of times that we see, whether it’s with weight training, cardio respiratory training like running,

or even like a plyometric protocol, you’ll see that people get Young’s modulus changed before they increase, if ever, cross-sectional area. Men have larger tendons than women on average, but that doesn’t necessarily mean that the tendon is always stronger just because it’s larger.

A larger structure is only as good as the microstructure within it, and the microstructure is more measured by Young’s modulus. So when we look at the studies that examine loading up the lower limb tendons, the patellar tendon, the achilles tendon, the glutes, what we see is that that Young’s modulus changes, and that does appear to change a little bit with age. So building that up while you’re in the prime years is perhaps beneficial, and then staying with it.

– Do we know the mechanism of action as why there is a decline?

I don’t know the body of literature when it comes to tendons and tendinopathy. You know, when I think about muscle, we know that there is motor de-innervation, there’s a decrease in the quality of the satellite cell. Do we know why tendons decline? – So one thing is, from a metabolic aspect, they do change a little bit. So they actually, tendons are minimally aerobic tissues. They don’t really go through, they don’t really use oxidative phosphorylation as a means by, they’re largely anaerobic, but they have some aerobic metabolism, and it’s actually a hallmark of the degree to which your tendon is conditioned, that it can actually engage in aerobic respiration. – That’s pretty fascinating, isn’t it? – It is.

I think because it’s such an on-off mechanism– – Meaning you’re either engaging the tendon or you’re not? – Exactly. You’re either crimped or on-tension, you can kinda get away with an anaerobic response. – Is it metabolically active tissue? – Less active than muscle. Highly less active than muscle. But the metabolism will change, and your blood flow may change as you age as well. Hypoxia, or the absence of oxygen, is considered to be a driving factor behind tendon degeneration. – That’s interesting because it’s mostly avascular. – Yes. – So it doesn’t have a good blood supply to begin with. – Yes. So minor alterations as we age, either due to the sedentary nature, or just the fact that we’re not moving well, or whatever else it is, or just time.

The other thing is we accumulate micro tears. And a lot of micro tears don’t heal, is a high rate of chronic tears in, say like your rotator cuff, or in other areas of the body, that may not heal, and you may not need them to heal. Ultimately, they may not progress to be a surgical issue. But that will weaken the tendon. Nothing in the body is as strong as when you originally made it. So if you have a collagenous structure, it’s relatively avascular, you’re gonna try to put down a scar tissue within it, it’s almost never gonna be as strong as when you first started it. The other tendon fireballs may take that load. They may be able to do 99% of what they did before, but it’s tough to say that the magnitude effect of the tendon at its best will ever be the same. So metabolism changes, and you also see cell senescence, or some cells just dying off. And we see that in a lot of tissues. So there’s an element of tissue hypoxia, there’s a little bit of a change in tissue metabolism, the collagen cross-linking, and perhaps it’s not as efficient, and so your young’s modulus goes down. And then we also see that some of these cells just die off with time, and so it gets harder.

I think if you can maintain it, it’s very good. It’s tough because there’s always the abstract element of this. We’re examining literature that takes a point in time, and typically these studies are over months. It’s tough to say what would happen if you informed a population of this when they were younger, and they engaged in certain exercises. Could they, in theory, maintain a lot of this? The same way that, in theory, we can maintain a lot of our muscle. – Are there activities that individuals should be doing? You had mentioned plyometrics, running, skipping, bounding. Will those things that maybe children naturally engage in help develop the health of the tendon, and that we should probably continue to do? Whether it’s should we continue to sprint? Should we make sure that we have bounding in our program? – Yeah, I think everybody should be training type two muscle fibers, and so you need to be getting some degree of explosive work. I think the biggest phase change that we see, when we look at a program for somebody, and we try to see how they could be, for instance, we’re seeing that they’re overloading their patellar tendon. So the tendon that connects the kneecap to the shin bone, and helps basically act as a mechanical lever for the quadriceps muscles.

Maybe they’re overloading the sagittal plane a little bit too much. – So explain to us what that is. – So sagittal is back and forth. So a squat is a sagittal plane movement. To some degree, a barbell squat, you’re doing some degree of frontal plane, so that’s left versus right stabilization, and you’re also not rotating with the bar on your back. So that would be a classic sagittal plane movement. The bench press is a sagittal plane movement.

But as we age, it does appear that we just generally spend less time rotating and running and cutting and doing the things that we did as kids. So when we try to go back to those activities, that’s when you’ll hear about an acute

achilles tendon rupture, and some 30 to 50 year old male who’s doing a backyard football game for the first time in a while. So you’ll hear about it, and they’ll pop their calf muscle, and that’s an achilles tendon rupture. So I like to look at globally in a program, how much time are you spending in the three planes? Are you rotating? Are you rotating under load? Are you stabilizing? A good example of a stabilization exercise in the frontal plane would be like a suitcase carry. I’m just gonna carry a kettlebell at my side. I’m gonna go forwards and backwards, and I’m gonna make sure that my body doesn’t lean either way. By engaging in sagittal and transverse movements, you engage different muscles than you do with sagittal, I’m sorry, transverse and frontal plane movements, you engage different muscles than you do with sagittal plane movements. A lot of the machines in the gym will keep you in the sagittal plane. And so this is something that I advise people to get off of machines. Get used to doing lunges, get used to doing rotational work, and really challenge your body. There’s some degree of, I think a very good scientific debate about what exercise is best for tendons. – I would love to know, and I wanna know if blood flow restriction has any influence on tendons. – Yeah, it’s a good question.

With regards to the types of exercise, we look at predominantly from the prevention aspect and from the treatment aspect. From the prevention aspect, there’s nothing to say that we can justifiably tack down something to the wall and say, you should only do isometrics or eccentrics or concentrics. It’s tough to say that. There’s a bit of conjecture in the literature about that. But what’s interesting is there was a very good study that looked at the rates of lower limb tendinopathies in soldiers in Israel, and basically looked at a prevention program, and then used an ultrasound to take a look at the tendon health of the lower limb tendons, and whether or not those tendons were aggregating those products that are hallmarks of tendinopathy. And what they found was, contrasting what you might think, it was like an Achilles prevention program, there were almost no calf raises in the protocol. The entire protocol was hip and knee. And it was all stabilization of the core, rotational movement, hip, airplane, stuff like that. So this is another concept that I very commonly bring up with patients, which is smoke versus fire.

Are your symptoms a representation of that tissue being at its end, it’s overloaded, but is the real problem a mechanical element that’s missing from your program or missing from your life? So in that particular study, where they looked at prevention, they did find that it was helpful when they underwent this prevention protocol, which is largely comprised of hip stabilization exercises. The entire kinetic chain is linked. We cannot divorce one element from the other. Your body has to achieve motion. It has to get range of motion from some element. So let’s say you go bend down to go get something you’re doing, a squat. There’s so many moving parts within that, from your ankle to your knee, to the intrinsic muscles of the foot and the bones in the foot, to your hips, to your low back and to your thorax, et cetera. So you’re gonna get mobility from somewhere. So as the answer to the question, how can we actually prevent some of these things from happening, it’s can we identify your mechanical weak points ahead of time? From a rehabilitative aspect, we use isometrics commonly as the starting point in a tendinopathy rehab protocol. – So would you explain what would be an example of an isometric? – Yeah, an isometric exercise is one where you’re contracting a muscle, but you’re not moving the limb. So if I were to be rehabbing a biceps, it would be just holding a dumbbell at my side, right? A concentric would be bringing the dumbbell up to my shoulder. An eccentric portion is when we’re actively mitigating the lengthening of the muscle, and those tend to be the hardest, right? So that’s when we’re lowering down a weight slowly. So as a scientist by the name of Alfredson who came up with something called the Alfredson protocol, and since then we’ve been really focusing on eccentrics as the sort of the go-to. That’s how we’re trying to get by week six of a PT protocol for somebody’s Achilles. And we’ve broadly adopted that for other tendons as well.

And good comparative study came out a couple years ago that looked at heavy slow resistance training versus eccentric training specifically, and found that heavy slow resistance training was non-inferior to eccentric-based training. So basically the time under tension with deliberate motion meant to restore the capacity in the tendon is as beneficial as doing heel drops off of a stair, for instance, for Achilles tendinopathy.

For blood flow restriction, I can’t say specifically whether or not it’s beneficial. The thought of hyperemia, so hyperemia is the process of getting more blood into a tissue, and we do use therapeutic ultrasound to heat up tendons. And we use shockwave to heat up tendons to basically break up microstructures in a tendon to treat it. When we put PRP, we’re putting blood products in an area. So the thought of getting blood into this relatively avascular structure is one that makes a lot of sense. – How effective is that? – Which one specifically? – Any modality that utilizes,

because the structure is a largely avascular structure. So now you’re introducing something that potentially it’s not exposed to routinely or with the amount of whatever you’re gonna use, PRP, or however you’re going to use any of these modalities. How effective in treating a tendinopathy is it? And tendinopathy would be something that would cause pain over time. And you eliminate the capacity. From a very practical aspect, the reason we are really focused on tendinopathy is because those seem to injure before a muscular injury happens. – It’s the common denominator that limits the quality of life.

