00:01:00.150 — 00:01:30.910 · Speaker 1
There are a number of topics that I’d love to discuss on this podcast, which included 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. But let’s start with one of the things that I think that we both see in clinical practice are issues with tendons.

Yeah. And why are tendons important? What are they. How do we think about them in a global sense?

00:01:30.950 — 00:02:20.190 · Speaker 2
Muscle is contractile tissue. Muscle is made of actin a mouse 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 tenderness 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 you 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 a tendons have this incredible quality called visco elasticity, which is a cool word.

00:02:20.190 — 00:02:22.150 · Speaker 1
But everyone is going to be quizzed on this later.

00:02:22.190 — 00:02:51.950 · Speaker 2
There you go. So visco elasticity. It means that the the mechanical, 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

00:02:53.510 — 00:05:21.370 · Speaker 2
sort of an organizational level. You know, muscles have the contractile elements. You have muscle fascicles and fascicles for those who are listening are bundles of proteins. So you have this structure. You have a larger structure, and then you also have within that these composition of these micro structures 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 don’t we’re not unipolar 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. Stress. Not the entire 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 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 and at the co-curricular joint you have your AC joint, and then you have your true glenohumeral joint and you have the the scapula, the shoulder blade that rests on the back of the ribcage.

So there’s a lot of mobility in it, which is why on average, unless you’re a Rockette, you can raise your arm higher in the air than you can your leg. Okay, so similar ball and socket joint with the hip but more stability there. Job of the rotator cuff is to stabilize the the head of the ball and socket joint.

It’s almost like think about like 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 muscle, we have it intended, and we also have it in nerves to allow us to be more athletic and multi-player motion. So it’s it’s very cool. And collagen itself is it’ll most, 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 tendons.

00:05:22.170 — 00:05:33.810 · Speaker 1
Um, 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?

00:05:33.850 — 00:05:54.520 · Speaker 2
Yes. So it is fair to say, and it’s fair to say, because we have general principles, you know, we use this word homeostasis to describe how everything is regulated. Healthy muscle to exhibit its mechanical effect of moving bone effectively. It needs a healthy tendon. You can develop your muscle. It’s actually muscle will develop more quickly than tendon adaptation occurs.

00:05:54.520 — 00:06:24.720 · Speaker 1
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? Yeah, nothing will take you out of the game faster than a ACL tear, than an Achilles rupture, right?

Tendon apathy, which then becomes chronic. Um, could you have a, um.

00:06:26.080 — 00:06:28.760 · Speaker 1
I suppose a better question is, which goes first.

00:06:28.800 — 00:06:39.560 · Speaker 2
Yeah. So this is a 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.

00:06:39.840 — 00:06:41.320 · Speaker 1
So I don’t either.

00:06:41.360 — 00:07:56.230 · Speaker 2
Yeah, yeah. Um, 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 neuro kinetic 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 going to be as good. I’m going to be much more gassed. I’m going to go deep into those energy zones. I’m going to really kind of stress to do the activity, but I get better at it with time.

Then in muscle tissue, after the first couple of weeks, you start to get sarcoplasmic 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 are engaging in. You’re almost looking at 6 to 9 months.

00:07:56.590 — 00:08:05.070 · Speaker 1
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.

00:08:05.110 — 00:09:52.580 · Speaker 2
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 as about 90% of a tendon is more or less static. And then you have maybe 5 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, etc..

So this is when my 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 loading? Where’s? Are we working towards a goal in 2 to 3 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 and it’s too true. And some people are very nuanced. They know their bodies really well. They’ve been training for 20 or 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 want to train. I have a I have a long term goal. Well, you’re a 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 training 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 guess I ask, what does your training program look like? Well, I do. You know, they’ll tell me a split. I do back end bys on Mondays. I do shoulders and tries on Tuesdays.

00:09:52.620 — 00:09:54.420 · Speaker 1
I do it on Monday. Universal chess day.

00:09:54.460 — 00:09:57.820 · Speaker 2
There you go. I do. Yeah. Sorry. Yeah. Probably chest on Monday.

00:09:57.860 — 00:09:59.940 · Speaker 1
Matt. Matt. All only does chest on Monday.

00:09:59.980 — 00:10:01.220 · Speaker 2
Matt. Matt has a good chest.

00:10:02.060 — 00:10:03.100 · Speaker 1
So lots of push ups.

00:10:03.140 — 00:10:23.140 · Speaker 2
Lots of push ups. Um, and, you know, 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 2 to 3 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 going to have to scale back?

00:10:47.610 — 00:11:03.849 · Speaker 1
So osteoporosis affected 10 million Americans in 2014, and it’s projected to increase by 50% by 2025. But what is so fascinating is we have an increased use in GOP ones. Yeah. Like

00:11:04.970 — 00:11:10.050 · Speaker 1
I’m curious as to what your thoughts on what we’re getting right versus what we’re getting wrong. Yeah.

00:11:10.050 — 00:11:11.610 · Speaker 3
So the GLP.