– I think it’s a huge limiting factor in training programs and progression. And I think it’s one of the first things we see when somebody starts weight training and we start to see these things arise. So we’ll go through a couple treatments. – Amazing. – All right, so we have this relatively avascular structure. It’s in a state of disrepair.

Let’s think about what that means. So the actual structural components are not as strong as they were. And you can think about this like you have a house that is not perhaps built as well as it could be. You have a leak, whatever else it might be. Well, first thing we’re gonna do is we’re gonna bring in a GC. And so that’s your general contractor. – I was like, what’s a GC? Oh yeah. – Yeah.

You have tenocytes. So same thing in muscle. You have your myocytes and you also have your osteocytes and bone. You have these cells that basically look at the tendin homeostasis and they help direct traffic. And tenocyte is a standard, it’s called a modified fibroblast cell. So it helps to lay down collagen and also helps to direct traffic.

The tenocytes will sense that something’s wrong and they’ll bring in other cellular products. One of which is that you will start to grow little blood vessels in the area. So part of tendinopathy is actually when we put color powered Doppler on ultrasound and we look at a tendon, we’ll see stuff light up. That was previously, that is a good telltale, one side versus the other. Do you have hyperemia in a tissue? That’s already a sign that things are going the wrong direction. Well, now we say, well, now you’ve aggregated the scar tissue, you’ve aggregated these other things that are there that are not that helpful.

Well, we might have to bring in an excavator. And the excavator is, we have a couple of different treatments for excavation.

One of our treatments is called PNT, so Percutaneous Needle Tenotomy, which is when under an ultrasound we’ll actually pass a needle through the tendon several times. – Is that where dry needling came from? – It’s very similar to dry needling. – Or this came first and then dry needling was adopted. – Yes, so dry needling, depending on your discipline, dry needling is something that could be performed by a physical therapist. For myself, I do these under ultrasound and visualize the portion of the tendon that’s in the dental pathic. – Which I just want to highlight that that takes a ton of skill. Ultrasounds are not easy to use. And quite frankly, I believe that that’s how it should be done because then you actually can see where the injury is, what tissue you’re putting it in. You’re not doing it blinded. You are being able to visualize. – It’s important to visualize. It’s also going to tell you whether or not there’s a tear there. You don’t want to needle a tear. So a tear is a different concept. A tear is a separation. So we don’t want an excavator in that area. It’s not helpful. So the thought of passing a needle through a tendon several times will actually help induce,

take this state of chronic disrepair and convert it to the acute inflammatory phase again, and basically help to cycle out some of that stuff. So that can be done through PNT. It could also be done through something called a 10X procedure, which helps to remove scar tissue, remove calcium that’s built up in tendons. The advent of PRP and why PRP is so interesting. So PRP is a distillation of blood products. So we spin down your peripheral blood. It’s still majority red blood cells, but PRP means platelet-rich plasma. And there are two subtypes of platelet-rich plasma, the exact concentrations of which do differ in the literature base slightly, depending on the study you’re looking at. So you have leukocyte-rich, so white blood cell-rich platelet-rich plasma, and leukocyte-poor platelet-rich plasma. If I were treating a joint, I would use leukocyte-poor. I don’t need white blood cells in a joint necessarily. But when I have this chronic state of disrepair, I need a whole construction crew. I need my white blood cells. So I’ll use leukocyte-rich preparations. And I typically perform it with a tenotomy too, to actually put some areas into the tendon where I can distribute that PRP. Now PRP has several growth factors, one of which is platelet-derived growth factor. And this helps to basically stimulate the tenocytes and another type of cell that resides in tendons called TSCs, tendon stem slash progenitor cells. So you do have a repository of stem cells within your tendons. It’s just a question of mobilizing them. So conceptually, we thought, well PRP makes a lot of sense.

Depending on the tendon and depending on the literature that you’re examining, it can be very effective. On a hold, I would say it’s probably a 50-50 proposition depending on the chronicity of your tendon problem, as well as whether or not you have a tear concomitantly and where that tear is. Not all tears are made equal.

The tendon itself, right, so you have the muscle coming towards the tendon. You have a mild tendinous junction, which basically looks like a finger where the tendon is interlocking with the muscle. And some tears do occur there, and those can be quite tough to treat. But then you also have something called the enthesis, which is where the tendon attaches to the bone. And so those are the most common ones we are treating. Now you can have a tear at any portion in that tendon. So they all have different prognoses. If you have a tendon on the bottom right by the bone, that’s a different prognosis than the one up by the top by the bursa. So we try to extrapolate from the natural history of this. What’s the percentage chance it’s gonna heal? Where is it? How big is it? How impactful is it to the amount of strength you can produce in the relevant muscle? How impaired is it? And then would we consider, is this a large enough tear that it should go to surgery? Is this something that we should try PRP in?

Important for people to know, if you do suffer a tendon tear, there are different types from a perspective of, if we’re just looking at a large tendon,

you can get what’s called a full thickness tear, which is when it’s like as if somebody punched a hole in a paper, goes straight through from top to bottom. – And you usually know when you do those. – Yes. – That is, I have had quite a few injuries and you know when that happens, it’s not like a tendinopathy. You don’t necessarily, you know, might be a little irritation and then you go back to the thing and then you irritate a little bit more. – That’s right. – But when you get a full thickness tear, that is an acute injury that typically will take you to your knees or whatever, yeah. – So the full thickness is the pothole and then there’s something called, so we say full thickness incomplete or full thickness complete? Incomplete would just be, I have a sheet of paper and I punch a hole with a hole punch. Complete means I literally take a pair of scissors and I cut the paper in half. If you have a complete tear, now the tendon is no longer attached to the muscle.

That is a surgical problem, okay? That is not something that’s likely to heal by itself. – That would be, for example, like a tricep tendon tear or a bicep rupture. – Yeah, so and depending on how important the bicep, so for instance, the bicep is interesting because the bicep is almost like a fifth rotator cuff muscle. There are people walking around with bicep tendon tears without significant, you know, without significant symptoms. But if you have a complete full thickness tear, what will occur in time is because the muscle’s not seeing any tension. The body deprioritizes it and it will atrophy. And if it atrophies, to date, I’m not aware of any way to stop that or reverse it. So those are the circumstances, you know, like I brought up that example of the 30 to 50 year old guy who pops his Achilles playing backyard football because that’s the most common age population to get Achilles tendon ruptures. But if that occurs and that tendon’s not reattached or it’s not approximated and you’re putting a boot and something like that, then foreseeably you’ll atrophy your gastroc and your soleus and that’s gonna be really tough functionally to go through. – So essentially don’t delay. I think a lot of the patients that I have and many people listening, they don’t wanna stop their activity. They’ll injure themselves and they don’t wanna stop. I don’t wanna get a bicep repair. I can still be just as strong. But if you’re going to do the intervention that requires surgery, one should do it swiftly. – Yeah, you should be evaluated swiftly. And you don’t wanna see on MRI or on ultrasound, you don’t wanna see those atrophic changes occur. That’s a sign that your, that muscle’s not gonna be as functional as it originally was and therefore your prognosis isn’t as good. – Why do you think that we see, again, you see patients often and it’ll be daily, either a shoulder, a knee or a hip.

Do you believe that it’s because of patterning? Why are those the common injuries? – Yeah, in the shoulder, I think it’s because we have mechanical compression underneath the bones of the shoulder and that’s known as a symptom they call it subacromial impingement. So basically you’re moving your shoulder around and the tendon gets caught underneath the bone. And that’s, you can sometimes hear a snapping sensation when you do something like a military press.

For patella, it’s because a lot of times patellar tendinopathy is part of a greater clinical concept known as patellofemoral pain syndrome, which by the way, is most often associated with weakness of the gluteal muscles. So the knee is overloaded trying to do too much work and the glutes are not adequately supporting the knee and the hips. – So the posterior chain is actually affecting the anterior chain. – Yes, and posterior lateral specifically. So hallmark of patellar tendinopathy, patellofemoral pain syndrome, we commonly will look at strengthening up the gluteus medii on the side of the hip. And then the really the whole goal there is can you get back to walking and running with stabilization at the hips so there is not so much pain at the knee. Once again, smoke versus fire. Your knee hurts, you do have a tendinopathy, but mechanically speaking, there’s an insufficiency of some muscles that are higher up in the kinetic chain. – It just seems really challenging as we think about long-term projection of people’s lives to figure out that, you know,

I have a weak glute medii and you have, I don’t know, just pick a different muscle. Are there things that individuals should all be doing? We wake up, we brush our teeth, we brush our hair, should we be getting up and doing glute activation? I don’t know, eyes, tees, and y’s for our shoulder. Are there things that we could embark upon now to very specifically prevent a mechanical injury from a tendon that we don’t even know that we have? – It’s a great question.

And in trying to distill what makes a lot of sense, I will give home exercise programs to patients almost to that exact effect. They come in with a back injury, but I say, well, now’s an awful time good to start rehabilitating and prehabbing your hips. – Is prehab a real thing? – Prehab is absolutely a real thing. It’s tough because prevention is difficult to study. So it’s more– – That’s a really good point. – It’s very, very difficult to study. So I’m recommending this because conceptually it makes sense not because I have a study to point to that doing, you know, side-lying hip abduction exercises helps stave off the onset of something. So what I see for the shoulder,

a lot of times the mechanical dysfunction is at the shoulder blade and how it’s moving. Either it’s elevating too much, it’s not appropriately what’s called protracting. And a really good test to see how your shoulder blades working is to do a pushup with a plus. So at the top of your pushup, you push out the ground a little bit more. If you’re trying to achieve that motion by rounding your thoracic spine, you can’t appropriately actually work through the back part of your rib cage and your shoulder blade to get that to work well. So pushup with a plus that I like. For the hips, a single leg stance squat. – Would that be a pistol squat? – So actually I prefer this like skater variety. So your trail leg is behind you. – And you guys listening, we are gonna go through these exercises. So while they’ll be in accompanying YouTube, which will go through a lot of what Dr. Gerard is talking about. – Yeah, so I like to see single leg stability. And single leg stability is a great determinant of how you are actually going to progress through your gait cycle. So a lot of people, this is a really good thing and I’ll show off my PMNR residency here. – And this is standard, so do all physical medicine and rehab physicians need to learn biomechanics? – Yeah, it’s a huge element of our training. – So it is a part of your training. – And I’ll tell you why, because unless you understand normal biomechanics through the gait cycle, you can’t rehabilitate somebody with a stroke.

Once they’re hemiparatic, once they have a foot drop, it’s really tough. So you have to know the normal mechanical determinants of gait to understand the dysfunctional elements of it. So I like to see how, with regards to the gait cycle, 60% of your time is in stance phase, 40% of your time is in swing phase, there’s a 20% portion that’s called double support where both legs are simultaneously on the ground.

So your glute med is actually active to stabilize your pelvis. So if you see somebody with a lot of hip movement while they’re walking, you don’t wanna have 100% stiffness, but you wanna have stability. If you have a lot of hip movement when you’re walking, it’s oftentimes an indicator, well, it’s not as stable as it could be. There’s not enough muscular tension to support the core. The center of mass in the body is in the pelvis. So I always encourage young athletes, I’m like, if you have to focus on a couple of things, it would be very stable through your pelvis. You can’t shoot a cannon from a canoe, okay? So you need stability in the pelvis to put force down through the legs. All athletes, regardless of what you do, are made in the legs. – All athletes are made in the legs. – Yes, and I believe that very strongly, great pitchers have a good set of legs. They know how to really drive off.

Even look at Mike Tyson, right? One of the greatest knockout artists that has ever existed in the heavyweight division, he had monstrous legs, right? It was a huge element why he was able to compete with people six inches taller than him. So I believe it’s a good stable core that can rotate under load, good strong glutes, and knowing how to keep your spine stable is really important. So good neutral spine throughout the range of motion. And then when you’re walking, yeah, you do swing the thoracic spine and rotation a little bit while you’re swinging your arms, but you want your body to be stable. You want to be able to walk slow and you want to be able to sprint fast. And if you could do both of those, you’d kind of check in with yourself. If you can’t walk slowly without feeling like you’re off balance, something’s a little bit off. – Do you think that everybody should continue to sprint or never lose that ability? – I would love for everybody to sprint. I think sprinting’s fantastic. It’s also a great check-in to see where you’re at. But if you are doing it, you need to be very careful with load management because if you haven’t done it in a while and you go back to it, it could be a major risk factor for Achilles tendon. – And to be clear, well, actually I avuls my hamstring doing a long stride sprint. Would you recommend, you know, people listening to this are thinking, because we’re going to cover zone two cardio and training,

because you and I really see eye to eye, excuse me,

about how there’s a lot of discussion about zone two and how that’s going to be so effective in cardiovascular health. There’s a lot of other ways to train.

But this idea of picking up where you left off may not be the best thing. So if you are at home listening to this, moving fast is important because you lose speed and you lose power,

but perhaps not picking back up if you haven’t sprinted or you haven’t done a lot of these motions like the guys that you’re talking about between 30 and 50, jumping on the basketball court, you probably have to build up to that. Is that fair to say? – It’s absolutely fair to say. – Can we talk a little bit about, well, I mean, let’s tie up the rest of tendinopathy because I’m curious about some risk factors, which in my mind would include medication. – Yeah. – Common medications that may affect tendon health. – Yes.

The first one that comes to mind is fluoroquinolones. So that’s like ciprofloxacin, levofloxacin, that’s a whole class of medications. Those are antibiotics.

Fluoroquinolones are very strongly linked with tendon problems and tendon rupture.

We believe that this impacts tendon metabolism and integrity to some degree. So those are of concern.

You know, there’s some, I think very good discussion around statins and tendons specifically. So whether or not they’re beneficial. So if you have somebody who has hypercholesterolemia, they can actually deposit, I’m sure I know you know this, but xanthomas in their tendons. So fatty deposits in the tendons. So in that case, a statin might actually decrease the size of their tendon and improve the tendon health.

– If they have familial hypercholesterolemia. – That’s right. – But not if they just have high cholesterol. – It’s tough to say. – Okay. – It’s tough to say because hypercholesterolemia, diabetes, gout, these are, gout and slash hypereurysmia are all risk factors for the tendinopathy and smoking. So if you look at the metabolic syndrome spectrum, obesity is also a risk factor. All of these things impair tissue healing anywhere in the body. So in a structure that does not have a great blood supply, that’s constantly under load, it’s very much magnified.

– That’s an interesting concept I haven’t quite thought about. Again, because I’m so fixated on muscle, if someone is obese or struggling with any kind of metabolic dysfunction, that would affect tendons in general. – Diabetes patients will rehabilitate more slowly than non-diabetic patients. And partly because tissue healing is slower. So there’s an excellent textbook that I came across that actually looks at all the metabolic influences on tendinopathy and chapter by chapter goes through it. And one of the aspects of it was just think about it like it’s another structure in the body, it heals more slowly. Bone fractures heal more slowly, microarchitecture and bone is more slow. It’s one of those things where it’s reasonable to make a leap from one concept to another. If tissue healing and tissue repair is not as quick as it could be or as comprehensive as it could be in one tissue, there’s no reason to suggest that it’s gonna be better than another. – So fluoroquinolones can cause a risk of tendon rupture. – Which it’s really important that physicians educate their patients. Don’t go sprinting, don’t go running when you’re on these statins. They may have a positive effect depending on the person.

Anything else that is known to affect tendinopathy. – Corticosteroids. So corticosteroids, I had a great attending while I was in residency. He said if you just draw a body diagram, you can find a place that corticosteroids impact every part of it. And it’s the truth. You can get hair loss, you can get your skin changes color and texture, and no surprise, it does impair tissue healing. Now the question becomes a very good question because it is part of my practice to provide corticosteroids. – And also it’s important to point out it’s a standard of care. – It is, it is. And so the question becomes why are we doing what we’re doing? And so in the circumstances of somebody has a tendinopathy and they’re getting a corticosteroid injection, that injection should be guided, it should be into the adjacent bursa. You don’t want to put corticosteroid into a tendon. That’s not gonna help anybody. But if you’re putting in the adjacent bursa, there’s theory that perhaps you’re gonna anesthetize and kind of decrease the pain signals coming from those little nerve inlets that have actually grown into the tendon themselves. And if I get you some short-term pain relief for three months, which is on average what we counsel people for corticosteroids, if I get you some short-term pain relief and you could do the PT and your mechanics are improved, are you in a better landing spot than if I didn’t do it? And that’s a conversation I have with everybody around a corticosteroid. Now, oral corticosteroids are prescribed for a variety of conditions. Rheumatologic conditions. – And we’re talking about a prednisone, a meteral dose pack. – That’s exactly right. I even use them to some extent when we’re treating low back pain patients who have a really bad low back pain bout and they have a flare and we can’t get them in for like an injection or epidural.

And we can’t get them through PT because they’re in such a bad spot. We’ll use a meteral dose pack. Now, meteral itself is gonna be absorbed by the body. Your body does not know exactly where to disperse this medication. It’s gonna be absorbed, it’s gonna impact hormone production, it’s gonna suppress natural production of things like testosterone and sex hormones, it’s gonna feed back on the pituitary and the hypothalamus and the whole chain and the adrenals. But at the tendon level, it can actually impact your ability to repair. And so if you’re susceptible and you have a predating injury and you go through a meteral dose pack and you go exert yourself, there is a potential that you can injure yourself. Now, once again, risk benefit ratio in everything we do.