00:11:11.650 — 00:11:54.440 · Speaker 4
One, um, agonist group of medicines is fascinating. Um, they are, you know, currently used a lot for weight loss and people lose a lot of weight. People also lose a lot of lean body mass. And you’ll see ranges in different studies as low as 15. I’ve seen 40 to 60%. Sometimes this is, you know, proportional to the amount of body weight lost.

Um, and, you know, so it is that bad. Are we like losing a lot of muscle mass? And is that going to affect our bone density? Um, you would think it would. But so far, studies looking at fracture risk in people using these medications are not showing any, um,

00:11:55.560 — 00:12:58.680 · Speaker 4
increased risk of fractures. And some studies are showing slightly less, uh, fracture risk. So, so that is not showing up to be a concern. The other thing we’re seeing is these are basically anti-inflammatory medications. They may even end up helping people with rheumatoid arthritis and psoriatic arthritis and things like that.

So you’re reducing fat. You’re reducing probably some of the inflammation associated with metabolic syndrome. And so people with body, you know, with a loss of weight have less stress on their joints. So people are having less joint pain. We’re not seeing an increased risk of fractures, I do think because they, you know, basically delay gastric emptying and, create a sense of fullness and maybe decreased appetite.

People have to be, I think, more thoughtful about what they’re eating. Um, you know, because you could easily fill yourself with things that don’t give you the nutrients you need. So I think, um, yeah, you’ve got to be really thoughtful about your your dietary choices if you’re eating less.

00:12:58.840 — 00:13:14.200 · Speaker 1
Yeah, I think that that’s fascinating. I’ve never I’ve seen the data that it looks like these medications actually can improve certain pathways in skeletal muscle. It seems like there are positive yeah. Benefits to it as opposed to this narrative that.

00:13:14.240 — 00:13:16.080 · Speaker 4
I know you would expect. It would be negative. Yeah.

00:13:16.120 — 00:13:43.310 · Speaker 1
But I’m not seeing that either. And I’m really interested in what you’re saying about how the use of these medications, which, by the way, we’ve never had anything work better when it comes to weight loss. Yeah, a bariatric surgery. But those complications are challenging and I love hearing that from the bone aspect.

You’re not seeing increase in fracture risk Surest because you’re hearing on TikTok. Not that I’m watching on TikTok, but all these other places that it’s affecting bone density.

00:13:43.390 — 00:13:47.430 · Speaker 4
Yeah, it doesn’t seem to be. And maybe having the opposite effect.

00:13:47.430 — 00:13:49.150 · Speaker 1
So, um, do you think that there’s.

00:13:49.150 — 00:13:54.430 · Speaker 4
So far they can’t lose unless you get them taken away from you and then people rebound? Yeah. Right.

00:13:54.510 — 00:14:00.390 · Speaker 1
Um, and again, if they’re doing the right things like strength training and, um, eating dietary proteins.

00:14:00.390 — 00:14:05.470 · Speaker 4
Oh, yeah. I definitely think people need to strength train while they’re, um, going through the weight loss process.

00:14:05.510 — 00:14:27.710 · Speaker 1
Yeah. When someone is thinking about osteoporosis prevention and I think I text you, messaged you, what do we have to do? Do we have to do plyometrics? Do are there certain movements that we should think as women that we should all be doing to prevent you? I think about my mom. So my mom is in her 70s. She would cringe.

She’s like, you can tell everybody because I’ve looked so young. This is my mom.

00:14:28.430 — 00:14:32.670 · Speaker 4
Um, I always round up by year. I always say, I’m 46 now. I just say I’m 47. Yeah.

00:14:32.950 — 00:14:43.740 · Speaker 1
But, um, you know, I watch my parents in the gym and I am concerned about them jumping or doing any kind of breaking. I totally.

00:14:44.300 — 00:14:44.620 · Speaker 4
Yeah.

00:14:44.660 — 00:14:47.100 · Speaker 1
So I put themselves in the gym.

00:14:47.260 — 00:14:48.220 · Speaker 4
Yes. Right.

00:14:48.260 — 00:14:50.340 · Speaker 3
So that’s been studied.

00:14:50.500 — 00:15:27.180 · Speaker 4
Um, yeah. The high impact activity. And in almost every study there aren’t injuries reported. Um, now, these are, of course, supervised programs, and there are people who have bad balance or maybe more of a fall risk. And I think all that has to be taken into account. But there’s huge heterogeneity in the studies on exercise programs for, um, addressing, you know, bone loss.

And many of them are on menopausal women with low bone density. Um, many of them show gains in bone density, like ranging from like 1%.

00:15:27.220 — 00:15:28.540 · Speaker 1
Training or with plyometrics.

00:15:28.820 — 00:16:16.860 · Speaker 4
Combined. Generally combined strength training and some impact training. It doesn’t have to be a ton of impact training like one of the studies showed. Improvement in bone density and using like 50 jumps per session a few days a week added to the you know, it made made a difference. So. But the most effective programs seem to combine some impact and some strength training and a few days a week.