I’ve used this phrase with you once before and I’ll use it again, there is no free lunch in biology. So, and it’s too true, it’s too true. So everything we do has side effects. Everything we do has a potential downside. Everything needs to be weighed for the person in front of you. So in the risk benefit analysis that you’re saying somebody has a tendinopathy, it’s been recalcitrant to PT, you’ve tried to do some stuff, they have nighttime pain. Well, now the nighttime pain is impacting the rest of their body because they can’t sleep well. – Is pain worse at night? – Depending on the tissue. So let’s say, so if you have a shoulder bursitis as a consequence of a tendon problem in your shoulder, nighttime pain is a hallmark of it. – And is it because cortisol is lower? Why does that happen? – Mechanical compression. So when you stop moving tissues that are relatively inflamed, they will touch other structures around them and sensitize them. And then specifically if you’re like a stomach sleeper and you put your arm up to the side around your pillow, you might feel like your adult wakes up really sore and that’s because you’re compressing a tendon. Tendons like load, they don’t like compression. – Tendons like load, they don’t like compression. – That’s right. So same thing– – We’re learning a lot of really good one-liners over here. Really, really great. – There’s a, same thing, somebody has a gluteal tendinopathy on the side of your hip, lying on that side will be very painful at nighttime. Extended compression on a tissue that’s irritated, you’re gonna know about it. Somebody has an Achilles tendon problem, shoe fits not correct, or they tried to say they were in the first time in cleats for a while that they weren’t in cleats before, you might inflame that area.

– Any other medications that can be harmful?

– There’s perhaps more as well. – But these are the big ones. – Those are the big ones. I think more about the, in some circumstances, some of the hormone replacement that’s helpful. – I was gonna ask you, I was gonna ask you on the flip side of this, are there potentially oral agents or injectable agents that could be beneficial for tendon health? – Broadly speaking, from a nutrition aspect or like a nutraceutical aspect, what we can take, hydrolyzed collagen has been proven to be a little bit helpful in studies.

Leucine, no surprise there, has been, I’m sure Leucine’s been on this podcast before. – No, never heard of it. – Yeah, right.

Leucine is actually a component of a proteoglycan around tendons called decorin, and it can help lubricate tendons. It’s also, once again, a concept that makes sense. If it’s good for muscle, it’s probably good for tendon. So in these circuits– – If it’s good for muscle, it’s probably good for tendon. I love this because we have really left tendon out of the conversation. (laughing) – We’re back to your neck of the woods and muscle. But the interesting thing is we know that you need, to some degree, it’s a substrate driven issue. You do need adequate protein intake. It is a collagenous structure. Whether you absolutely need collagen, because your collagen is gonna be broken down your stomach and brought back, is I think a better question to ask. So it has been proven to be somewhat helpful. Omega-3 intake has been associated with decreased in tendinopathies. – And is that because of its impact? I always think, okay, well, what would the mechanism of action, would that be an inflammatory perspective? – I think it’s the low-grade anti-inflammatory aspect of the resolving pathway. So I think that that’s it. Now, for that reason, it’s important to point out, a hallmark of tendinopathy is expression of prostaglandin E2. And so if people don’t know E2 is something that is present in acute inflammatory processes, it’s why a lot of anti-inflammatory medications work. So omega’s act on the same aspect without a lot of the potential downsides. So I will counsel patients to take omega-3 supplementation. DHA and EPA are superior. So I will counsel them to do that as well. Now with other aspects, protein intake, loose intake, vitamin C is a cofactor and collagen synthesis. So vitamin C makes a lot of sense. – And are there doses that we know of? – You know, I’d have to get back to you with exact dosing. I just know that it’s dietary intake of vitamin C is associated with improved tendon healing. – And have you heard of, I don’t know if you ever use these in clinic, but SPMs, the specialized pro-resolving mediators orally? – I’ve not used them. – Yeah, I am not so sure on the data, but we’ve used them, some of my colleagues have used them a lot with operators.

But you and I will have to look at some of the actual data, but I am curious. – Yeah, and vitamin D can be helpful as well. So vitamin D has been proven to be helpful and tendonopathies as well can help decrease some of the pain. Vitamin C and vitamin D deficient rats have decreased rotator cuff healing after an injury. So it’s interesting to think about leucine, glycine, and lysine are the amino acids that are most helpful. But having a good amino acid rich diet with good amino acid profile is probably best.

From a hormonal aspect, hormones are really interesting here because I think when we were speaking about this, you had mentioned that when you were back in training, you came across some patients and one of the first signs of some of their hypothyroidism was actually the acute development of tendonopathies, which is fascinating. – Yes.

– Thyroid hormones, basically T3 and T4 play a role of stopping apoptosis or programmed cell death in tendons, in tenosites. So in your general contractors that are overseeing work on your tendon.

So if you have insufficient thyroid hormone circulating, that’s perhaps a major risk factor. Another thing that’s a potential major risk factor is T4 actually mediates collagen metabolism. So you need enough circulating.

The sex hormones are also interesting too.

So estrogen is the interplay of female sex hormones and what these deeply collagen structures like tendon and ligaments is the subject of fascination for a whole body of literature. So I don’t wanna do them into service by speaking about it very quickly. But there’s been a good degree of insight into phases of the ovulatory cycle and risk of injury in adolescent females who are in the developing stage there and engaging in sport that perhaps you could have a two to six times increased risk of ACL injury during specific phases. And then we know in the post-metopausal population that tendinopathies tend to develop. So the absence of estrogen appears to be a problem.

Same thing goes for testosterone. Now testosterone, there is a clear,

in that same post-metopausal population, the testosterone’s gonna decrease as well.

So testosterone appears to be beneficial for tendon. Where the conversation gets very interesting is are the testosterone analogs, are the synthetic analogs detrimental?

– That’s a really good question. So basically what he’s saying is the use of certain anabolic steroids going to injure tendons. I think it’s a really good question. And the answer is they appear to be, clearly due to the use of them, the skeletal muscle is enormously sensitive to them. But does it need to be testosterone specifically to help tendons? And that’s one of the great questions. So I’d say somebody starts on an anabolic steroid regimen and they’re drastically increasing their muscle size. Well, the athletic adaptation curve does not change. You might retain more muscle, have less catabolic effect. You might get more week over week training benefits. But you still need time for the soft tissues to accommodate. So it’s one of those unfortunate things that plagues people is bicep tendon ruptures, pec tendon ruptures. That’s what we see a lot of time in the gym. And so it’s something important to think about. Does it need to be testosterone specifically or can it be something else? The literature that I was reading, it seems like it needs to be testosterone specifically. So both estrogen and testosterone play some protective element. And therefore another question is, in individuals who are taking synthetics, who are on aromatase inhibitors, are they doing themselves some degree of disservice? Are they throttling down estrogen so much so that it’s not beneficial? – You bring up a really good point. And what he’s talking about is medications, aromatase inhibitors that would decrease estradiol or overall estrogens. And we know that estrogen is important for both men and women. I can say clinically, I like to see my men, it’s interesting for women, there’s a lot of ebb and flow. Obviously we don’t want their estrogen suppressed. But for men, I am happy with an estrogen level between 30 and 50.

Individuals you will see sometimes are on something like a rheumidex and they will suppress their estrogen and they’ll feel terrible. They’ll feel terrible, perhaps they’ll get injured. You know, in menopause, I’ve seen somebody of literature talking about frozen shoulder.

And I’m curious as to why frozen shoulder and menopause, wouldn’t that be, whether it’s shoulder, whether it’s a knee patella tendon issue or hip, why shoulder? – Yeah, it’s adhesive capsulitis, there are rare clinical accounts of it occurring in other joints, but that’s the clinical term for frozen shoulders, adhesive capsulitis, which appears to be an acute thickening and contracture of the joint capsule. So when we think about a joint, you have two bones articulating with cartilage. And so you have a cartilage interface that allows that. You have typically have a pressurized area of joint fluid. That joint fluid periodically gets turned over by the body. And you have a capsule, which is made of collagen and basically envelops the entire joint to provide stability. This is what, if you ever like carved a turkey and you take out the hip and you hear the suction break, you’re breaking the suction seal that’s within the joint. So adhesive capsulitis is sort of most common

in women between the ages of 40 and 60. It can occur in men as well. And it is, the hallmark is this very rapid onset of decreased range of motion of the shoulder to the point where some individuals can’t raise their arm above their head without necessarily a predating injury. Some predating injuries can predispose you to it. So let’s say you have an acute rotator cuff tear, you stop moving your shoulder altogether just to protect yourself. And you’re not undergoing the rehabilitative process. Perhaps that could actually predispose you to getting your shoulder frozen. It’s also interesting because frozen shoulder is one of the few times in medicine that we can say corticosteroids are meaningfully disease modifying. So we use corticosteroids in sports and spine practices for pain relief. That’s the main purpose, their pain relief. But in the process of frozen shoulder,

depending on which article you reference,

I like to look at the, there was one article that described it in a way that I think is very easy to understand, freezing, frozen and thawing. Okay, so it makes a lot of sense.

If you catch it in the freezing phase and you give it a corticosteroid injection in the joint, it actually decreases the duration of symptoms. Frozen shoulder untreated can lead to potentially years of symptoms in the shoulder. So the question is, is there, is the absence of estrogen and the increasing rise of the precursor LH and FSH that are present in the state of menopause? Are these things predisposing to that? Because we also see it in premenopausal women as well. So it’s tough to tell, but we know some risk factors for frozen shoulder. One of them is obesity, one of them is diabetes. And then the other one is perhaps a lot of these perimenopausal females are seeing. So tough condition to treat. – Yeah, and these are all really important conversations because if we just focus on muscle and we miss tendons, then when people get injured, I hate to say it, it’s not an if, but it is a when at some point, if you are pushing yourself or sedentary and then getting back in a blend, you’re going to get hurt.

And I would also say arguably it’s not always the muscle, it’s probably the tendon first. – Yeah, it is. And you know, it’s interesting too.

Tendons degenerate at a speed that’s quite rapid. So if you stop using it, it is a, so I was thinking when I learned about this, it’s very slow on, right? So it’s six to nine months for accommodation and tendon for the on phase, but it can be a relatively fast off.

So depending on the degree of immobilization post injury is a potential that your tendon could be the weakest element coming back. So injuries will find the weakest element,

biomechanics, whatever it is, you’re going to find the weakest element in the chain. That’s how a lot of times we diagnose pediatric injuries with tendon. So in pediatrics, the bone is weaker than the tendon. – The bone is weaker than the tendon. – Yeah, in a majority of circumstances. So you’ll see this interesting convergence of pediatrics and geriatrics, where because bones are weak, relatively weak, relative to tendons and muscles in both segments of that population. So if you have say an osteoporotic person and they go and they trip and they catch themselves and they evulse their hamstring right off of their ischotuberosity on the bottom of their pelvis, it happens. – I know, I did it, but not for that reason. – Sorry. So, – Terrible. – Tough to treat. Now, same thing goes for when we have kids. We will find bone fragments, things called something called attraction apophositis, which is like your Osgoods, you see somebody’s knee who has a little bit of a lump on it. Basically, the tendon was pulling on the bone, the extensor mechanism of the knee was overloaded. And because the tendon was stronger than bone, it convinced the bone to do what it wanted, which was pulled the bone more towards it. Now we’ll see that to some extent in the population in between. So if you have, say you have a long standing Achilles problem, but it’s Achilles tendinopathy, or you just overloaded your Achilles, you will see the actual attachment point, the bone changes form. It’s as if the tendon is pulling the bone up and actually, because bone is constantly remodeling. – Interesting. – Yeah, so x-rays, despite the fact that tendon is a soft tissue problem. – So you wouldn’t see a tendon on x-ray? – You would not see the discrete, yeah, you’re not gonna evaluate it to the same extent. – So as the listener is thinking, well, how do I know if I have a tendon apopathy, should I go get an x-ray, you would not go get an x-ray? – I would get an x-ray only to look at the other elements of it, but MRI and ultrasound are superior for tendon imaging. So, MRI has a very good degree of resolution, and a very high degree of penetrance. So the benefit of MRI is we can see to the level of the bone and beyond.

Ultrasound will stop at the bone. So, very high resolution, in some instances, higher than MRI. And so I will find commonly on someone’s, in a shoulder, I’ll find little, what are called interstitial tears in the middle of the tendon that were not visualized on the MRI. Because the MRI takes certain cuts, the other benefit of ultrasound is dynamic. So I can actually put the probe on somebody, have them move their shoulder around, and if I’m gonna make the clinical diagnosis of you have shoulder impingement, I can prove it. And I can see, is this something where you’re acutely catching your shoulder under a structure? That’s gonna help me formulate a therapeutic exercise routine for this person. On the topic of not if, it’s when, it’s a tough pill to swallow. – I know, and I hate to say it. – I hate to say it as well because I do believe, on one of those people, it’s like, in the ideal circumstance, could we avoid it? – Yes, if you didn’t do anything, you absolutely could avoid it. – But in that case, you’re gonna be on a freight train towards a bad state of health. So you have to make a trade-off at some point. Now, with restoration of normal mechanics and loading and periodically de-loading, I think we can do a lot for injury prevention. – And we know what normal mechanics are, despite the fact that everyone has different arm lengths and different leg lengths. There are standards of mechanics. – If you look at like an orthopedics textbook, you know, look at joint ranges of motion, it’ll look at specifically what’s a norm. And these are all Gaussian distributions, bell curves. So you’re gonna wind up with, here you go, you have majority of people should have 180 degrees of shoulder flexion, they should have 90 degrees of shoulder external rotation when the arm is abducted. You can find these things. Now, if you restore a range of motion, a very important principle in musculoskeletal health is mobility and stability, okay?

When I evaluate somebody, I’m looking at them on a two by two table. Are you weak? Are you strong? And we’re talking about a specific element of the mechanics, not generalized. – For example, raise your arm up, right? Is this strong? Can you push it against resistance? – Exactly. And what I like to look at is, say I’m examining somebody’s hip and I’m gonna isolate one of their gluteal muscles with a specific range, are you weak in that muscle? So I like to look at weak versus strong and mobile versus stiff.

– Weak versus strong, mobile versus stiff. – Yeah. So to give you an instance, for instance, of who kind of fits in each category. So for our elderly patients who have unfortunately accommodated a lot of time and where, they are most often stiff and weak.

So joint ranges of motion decrease with time, you get calcification of soft tissues, your joint capsules harden a little bit, you stop moving them as much, so it’s natural to see a normal decreased range of motion as we age. So now if you pair that with inactivity, if you pair that with somebody who’s not engaging in a lot of resistance training, it’ll be paired with weakness, so stiff and weak. – Because you hear a lot about that people are very hypermobile. – Yes. – And it’s interesting to hear, but as they age that they would stiffen. – Yeah, just about everybody stiffens to some degree as you age, and just about everybody’s more mobile when they’re younger. Now, there’s obviously variations within that, depending on what modifiable behaviors you engage in. Now let’s take for instance, the hypermobile patients. So hypermobility does come, it’s not always a dedicated Ehlers-Danlos diagnosis, we have something called the Biton score. – You should mention Ehlers-Danlos, because I do have a few patients with it, people are very curious about that, just as we’re talking about mobility, because there’s probably a spectrum of it that’s much more common than individuals recognize, and it could predispose people to injury, and other things. – So there is a good evidence-based score, it’s called the Biton score, that can actually be performed in the office to test for hypermobility. What we look at is, can you bend down to the floor, touch your palms on the floor, can you bend your pinky back, getting greater than 90 degrees? – Everyone’s gonna be trying it. – Yeah. – Go ahead Mia. – Yeah, so there’s other tests within it, but there is a spectrum of hypermobility, and it’s likely due to genetic determinants of collagen. And so when we think about– – It’s not treatable, correct? – Yeah, so it can be treatable, modifiable with exercises, and I’ll explain that in a moment. – Wonderful. – But these are things, these are relative, not absolutes. So your mobile and weak patients are most commonly hypermobile.

– The mobile and weak? – Yeah, so on the two by two stiff and weak is elderly, your mobile and weak are hypermobile.

Now stiff and strong, or stiffer and strong, is like an offensive lineman. If you examine an offensive lineman’s hips, they’re not gonna rotate a whole bunch, but they’re as strong as heck, and they could put the power down. So that’s stiff and strong. Stiff and strong is not a bad place to be.

Then your mobile and strong, those are your Michael Jordans. Those are the people– – Mobile and strong. – That’s the grill. So if you can, for every bit of mobility that you gain, you have to be stable. So range of motion, if I just stretch myself into a range of motion, but I don’t know how to activate muscles to protect my body in that range of motion, it’s just range of motion for range of motion’s sake. Not all mobility is uniformly beneficial, in my opinion. I believe that if you’re gonna have mobility, you need to have accompanying stability. And if you’re a more mobile person, you have a larger responsibility to be stable through a larger range of motion. Now, what are the determinants of mobility? It’s a really complicated topic, but you have your bony determinants, so not everyone’s hips are shaped the same, not everyone’s shoulders are shaped the same, and those are your more mobile joints. Then you have your soft tissue determinants, things like collagen play a much more of a role there, so whether you’re hypermobile in a joint capsule, women are more mobile in their joint capsules than men. Women have more type three collagen in their tendons than men, so that’s gonna influence– – I didn’t know that. – Yeah. – Just– – Broadly speaking. – Okay. – Broadly speaking.