They’re all over the map in terms of numbers of exercises, numbers of reps. The intensity is at 50% of your, you know, one time max, or is it 80% with lower numbers. And they’re they’re really variable. But um, in general, like I’ll just sort of like forest view. Um, higher intensity strength training does seem to yield more benefit.

00:16:17.340 — 00:16:18.620 · Speaker 1
Uh, than capacity.

00:16:18.820 — 00:16:53.250 · Speaker 4
In terms of bone density. Then then the um, more moderate or low intensity, but the other forms are not without benefit. So you’re kind of seeing some gains in bone mineral density with the higher intensity strength training and the impact training. But you’re still there still benefit from the less intense, you know, lifting regimens.

And to be honest, not everyone people get injuries like, I don’t mean injuries like falling and breaking your hip while doing these exercises, but just like tendonitis or overuse, I mean, it happens to all of us. Like I love to do pullups. And every time I.

00:16:53.290 — 00:16:53.930 · Speaker 1
Aim, every time.

00:16:53.970 — 00:17:03.770 · Speaker 4
Every time I do more than ten sets of ten, I get biceps tendinitis and I have to take a step back. So or, you know, if I do, for me, I can’t do

00:17:04.890 — 00:17:19.770 · Speaker 4
a really high overhead pressing weight because every time I do, I flare up my AC joint. So that is not one I choose to do it the high intensity. I choose to do that when I lower intensity. But but my point is, yeah, these programs strengthening

00:17:21.089 — 00:17:49.400 · Speaker 4
some impact training and balance training combined are things that help with increasing bone density and reducing risk of falls and fractures. But, you know, honestly, they’re quite effective. A lot of the studies range from 6 to 8 months. And follow up will show a few. You know, I would say on average a few percentage points and increase in bone density.

Now if you look at what do you get from something like a bisphosphonate over a couple of years, you’re going to get like 6% increase in bone density.

00:17:49.440 — 00:17:52.760 · Speaker 1
For someone who’s listening. A bisphosphonate is a medication.

00:17:52.800 — 00:17:57.920 · Speaker 4
Medication that would, um, inhibit, uh, resorption of bone. Yeah.

00:17:57.960 — 00:18:02.120 · Speaker 1
Is a quality different of the bone that you get on a medication like a phosphate?

00:18:02.160 — 00:18:29.160 · Speaker 4
Yeah. Probably. Yeah. So. So the natural, like loading of your bone, you’ve got the pulling and the pushing all the tension of the skeletal muscle on your bones that, um, stimulates the bone, you know, for to to grow and have more density. Axial loading or impact stimulates new bone formation. Our bones again we talked about disuse osteopenia.

That’s the opposite of use. You know use increases density. Um so. uh,

00:18:30.360 — 00:18:31.280 · Speaker 4
where was I going with that?

00:18:31.560 — 00:18:34.760 · Speaker 1
Well, I’m curious as to how if we know that, um.

00:18:34.760 — 00:18:35.720 · Speaker 4
Oh, the quality of the boat.

00:18:35.760 — 00:18:40.160 · Speaker 1
We’re looking at 20 million Americans. We’re going to have osteoporosis this year. I’m scared.

00:18:40.200 — 00:19:19.080 · Speaker 4
Yeah. So the quality of the bone, I think, uh, is, is better when you get it from actual loading of the bones. You know, one thing we see, for instance, with bisphosphonates is you can increase the density of the bone, but is it, you know, as normally organized and is it actually laid down in the areas where the stress occurs?

Probably not. As well as we get with our own efforts that that lead to that. Um, and, you know, one example of that is it’s not a common problem, but there is something that occurs where people get an atypical fracture who’ve been on like a bisphosphonate for many years. It’s called a sub trochanter fracture of the hip.

So it’s like below the level of the hip joint.

00:19:19.320 — 00:19:21.360 · Speaker 1
That when the hip breaks and then they fall.

00:19:21.400 — 00:19:33.229 · Speaker 4
Well it yeah, it’s like a break below the level of the hip. And so that’s probably, you know, over time, there’s probably micro damage to the bone because it’s been, you know, normally bone is dynamic. It kind of

00:19:34.230 — 00:19:44.790 · Speaker 4
reserves and forms in relation to the stress that’s applied to it. But if you’re on this medication that’s, you know, just preventing resorption, it can become maybe abnormal. And it’s not a common problem. But just an example.

00:20:09.590 — 00:20:23.710 · Speaker 1
This book does something that I’ve never seen. It brings history, the history of muscle, the history of movement. And it integrates science. Really well done. Tell me about why. Why this book?

00:20:24.190 — 00:21:27.060 · Speaker 5
The choice to see ourselves as split down the middle. Um, is that it comes from a history of choices that people have been making for thousands of years, and those choices, in many ways, focused on muscle. In ancient Rome, doctors and trainers had a big fight over who would corner the market in what we now call health care.