So these are some determinants that are gonna predict some of the soft tissue extensibility, and then the mobility aspect and really how stable you are, a huge element of that is that same neurokinetic element we spoke about before, and the athletic accommodation timeline. So if you can be stable, and you know what muscle to contract in what position, mobility’s fine, but I, for instance, I would prefer for a lot of patients to be in a narrower range of motion, but much more stable through it than as opposed to having just a very large range of motion. If you think about the ranges of motion that we need to accomplish your day-to-day life, you need to be able to do a good hip hinge, you need to be able to do a good squat, you need to be able to rotate, and you need to make sure that you’re producing enough body tension that’s centralized in your core

to mitigate injury in those circumstances. You don’t have to be an elite contortionist to achieve everyday life, and that’s why the concept of stretching is a very interesting conversation to have, what we’re achieving with stretching is a very interesting conversation to have. – Should we do it? This is gonna bring me to the yes or no section. – Oh dear. – Okay. So you’re not gonna like this, because you’re very academic, but I’m going, you can only answer yes or no. – Okay. – Pilates. – Yes. – Steroid injections. – Yes. – Zone two. – Sure.

(both laughing) – We’ve never had a guest answer, sure, ever. – I think it’s beneficial, I think it’s the question. – Not, not, not. – The question is the dose, the type. – Not, not, but see, this is very difficult for people. I always have to do it. – This is why, this is why I’m not on the hill. Okay, if I wanted yes or no, it would be a politician. – Okay, fair. Yoga.

Whoa, I love this section of the podcast. – Yeah. – Is that a yes or no? – I’m not, no, and I’m not yes. I’m gonna bow out of that one. I’m gonna use my fifth amendment on that one. – This then leads me to stretching.

– Stretching can be beneficial. – Okay. – So it’s not uniformly beneficial. The question is what you’re trying to achieve with it. – Now then let’s talk about, so that we do a, so Matt loves having the yes or no, because it, obviously, no answer is typically yes or no. – Yeah. – But stretching. Tell us about, should we be stretching before activity? Should we be stretching after? Because I ran out of the gym yesterday because my sister said we trained with Carlos Moda, he’s my coach, and my sister said, we are done working out, we should stretch. I’m like, what are we stretching? Why are we doing this? And then I said, I’m gonna talk to Dr. Gerard because I think you’re wrong. We probably don’t need to stretch after we work out. – Okay. – And now I’m about to be schooled. – Oh, well, let’s see. So there is, this is one of those topics that I have some relevance in, but I don’t feel 100% at expert level with. I have a lot more to learn on it, but I’m gonna give it a shot for you. So stretching preactivity,

decreased neuromuscular firing, decreased stability, not beneficial for power athletes.

– And can we define power athletes? – So pitcher, shot putter, elite power lifter. You could even throw fighters in there. That’s a powerful sport. So you’re producing power as force over time, so you’re gonna produce a force over a very short period of time.

So static stretching, probably not beneficial. – For anything or just we’re talking about power. – Pre-exercise for power generation. Now, stretching, there are different categories. There’s static stretching, so I’m gonna hold a pose for a while, typically 20 seconds or more, and hopes to elongate the tissue. Now, you’re not just stretching the tendons. You’re not just stretching the muscles. You’re also providing neural feedback that can actually turn off some sensors that help to protect you under load. – Are these the Golgi spindle virus? – Yeah, so Golgi– – Okay, just curious. – You must– – Just wanted to see if I remembered anything. – Hey, so the Golgi’s interesting.

You know, the other apparatus are also interesting, but the static stretching component perhaps has some benefit post-exercise with relation to tendon health specifically. And it may actually help just elongate the tendon and actually, if you’re holding a pose, maybe with an isometric or let’s say you’re gonna do a heel drop and just hold it there. That could have some benefit. Now– – For power or for– – For recovery. – For recovery. – Yeah, now I say a lot of, I’m gonna heavily weight the may here. – Okay, I’ll take it. – Because I think it may help. But I’m also gonna tell you from a personal aspect, I don’t do it. So I think it’s important to note that I don’t– – Neither does my husband. I’ve never seen that guy stretch, ever. – He’s a smart man.

Now, if you’re going to stretch with the hope to teach your muscles how to engage at a larger range of motion, then you do PNF, so proprioceptive neuromuscular facilitation. And the answer for that is– – PNF. – PNF. – Proprioception. – Nuromuscular facilitation. – So PNF is a process by which, okay, so I’m gonna stretch, say, my hamstring, and somebody’s gonna push against my leg, and I’m gonna actually try to contract my hamstring at a larger length than I did pre-stretch, and then I’m gonna stretch from there. And so there’s typically these on-off cycles, like a 10-second isometric at one length, 10-second stretch at another, and you can do that. Now– – And the benefit of that is– – The benefit of that is you are teaching somewhat that the muscle can relax at a larger length. Okay, so whether pre-exercise or post-exercise, I’m not clear on. – And this seems to work with, a lot of people do it with pain. – Yes. – Is that, so is PNF used for mitigation of pain about muscle or– – Yeah, it’s used in rehab. So it’s used by physical therapists and ATCs and other people who will rehabilitate patients. So it’s definitely part of it. When I design physical therapy protocols for patients, I like eccentrics for lengthening. So once again, eccentrics, your muscle is contracting periodically or mitigating the elongation process. I think that could be very beneficial. The stretching component is interesting because once again, we’re not just stretching the muscle, we’re not just stretching the tendon, and we are also gliding the fascial layers. So here’s another– – I love that you brought this up. – So here’s fascia– – Another, that’s it. Would you consider that an organ system? – It’s interesting. It’s part of the musculoskeletal system, but it’s so richly innervated and so large, it could be its own category. – What is fascia? – Fascia is interconnected connective tissue that can run the entire length of the body. – Incredible. – Here’s why we don’t get taught about fascia as much as we should be.

A lot of it is almost as if we, during the process of medical school, well, me dissect the dissect cadavers. – It’s gross. – It’s necessary. – It’s absolutely disgusting. – It’s also– – Important and meaningful. – It’s important, and thank you to everybody who donates their bodies of science. – It’s absolutely incredible that people are willing to do that. – When we dissect cadavers,

most fascia dries out so much so that it adheres to adjacent structures and becomes incapable of dissecting it off of.

Now, I’ve spoken to some scientists in Italy about this, specifically. – You did? You were just– – I wasn’t in Italy, it just happens to me. – But you were just thinking why– – I spoke to somebody, basically because ultrasound is one of the main ways to evaluate fascia in the living specimen.

So there are specific cadaver preservation techniques for preserving fascia. One of the reasons we don’t really understand it or appreciate it’s the level that we do is we just don’t see enough of it.

So fascia can adapt. Fascia is, if not the most richly innervated structure in the body, one of the most richly innervated structure by that means the most nerves. – Does it have pain? So does it feel pain? – People feel myofascial pain. I believe it is a, it’s part of the diagnostic spectrum of pain, so you can have a muscle that hurts, you can have a tendon that hurts, you can have a joint that hurts, you can have a ligament that hurts.

And fascia also can hurt, in my opinion. – Did you feel it if someone were to say, would that have anything to do with fibromyalgia? – It’s interesting, yeah. So the concept around fibro is, I think it’s part of it, that fascia is part of the issue, but we also see myofascial pain in people who don’t have fibro. And so we see myofascial pain in overuse syndromes, a very common myofascial pain that perhaps some people will experience is if they have a pretty large asymmetry in their hips, how their hips move and function, they feel a lot of myofascial pain in the top of their glute low back area. Now, it’s tough to discern, and I spend my job doing this every day, discerning what the main pain generator is and then describing how we can appropriately rehabilitate it and treat that pain. Now, fascia specifically do adapt to exercise.

And one of the best books I’ve read about this by a guy by the name of Bill Parisi. And the forward was written by Stu McGill.

So it talks about fascial adaptation to training. And that basically this fascia system that extends in some circumstances, the length of the body connects your glute on one side to your lat on the other, is a lot of the reason that we don’t move like rigid robots. So allows us to move much more coherently. Now, the question in this circumstance is how much of a role is that in pain? How much can we do about it? Now, we know that it adapts in some circumstances because there are some athletes that when you take them and train them a certain way, they get athletically worse at what they’re doing. Now, there’s changes at the neurokinetic level there, there’s changes at the muscle level there. Presumably there are some changes at the fascial level as well. One of the accounts that Bill talks about in his book is about an elite quarterback who was training like an offensive lineman. So basically they were putting the quarterback through the lifting protocols on offensive linemen and the quarterback, all the numbers around throwing got worse. Spiral got worse, velocity got worse, arms started to hurt. So maybe everybody needs to train towards a specific goal because on some level or another, your entire body’s adapting to that stressor. So you always have to keep that in mind of when you’re training an athlete, they can’t all be treated the same. Not any exercise is uniformly the perfect one for everybody. For their specific needs, you have to do an individual needs assessment for that patient. So fascia is very interesting.

We do visualize it on, and specifically, where fascia are where the small nerves, like say, for instance, the nerves that talk to the muscles of the back,

the fascial layers are where they travel. So the thought is behind myofascial pain is could you have these layers that are not appropriately gliding on each other and patients who have chronic pain, there’s some evidence to suggest that they don’t glide that well. Rounding this back up to the initial question around stretching, stretching also glides fascia. And so does that have its own therapeutic benefit? Could that actually be helping produce these proteoglycans, these lubricants that are present in the body, the same way that they’re intended? So is it a lubrication problem and can we facilitate that with stretching?

So then there’s also the question of myofascial release and what we do for individual people.

I’m less concerned about the modality we use to get people mobility, so much as I am more concerned with us restoring stability through that mobility.

– Really well said. I’m learning just so much.

How are you doing? – I’m good. – You’re doing great.

Can we talk a little bit about training? – Yes. – I’ve learned quite a bit and you really have helped me reframe. In fact, we’re working on a second, I’m working on a second book proposal and I’m hoping you will be so gracious as to impart some of your wisdom in part of that process. And I’ve learned a lot about thinking about how we train the current paradigm, the current narrative is all about zone two. It is that zone two is where we need to focus and then we have other groups that we talk about resistance training, do it three to four days a week. And understandably so. There’s only so many ways that we can make global recommendations. – Yes.

– That being said, I would love your take about you and I have spoken about minimal amount of movements, exercise, kettlebells, more effective ways to utilize our body. I’m just gonna leave that for you to take it wherever that you’d like to. – Sure. So the concept of zone two is an interesting one. I think that a lot of the excitement around it is that it’s helping to promote mitochondrial function and that mitochondrial function appears to be absolutely essential as we age. And can we improve mitochondrial function to decrease things like insulin resistance, improve metabolic health, improve our athletic performance. And the concept there, it’s interesting to see how, depending on what you look at, these different terms that describe similar phenomena. So sub max VO2 training, zone two, moderate intensity continuous training. I did a presentation a while back, specifically as it regarded patients who were recently diagnosed with cancer, undergoing cancer treatment or finished cancer treatment and what exercise recommendations we could make for them because their VO2 max and muscle mass help predict how they do. And we know that quality of life, mortality, morbidity, the more fit you are from a cardio respiratory and muscular aspect, the better you will do with treatments. So how can we help people? And so the question was in the presentation, should we be engaging in high intensity interval training or moderate intensity continuous training? And the answer is of course, both can be helpful. Per unit time, high intensity training might be more beneficial to jack your VO2 max upwards. But what are we really thinking about with VO2 max? One is if we’re gonna test VO2 max in somebody, they should be familiar with the movement of which we are testing them. It’s not fair to say somebody has a sub optimal VO2 max but it’s their first time doing a certain athletic activity. You’re gonna be gassed. Even if I’m an American runner, if you throw me to a box hearing, I’m gonna be gassed in two rounds. No, you might be amazing but a normal person. But the truth is I would be gassed and it’s because I’m not familiar with the movements is the way that I should be. So it’s important, that’s important caveat. Don’t get down on yourself if your VO2 max is not where you think it should be because you did some modified Bruce protocol in a gym. It might not be where it should be because you don’t have familiar with the movement. If you’re on a bike, there are so many determinants of your performance on a bike. – Absolutely. – You’re positioning, you’re familiarity with it. What muscles you’re activating, your shoe angle with the actual pedal. And I’m out of my league there. I know that that’s the very, very surface layer of it.

So we’re looking at substrate utilization, fats versus carbohydrates versus creatine phosphate.

And we’re looking at what can be done to maximize fat oxidation. So this concept around zone two, as I understand it is fat max. Like we’re trying to maximally use fat for fuel while we exercise to teach our mitochondria to metabolize fat more readily to decrease insulin resistance. That’s what makes sense to me at least. Now with high intensity interval training, there’s no, I think the downside of zone two is time.

I think that’s it. – And you have two children and a beautiful wife and a full practice. – Yes, and time is tough. So I don’t engage in a ton of zone two myself. If I had more time in the week, perhaps I would. But then high intensity interval training appears to be as beneficial for VO2 max as the zone two. But you’re training it two different ways. From high intensity interval training, you’re like raising the ceiling of your house higher. You’re getting better at pushing it higher. But the zone two training appears to be like you’re solidifying the foundation. You’re getting better in the lower levels that predict success at the higher levels. So we might be describing it this way, but athletes have intuitively known this for decades. When they run, they’re not gassing themselves every workout. They leave a little bit on the table and the body goes through a period of compensation to basically mount a response to that stressor. And then when they do peak one or two times a year, they’re in really good shape. So same principle applies to weight training. So should we or could we be going to neuromuscular failure? If our goal is muscle hypertrophy, should we be focusing on just muscle hypertrophy in specific muscle segments or generalized strength and stability? I think these are good questions. But I find the way I train with kettlebells is I want to be number one thing for me is don’t lose stability in all three planes of motion, sagittal, transverse, and frontal like we spoke about before. When you work a kettlebell,

most of the time it’s in one hand and that by nature destabilizes you. And you’re not gonna get destabilization if you’re working only with barbells. So if you’re– – You’re not gonna get destabilization working with barbells. – Only, you know, as it relates– – Right, as it relates to the frontal and the transverse plane. So, Yobi Stable is all heck in the sagittal plane if you work with a barbell. I was the sagittal plane hero. I went to the gym and I did– – Well done. – Bench, lats, I did squats, I did deadlifts, and I became very proficient in those areas. But then I would go play golf and things would hurt. And I’d be like, “Well, that’s interesting. “I’m not the world’s best golfer, “but it shouldn’t hurt as much as it did.” And I thought it was basically because I wasn’t as proficient in translating force in rotation. So I like to use a kettlebell. I think you can get a lot out of it. I think the work from the Strong First organization and Dan John online in his own endeavors have done a great job elucidating the cardio-respiratory benefits of kettlebells that you can get strength and conditioning.

And so I try to follow that. I also do something, and we spoke about this term, exercise snacks, which I don’t particularly love. – I don’t either, but I can’t think of anything else. – We’ll find a way to re-brand it. – Definitely.

– I call it farmhand strength. So if you’re working on an outdoor, let’s say you’re not a farmhand, let’s say you’re just somebody mulching your yard, you’re not going to basically go to the point where you’re falling down every single time. You’re gonna leave a little bit on the table, you’re gonna come back to it, you’re gonna go do a different activity for a short period of time, and then you’re gonna come back to it. And so what I’ll do is I’ll intermix some sets of kettlebell swings throughout the day. I might do a set at 9 a.m. and do a set at 10.30. I’m not looking to build a sweat, I’m just looking to get better at the movement. So I’m really stressing that neurokinetic element. Am I getting better at the movement? Am I doing a little bit of stimulation of muscle? But by no means am I getting a skin ripping pump out of it. – But potentially you could build a workout like that. – Yeah.

When we look at some of the really good people who are training and what they do, and a lot of rehabilitation from injury, sometimes it’s three, five, 10 minute rest. And so the question I think in there is, do you want to be super proficient with a movement? Or do you want to get as much training in in a short period of time as possible? So there’s different strategies there. But we move throughout the course of the day, it’s not like we only move for 30 minutes, and then we’re immobilized for 23 and a half hours. So the concept of going to the gym, I think is something that needs some work. Where we think about going to the gym, we dedicate time, but should we be interspersing movement throughout the day, I think some people, fortunately in their jobs, can do that, and some people unfortunately can’t do that. But I like, I saw you both do a set of pushups before, as its own little stimulant part to the podcast. – That’s our pre-game pushup. – There you go. – We do a pre-podcast ritual. – Now is that not helpful because you only did one set? – No, one set. – Of course it’s helpful. – You didn’t know that we’re doing some after this? – I’m happy to do it. But you did one set in isolation, and you benefited from not overloading your tissues, you benefited from a short-term increase in your heart rate, you learned how to become a better push-upper. And that has something to do with it too. So I think coming back to the concept around zone two, it’s, if you were to train, I think that probably what makes sense from a metabolic corollary with weight training is like, if you’re going to neuromuscular failure, muscles are on fire, you’re not in zone two. I think we can comfortably say that, right? – Yes. – So you’re probably in zone five, or four or five. So you’re really getting there. Now, if you train and you say you do 10 repetitions of something explosively, and then you wait a couple minutes and do it again, could you still be in zone two? And that’s this concept that has come up called anti-glycolytic training, which is a way to build endurance and strength, which has been subject to my own personal fascination. I’m not in a position where I could speak from an educated perspective on it. A lot of the literature behind it is in Russian. So I can’t really– – Better get learning. – But I’ve read Pavel’s work and Pavel does a great job with that. And I’ve recently read a couple of his books. And I think it’s something I’ve experimented with. The same way that we might all experiment with zone two, or a HIIT training, or powerlifting, or whatever it might be.

A lot, I think one of the benefits to my patients is that I’ve gone through the process of experimenting a lot with this. I played baseball and football. I was a personal trainer.