And the doctors who won that fight won it in large part by putting down athletes who trained to build mass to build muscle. There was one Galen of Pergamon, and he said that athletes who trained to build mass were incapable of rational thought. He said that they actually smothered their souls with the slime of this muscle.

Right. And that kind of marked muscle as a locus of anxiety and marked it as

00:21:28.340 — 00:22:08.060 · Speaker 5
something there was something wrong about building muscle that has in a way that has lasted right up until today. So I had an experience when I turned 40 of starting to train in a more serious way than I ever had before, and it really changed me, and I was fascinated by that. I wondered why I didn’t know more about muscle, and I went looking for a big book that could kind of help me understand muscle in all the ways that you just mentioned.

I couldn’t find it, so I had to write it.

00:22:08.100 — 00:22:47.290 · Speaker 1
And to be fair, you are an acclaimed journalist and author. You have been contributing editor at Vanity Fair. You have contributed to the New York Times, GQ, the list goes on. You’ve been a very curious person, which is evident in this book. After you had this moment of understanding, we had really missed the mark on skeletal muscle.

How did you decide about the sections in this book as you began to formulate? There’s three big characters. There is this story that becomes interwoven. How did you begin to break that down and think about it?

00:22:47.610 — 00:23:43.650 · Speaker 5
Most books about muscle tell you what to do, and this one’s different because it’s descriptive. It’s not prescriptive. So I knew from the beginning that my way into talking about muscle was going to be through individuals, really fascinating people. I knew that one of them had to be a doctor. I knew that one of them had to be an ancient, a scholar of ancient Greece in some way, because we get so many of our ideas about athletics and medicine from there, and I knew that at least one of them had to be a really high level athlete.

And so I found I found these people. It took a long time hunting for them, but it’s just kind of like casting and you find the right balance of characters, and then you let them, let them start playing on the page.

00:23:44.010 — 00:23:45.850 · Speaker 1
How long did it take you to write this book?

00:23:46.130 — 00:23:48.010 · Speaker 5
Eight years full time.

00:23:48.290 — 00:24:15.250 · Speaker 1
Eight years full time. And for the listener or the viewer to give you a perspective of how in-depth this is on the history of muscle, it is exactly that. There are many things that really struck me about this book. I would love for you to touch a little bit about the history of muscle performance, the idea of the gymnasium.

I’m fascinated by the way that the the ancient Greeks looked at skeletal muscle.

00:24:18.520 — 00:24:30.280 · Speaker 5
The first thing to know about how ancient Greeks looked at skeletal muscle is to really sit back and take in the fact that they didn’t see it.

00:24:31.880 — 00:25:22.510 · Speaker 5
Now, that sounds impossible because you look at an ancient Greek sculpture, and to us it seems that they’re obsessed with muscle, but it’s really the lines of articulation around muscle that they believe do the work of movement, and specifically the tendons. They thought that the fleshy part of muscle, the muscle bellies, the contractile tissue that we now know moves us.

They thought that was just dumb stuff. That was maybe for padding, maybe for insulation. Like Aristotle thought that your glutes were built in beanbag chair. He called them useful for resting the body. It’s not until just before the classical period of Greece that scientists start to

00:25:23.590 — 00:26:10.190 · Speaker 5
open up the human body that had been proscribed in Greece before, and they begin to see how muscles work. They know that somehow muscles are part of movement, but they believe that there is a portion of hot air that gets trapped at the body in birth at birth, called pneuma. Pneuma is the word for breath or wind from which we get pneumonia.

Um, so pneuma is circulating in the body, and pneuma basically blows up the muscles like a balloon. And and then they deflate. And that is part of the process of, of of muscle.

00:26:10.230 — 00:26:14.230 · Speaker 1
This is crazy. The idea of how wrong we got. Skeletal muscle I mean.

00:26:14.310 — 00:27:25.940 · Speaker 5
The next big beat in the story of discovering skeletal muscle is under the Roman Empire. And the doctor Galen. He understands that muscle has to do with movement, but he still thinks that there is a mysterious substance, like a portion of hot air trapped in the body called pneuma that causes us to move. And he says that the brain is completely in charge and muscle is just something it uses.

We don’t begin to understand that the contractile part of muscle actually moves us until the 17th century, and then we don’t really begin to understand how it’s integrated with the neurological system, how the brain and muscle are partners, not it’s not a hierarchical relationship until the late 19th, early 20th century.

Even though I don’t think we’ve accepted that yet, I think we’re still pretty intent on thinking the brains, the boss, and the muscle is always, uh, second fiddle.

00:27:26.060 — 00:27:55.900 · Speaker 1
That’s really fascinating. Did they look at muscle as something different? I mean, there was we can think about words as, uh, words like victory. I know that that was something that you had wanted to put in the title before. Have we really changed the way that we have thought about muscle? Was it something to be revered back then and then transitioned to now?

It’s okay. Well, your knuckle dragger or just what do they say? Uh, all brains and no brawn or all brawn and no brains.

00:27:55.900 — 00:28:20.810 · Speaker 5
So Greeks were fascinated by muscle even before they knew what muscles did. They were running races at the Olympics for hundreds of years before they had any idea that muscles had to do with movement. Okay. But we know that its muscles that are making the sprinters win the race. They believe that.

00:28:23.330 — 00:28:42.010 · Speaker 5
They believe that strength is actually it’s not only something that an individual builds through training. It’s not only an individual accomplishment, it’s a collaboration with the gods. You have to train, but then you also have to be given the gift of strength. And this.

00:28:42.010 — 00:28:44.330 · Speaker 1
Is fascinating. The gift of strength.

00:28:44.410 — 00:28:55.530 · Speaker 5
Yeah. I mean, Greeks were as likely to talk about strength as something you receive as to talk about strength as something that you have.

00:28:55.570 — 00:28:59.570 · Speaker 1
That is an unusual way to frame it.

00:28:59.970 — 00:30:22.960 · Speaker 5
But there is a connection between that and current physiological Logical thinking in that there remain there remains an element of mystery in performance, an element of unpredictability in performance that you see in something like the super compensation effect after a period sized training regimen.

And Charles Stocking, who is one of the main characters in this book, he’s a classicist who worked his way through graduate school as a strength and conditioning coach for Bruins athletes at UCLA. Um, he’s become the really the world’s greatest expert on the Greek language of strength. And Charles says that he thinks the super compensation effect is a modern analog for Greeks description of great performances on the battlefield or in athletics as being a gift from Zeus.

It’s it’s something. It’s their way of explaining what we have come to understand as a physiological adaptation.

00:30:23.480 — 00:30:27.320 · Speaker 1
And what is super compensation? The super compensation effect.

00:30:27.480 — 00:31:12.310 · Speaker 5
Super compensation effect, um, just in simplest terms is, uh, it’s the outcome of a certain kind of cyclical training. So, you know, you can’t push harder and harder all the time. You’ve got to take a couple steps forward, a couple steps back. Periodization. The many forms of it are ways of organizing our training to build up to a moment where we have a a high level of performance.

Just before we reach that highest level, we take a rest. And in that rest we our bodies, repair ourselves so that we can leap ahead of where we were before that rest began.

00:31:12.310 — 00:31:33.710 · Speaker 1
And I have a quote from your book and its ancient Greeks considered strength not only as a quote, an individual accomplishment based on individual effort, but as a paradoxical phenomenon that depended partly on what a person did and partly on what help and gives the person received from the gods.

00:31:33.750 — 00:31:34.710 · Speaker 5
That’s right.

00:31:35.270 — 00:32:16.470 · Speaker 1
You know, I’m sure the listener, well, you guys better be interested in muscle, but really understanding. We talk about it in terms as if we’ve always known it. This is the bicep, this is the quadriceps. But very few of us, myself included, has have thought about the history and putting it into context of what was thought of it before we knew it was actin and myosin and that these muscle fibers and muscle bellies were attached to various parts of the body.

And there’s a whole history of what we imagined it was.

00:32:16.510 — 00:34:16.020 · Speaker 5
And let me give you a really concrete example of the gift and of strength in action, as the best as we can tell. The very first Olympic event was called the Stadion. The stadion was the equivalent of the 200 meter sprint now, and the way the stadion was set up, it started. The stadion was a race between two altars.

The first one was an altar to a hero who was a human who lived a long time ago, but was especially blessed by the gods. The other altar was to Zeus, the greatest of the gods, on the altar to Zeus. They had laid out their sacrifice to him, which was the best part of the bull, the fleshy thighs. Now, this is a time when meat is not a part of anybody’s regular diet.

So the whole community is there, and they’re looking forward to this feast on meat, which they never get to taste at the end of the day. Everybody’s watching this. The priest of Zeus is standing right by that altar, and he’s got in his hand a torch. And what the athletes are looking at as they’re getting ready for the race is the torch in that hand, because what they want to do is be the first to get there.

Take the torch, light that meat on fire and give everybody this just great gift. They’ve been wanting for the whole for the whole four years. And you run faster if you’re trying to complete the sacrifice that brings your community together, then if you’re just going for a run and they all believe that the person who wins wins because Zeus gave them a very particular kind of strength called Kratos.

Spell at Kratos. And Kratos is only given by Zeus. It is the strength of winning.

00:34:41.220 — 00:34:43.980 · Speaker 4
So, for instance, like impact, exercise in particular.

00:34:44.020 — 00:34:45.860 · Speaker 1
Seems to find impact exercises.

00:34:45.899 — 00:34:56.340 · Speaker 4
Like a jump. Like it could be jumping rope or a box jump, jumping jacks, running something where there’s like some takeoff and landing. There’s a little flight basically.

00:34:56.379 — 00:35:12.970 · Speaker 1
So that’s different. And you know, when we think about that, that’s different than doing, say, a leg press, because I would think that a leg press would build more muscle. But what I’m hearing you say is that the takeoff and landing, actually that that targeted activity.