I did a good bit of just casual powerlifting. I tried to be a crappy bodybuilder for a period of time, and I wasn’t great at it. But, and then on top of that, I might not be running a marathon like Shane in a couple weeks, but I did run a half. And you learn so much going through those individual experiences. So I try to maintain a radical open-mindedness about what could be helpful. And try it myself, if I can. – And that’s really valuable. A physician that sees patients and also walks the walk and experiences it. And I do think that you bring a very unique perspective.

In your practice, how do you incorporate some of these things? So you practice in, where are you in practice right now? – I’m in Florham Park, New Jersey. I work for Summit Health. – Okay. And people could make an appointment with you if they would like to. So let me just tell you guys something. Every guest is incredibly vetted before they come on the podcast. I have so much respect for Dr. Gerard. I send patients to him. If you are in the area, if you are not, he is definitely worth the trip. I would love to hear a little bit about what makes your practice different, unique. We’ve heard a lot about your philosophy and how you think about things from both a biomechanical aspect. I know where you sit from a nutritional aspect, but also your fellowship train. – Yes. – I’d love for you to expand upon your training and just your individual practice. – So my practice is a sports and spine practice. I did a sports and spine fellowship at the Hospital for Special Surgery. – Which, by the way, is one of the best in the country, if not one of the best places in the world. – Yeah, it’s a great place to train, a great place to be. I think the very important take home for anybody who’s listening outside of me kind of speaking about myself for a moment is, if you can find mentors that are really good for you, really pursue their mentorship. – Yes, great point. – That’s how you and I have developed this relationship. I have a mentor almost at every different phase of the career, so I kind of have mentors that are closer to me in age. I have mid-career people. I have later stage career people. And I also have mentors who are non-clinical, or not even doctors, who are people in different fields. Getting their perspective has been so important, and anything that I do is the great fortune of having a great family and a great upbringing, great wife and kids at home, and parents and brother and friends. So I’m fortunate that every day I go to work, I feel like I bring the best version of myself because I have a great backing. – Amazing, amazing. – Now, for my practice, my practice focuses heavily on the biomechanical determinants of pain. And when a patient comes in, let’s say I see a back pain patient, it’s less difficult to make the diagnosis of a pinched nerve in the back from a herniated disc, and more difficult to discern why the disc herniated, and to unravel in a relatively short timeframe what determinants in that person’s life, or in their training, predispose them to that injury. And how are those things going to be encumbrances to them getting better in the future? So that takes some refining, and I’ve gotten better at it with time, but every day we try to build a little bit. I try to find what is motivating this person, what are your goals? And I ask every patient, what are your goals for this visit? Some people just want clarity of diagnosis. Well, the first thing we need to do beyond anything else is clarity of diagnosis. From a biomechanical element and from a tissue layer element, do you have a herniated disc? Yes, why? Repetitive flexion movements without appropriate lumbar stabilization, insufficient hip mobility, and then they didn’t have the appropriate brace from the obliques. That’s a good starting point.

Now let’s use this inflection point of injury, and let’s build you back to a point of anti-fragility. So the concept of anti-fragility is one that I borrowed from Nassim Talab’s book, which is one of four books in the “Encherto,” which are very difficult and fun to read. I love– A very thick book. Yes, very thick. They’re books about everything. If you ask me what they’re about, they’re about everything. But this concept of anti-fragility is actually a concept that is exhibited in muscle and tendon and bone, which is you provide a stressor to a structure. It doesn’t break, but in time, if the stressor is adequate, the structure can actually get stronger. So I branded myself anti-fragile MD because I love that concept. I love, that’s the essence of my practice. Can we use stressors rather than hurting you and disabling you to make you stronger? Yes, sir, well said. And I know that’s you, too. I know that’s you, too. So I look at,

is can we get people from a point of injury to back to a state of athleticism, and what are the goals? Do you want to be on the ground playing with your grandkids? Are you somebody who’s gonna run a marathon in a couple weeks? And we kind of look at all these things and the variety of treatments that I can offer. And when there is an evidence base to draw from, we will draw from that evidence base. If there’s no evidence base to draw from, an area will extrapolate based upon the knowledge of my biological foundations. So, but my practice is a sports and spine practice, so I see a lot of hip pain, back pain, shoulder pain, neck pain, to a living extent, elbow, and then of course, knee, and some ankle foot as well.

And the three or four main conditions I treat are

specifically low back pain, tendinoptys around the body, and then a lot of neck pain. And you’ll find that patients who have low back pain have tendinopathic problems as well, and you’ll find– In the shoulder, it’s a whole sling, essentially? So the whole sling can have problems, but I think it’s, you’ll find specifically that there are insufficiencies in the pelvis and the peri-pelvic muscles like the glutes, and so it’s not uncommon to find a tendon problem there. So I like to uncover what the root cause is, and that’s really what gets me out of bed every morning, is root cause diagnoses, and then if your diagnosis is accurate, and you can correlate it with the diagnostic testing we have, X-rays, MRIs, ultrasounds, et cetera,

and it matches up with a good physical exam. Now we have a clarity of diagnosis, then the treatment, everything we provide from a treatment aspect there out is much more beneficial.

– And what I love about what you’re saying is it’s not about the end pain or the end symptom. It’s a root cause approach, which traditionally, medicine is not about a root cause approach, and that’s what I think what makes you and your practice so exceptional is that

what is at the foundation so that you can get people better. Where do you see the field going? – So I think that there’s a good interest around regenerative medicine, and there are a variety of regenerative therapies that we have now. PRP, we spoke about the athletic accommodation curve. There’s also the innovation curve of companies and products, and instead of being on the absolute first phase of stuff, I’m probably one phase delayed. – I feel the same way. We have to make sure that things are safe, effective, worthwhile for patients to spend their money, yes. – Agreed.

And first rule of medicine is do no harm. – That’s right.

Do no harm. – Anything we do, we wanna understand what we’re doing, why we wanna put it in the right place.

So I think there’s some very interesting work that’s going on from a stem cell aspect,

fat concentrate procedures, further sub-categorization of PRP, when to use it, when not to use it. And I think the field will continue to develop that. I think as we evolve, as a field going forward, we’ll begin to understand a little bit more about things like fascia. We’ll begin to understand a little bit more about mechanics other than just isolated joint range of motion and whole body movement. I think that it takes a lot of interest in that and study to do it, but I think we’re getting there. And I think that the last frontier is in a lot of ways, the first and most important, which is prevention. An ounce of prevention is worth a pound of cure.

And how can we prevent these injuries? Or you see this word circulated online, bulletproofing. Like, are we gonna bulletproof your shoulders, bulletproof your knees?

And so that’s where a lot of my own self experimentation comes in and trying to learn that as well as watch people do it and experiment with that. But as a field, I hope we study more of that. And then of course, predictive. Predictive analytics around who’s gonna wear a joint in a specific pattern based upon their bony development. We have some evidence to understand that now, particularly in the hips. But we’re starting, I think, to integrate a degree to look at that in the shoulders. And surgeons specifically are doing a great job of looking at that. And then from a tendon aspect, like we said, are the exercises we can engage in? I’m certainly gonna do my best to find out. And I think, and to figure out what is the most effective ones. I think that the question becomes minimally effective dose. – Of everything, yes. Training, medication. – Yes, how much is too much? And are we over training tissues? And that’s why we’re seeing so many musculoskeletal problems. Or are we just inefficiently training? And is it because we just don’t know how to do it? If you can restore, you know, quote unquote normal mechanics, it varies from person to person. But if you can restore normal mechanics, a lot of things get better. And I think what we’re seeing now is people like yourself are doing a great job of highlighting.

Well, we need power, we need muscle mass, we need cardio respiratory potential.

What movements can get all of those in a minimal dose of time because we’re all busy. And then what nutrition can empower those goals and what sleep, you know, determinants can help us. So I love how holistically you look at everything because you can’t look at one thing in isolation. The body is not isolation. Everything works. Everything works together. And it’s funny, we have this concept of organ systems and things like this. And it’s when you look at the musculoskeletal system, it’s like, well, B cells are present in chronic tendinopathy. Does that mean it’s now part of the immune system? You know, it’s, they all work together. They’re all constantly connected and communicating with one another to generate our homeostasis. So hopefully we understand more about the aging process, what we can do in the prime years to arm ourselves to that. And then what activities we can really get people back to as they age and age gracefully.

– Dr. Gerard D’Onofrio, thank you so much for spending time with us. You are a wealth of knowledge. I’ve just been very impressed with you over the years and you continue to impress me. – Thank you for having me on. – Where can people find you? – So I’m on Instagram as antifragilemd. And then my website is with my employer, Summit Health. So if you search my name, Gerard D’Onofrio, you’ll find that I have a webpage there and you can book appointments from that point. And over time, I think I’m also on YouTube at antifragilemd. And we’ll be publishing more content in the coming months and years. – Yes, sir. Thank you again. – Thank you.