00:35:13.250 — 00:35:15.170 · Speaker 4
Stimulates formation.

00:35:15.210 — 00:35:17.730 · Speaker 1
Bone. Uh, a more robust.

00:35:17.730 — 00:35:18.010 · Speaker 4
Way.

00:35:18.250 — 00:35:19.890 · Speaker 1
Or differently is that. Is that true?

00:35:19.930 — 00:35:51.610 · Speaker 4
Am I? Yeah. Because you’re kind of like, um. It’s more like twice the ground reaction force that you would have with just like, standing or walking, for instance. So, um, like a leg press is a load bearing exercise. Load bearing exercise is good for bone density. Like in the opposite. That would be not load weight, like being on crutches and getting again.

Being in the disc or being an astronaut is the extreme example of disuse osteoporosis. Uh, so yeah, load bearing, muscle pulling on bones. Those things do stimulate bone formation, but you get an extra oomph from from impact.

00:35:51.770 — 00:35:54.210 · Speaker 1
Even though you can’t wait it as much.

00:35:54.930 — 00:36:14.680 · Speaker 4
Yeah. There’s it creates it. There’s a response in the bone that increases bone density. So now not everybody can jump because they’ve got some people have some nearsightedness. So I don’t want people to think they need to go like jump rope for 30 minutes. You could just do at a little impact, um, you know, to your routine a few days.

00:36:14.760 — 00:36:18.040 · Speaker 1
Yeah. What else could they do? So they could do a small jump.

00:36:18.120 — 00:36:48.920 · Speaker 4
You could just hold on to the back of a chair and jump, you know, 30 times you could do some jumping jacks. Um, there’s some evidence that actually pool based jumping can increase bone density. So, like, you’d be in a pool and you would jump out of the water, but then it’s still land. And that’s probably a combination of the resistance exercise it takes to overcome the water to jump out of the water, but then land into it.

So you obviously you’re in a place where you’re not completely submerged to do that. But, um, that may be an option for people who can’t, you know, do a lot of land based jumping.

00:36:48.960 — 00:36:58.600 · Speaker 1
And if you were to think about how you would design or what you would tell everyone to do, do you say have them jump. And this might be in your book because I haven’t gotten a copy of it yet.

00:36:58.920 — 00:36:59.840 · Speaker 4
Sorry, I just wanted.

00:36:59.840 — 00:37:02.080 · Speaker 1
To throw that out there, just waiting.

00:37:02.080 — 00:37:03.880 · Speaker 4
For that. I was thinking about that on the way here. Yeah.

00:37:03.960 — 00:37:22.280 · Speaker 1
Um, but, you know, in all fairness, I’ve looked at multiple research papers that you’ve put together, so I’m just. I’m so excited for your book. I think it is going to be tremendous because there’s a lot of information out there about building muscle and body composition. But really, when it comes to bones and joints.

00:37:22.320 — 00:37:23.600 · Speaker 4
Yeah, not all in one place.

00:37:23.640 — 00:37:25.800 · Speaker 1
Yeah, that’s I mean, I think it’s going to be tremendous.

00:37:26.080 — 00:37:34.080 · Speaker 4
I tried to put everything all in one place that all of my patients ask me all the time, and just, I just wanted it so badly to be in one place for people.

00:37:34.080 — 00:37:39.000 · Speaker 1
That was what’s not going to stop me from calling you from with these questions that I have. So we’re all good?

00:37:39.040 — 00:37:39.520 · Speaker 4
Yeah.

00:37:39.560 — 00:37:56.670 · Speaker 1
What would you have someone do if they were to prioritize? Because it’s tricky, right? You have to prioritize muscle for metabolic metabolic health, but you also need strong bones. So I’m curious as to how often someone would need to do some kind of activity. What is the volume look like?

00:37:56.710 — 00:38:05.350 · Speaker 4
Yeah. So first of all, bone health starts very early. So I think we need to like, backtrack a little bit. Um, when you’re like a child.

00:38:05.590 — 00:38:05.830 · Speaker 1
So.

00:38:06.590 — 00:39:20.220 · Speaker 4
Yes. Uh, one of my very close friends who’s a brilliant woman, Tammy Scarpelli, who’s chief of orthopedics and sports medicine at University of Wisconsin, which is very unusual, a female chair of orthopedics, an underachiever. I’m not actually a total underachiever, but she has this amazing body of literature.

It’s like a 25 year project where she took kids as young as seven up into their teenage years and followed them for like 25 years, and they were gymnasts. So this is loading on the bone, including upper extremity, lower extremity, back. And compared them to kids not participating in organized sports. And she followed them into adulthood with Dexa scans and other studies of the geometry of bone.

And what she found was that these gymnasts ended up depending on what part of the body, with 15 to 40% more bone density than their comparison group maintained even into adulthood. Now, at around age 30, we typically say that’s when bone density starts to decline. So you’re, you know, adolescence and early adulthood years are when you build up your base.

And if you don’t build up your bone density before the age of 30, like that’s where you start from. So now we can maintain from there with interventions and try to not fall into the 1% loss per year.

00:39:20.260 — 00:39:22.460 · Speaker 1
Can we build after 30 and 40.

00:39:22.500 — 00:39:28.900 · Speaker 4
So some of these you know, you’re kind of trying to slow the loss right. Because you typically will lose 1% per year.

00:39:28.940 — 00:39:30.060 · Speaker 1
No matter what.

00:39:30.340 — 00:39:41.420 · Speaker 4
Uh, typically. Well these these resistance strength training programs and impact programs do show that we can gain bone mass back. You’re probably not ever going to get you’re never going to get above where you were when you were really age 30.

00:39:41.460 — 00:39:47.540 · Speaker 1
I mean, because from from muscle mass, you can get above where you were when you were age 30. Do you think that it’s possible?

00:39:47.580 — 00:40:35.900 · Speaker 4
I think you would gain muscle mass. I don’t I, I haven’t seen any literature to suggest that you would gain, that you would ever be higher than you were at age 30 with, with bone density. Um, but uh, and again, these studies but however, these studies on now, Tammy’s work is unusual because there aren’t many studies looking at the younger population like like that.

But if you look at, you know, most of the studies on these interventions, we’re already we’re taking people already osteopenia or osteoporotic and trying to reverse some of that. You know, with the interventions and the and the gains aren’t huge, but they’re enough that like if you gain a few percentage points, you might tip yourself from osteoporosis back into osteopenia.

You know, take your t score from -2.6 to 2.5. Yeah. But if you’re not losing you’re winning because the not that. Yeah.

00:40:36.100 — 00:40:36.980 · Speaker 1
You’re not losing your winning.

00:40:37.020 — 00:40:43.860 · Speaker 4
Yeah. Because the natural history would be to lose 1% of your bone mass per year. Or if you’re if you’re a menopausal woman, 2% per year.

00:40:43.860 — 00:40:51.530 · Speaker 1
You do a lot of surgery. And what are some of the perioperative risks associated with oral contraceptive use. What should we be thinking about?

00:40:51.570 — 00:42:32.480 · Speaker 4
Yeah. Well, number one, a lot of your patients or my patients, if I asked them if they’re taking any medications and they’re a teenager, college age girl, they will say no because they don’t think an oral contraceptive pill is a medication. Uh, so you have to specifically ask. And I always ask my patients this when I’m thinking about surgery or scheduling surgery.

Um, do you have any personal or family history of blood clots? Do you smoke? And do you take any contraception? And then if they say yes, ask them what type of contraception, if it’s a combined oral contraceptive pill, meaning an oral pill that has estrogen in it, there is some increased risk of blood clots from even an outpatient sports medicine surgery, like an ACL surgery, for instance.

It’s been shown to double the risk of a blood clot. And if you’re also obese or a smoker and using an oral contraceptive, it quadruples the risk. So that’s not good. So we need to do some risk assessment. You also do have to pay attention to things like a nouveau ring because that’s, you know, an estrogen delivery that’s exogenous.

We don’t know. The clotting risk is as high as it is with an oral contraceptive. But that’s that’s still a risk. So basically exogenous estrogen that’s you know, part of uh, contraceptive delivery is is a risk for perioperative blood clots. So sometimes that may affect our post-op plan in terms of blood clot prevention or just kind of raise our antenna in terms of concern for screening for a blood clot if someone has calf pain or swelling.

But there are a lot of contraceptives that don’t have a risk, like progestogen only pills don’t have that risk, and an IUD doesn’t have that risk. One that I hate the most to see young women on is Depo-Provera. It does increase risk of blood clots by.

00:42:32.480 — 00:42:33.160 · Speaker 1
The shot, right?

00:42:33.600 — 00:43:13.000 · Speaker 4
Yeah. Yeah, it increases risk of blood clots. But it also has a a supposedly reversible effect on bone density. It reduces bone density. So I had a patient recently who, you know, had a knee injury and I was trying to fix a fragment of bone on her tibia. And this is someone who has some nicotine exposure and is on Depo-Provera.

And the bone was just crumbling, just really poor quality. And, you know, while the bone loss may be reversible when someone goes off of Depo-Provera, you never know when someone’s going to injure themselves and need a surgery. So they have the bone loss while they’re injured. That’s that’s nice.

00:43:13.040 — 00:43:27.920 · Speaker 1
So you said something there that I wasn’t anticipating. And I’m looking at my producer over here smiling. Um, a lot of individuals use nicotine. Nicotine gum? Oh, yeah. Nicotine mints. Do we know is it the nicotine or is it the smoking that the nicotine?

00:43:27.960 — 00:43:28.960 · Speaker 4
Oh, gosh.

00:43:29.240 — 00:43:32.520 · Speaker 1
Everyone is crying right now. Including my husband. He loves.

00:43:32.560 — 00:43:43.280 · Speaker 4
Nicotine. Is bad for all things orthopedic surgery, wound healing, infection. Uh, your bone fracture healing, tendon healing, rotator cuff tear healing.

00:43:43.280 — 00:44:05.470 · Speaker 1
You just hurt a lot of people’s heart, right? Yeah, because it’s a it’s a thing. So I did my fellowship in geriatrics. And one of the things, actually, I did it wash you. Um, it was really hard. I don’t recommend anyone doing. Just kidding. You know, they’re always looking for fellows. Uh, please. But one of the things is they were talking about nicotine use and the impact on brain.

Brain function.

00:44:05.510 — 00:44:05.910 · Speaker 4
Oh.

00:44:06.190 — 00:44:23.230 · Speaker 1
Positive impacts for Parkinson’s and other type of memory challenges. And now we’re hearing from you from from your mouth to God’s ears. Nicotine exposure is not good for bone, tendons and anything orthopedic. Good to know.

00:44:23.310 — 00:44:25.310 · Speaker 4
Yeah. Okay. Unfortunately.

00:44:25.790 — 00:44:37.350 · Speaker 1
I’m. We’re all crying now. Yeah. You said something else. You said oral contraceptive or exogenous estrogen use. What about individuals that are using the patch?

00:44:37.390 — 00:45:18.300 · Speaker 4
Transdermal estrogen used at the level in menopausal hormone therapy has no increased risk of of clotting as opposed to the oral versions which do. And that’s because the transdermal delivery basically bypasses that first pass through the liver that can affect the clotting cascades. So transdermal estrogen is quite safe.

Um, now, one question mark is if you were having like a major orthopedic surgery, you know, where you have another risk factor. Does transdermal estrogen add to that? I mean, in the non-Indian population, there’s just really almost no risk for for transdermal delivery. So transdermal delivery is very safe.

00:45:18.700 — 00:45:25.499 · Speaker 1
I don’t want to open up a can of worms here. But we talked about estrogen. When you are

00:45:26.500 — 00:45:37.260 · Speaker 1
discussing menopause hormone replacement therapy. Are you thinking about estrogen or are you thinking also about progesterone and testosterone? Oh, right.

00:45:37.260 — 00:46:03.940 · Speaker 4
So, um, if you have a uterus you can’t use. Again, I’m not a women’s health doctor, but I do know this. You can’t use unopposed estrogen. You have to have some form of progesterone to protect your uterus from uterine cancer. So that could be in the form of a morena IUD combined with a transdermal patch. Or you could have oral progression, you know, something which has other benefits like sleep and things like that.

00:46:04.140 — 00:46:10.340 · Speaker 1
In terms of bone health, is it something that you are thinking about for bone health? Yeah, testosterone.

00:46:10.380 — 00:47:09.130 · Speaker 4
So testosterone therapy is of course, not FDA approved for women unless it’s for low libido, which it is approved for. And I think probably many of your listeners know that, yes, women have testosterone is just at a much lower level than men, about like 10%. Um, so there’s a lot of research going on in terms of, yeah, like, should testosterone be used for bone density and maintenance of muscle mass?

And um, I think currently that’s certainly not, um, a common use for it. And I think we’re still gathering data on that. But it would make sense that for at least women who have lower testosterone levels than they should, that the testosterone would contribute to certainly muscle mass. And we know muscle mass contributes to bone density.

So, um, but yeah, right now that’s not sort of a typical part of a regiment in terms of menopausal hormone therapy. Not yet. Not yet. Yeah.

00:47:10.050 — 00:47:17.090 · Speaker 1
If you are young, you suggest you have five kids. Mhm. Did you have them start your kids. Yeah. Early.

00:47:17.130 — 00:47:27.890 · Speaker 4
Yeah. Yeah. They all have participated for us. And we have a couple that didn’t love sports. But we sometimes we would go on walks and they would call them forced marches. But you know like most of our kids enjoy it.

00:47:28.090 — 00:47:29.210 · Speaker 1
I mean, you know.

00:47:29.730 — 00:48:27.250 · Speaker 4
Um, but, uh, yeah, I think sports participation in athletics is really important in adolescence and very important. And girls. Yeah. Because, you know, if girls aren’t participating in, like, high school sports, that they’re probably not going to go off into college and then, like, go do a regular workout.

Like, I can’t imagine not exercising every day, right? But I grew up always being active. And, um, I also think it’s really important to model activity for your kids, like work out with them or them seeing your workout. Like, my husband and I were very much prioritize exercise and strength training and our kids.

Now we have to get a workout in every day. And they’ve over the years been, you know, we always have a workout room in whatever house we live in, and they’ve always spent time in those rooms or use the, the equipment or whatever. So I think you need to model for your kids, but also you got to get them involved in activity.

Um, you know, at a, you know, so they’re active through those years.

00:48:27.290 — 00:48:31.050 · Speaker 1
And that’s from bone density cartilage tendons, muscles.

00:48:31.090 — 00:48:55.880 · Speaker 4
Mhm. I think um, yeah. Now you don’t want to over develop muscle too quickly and pull on tendons too hard before you’re done growing, because that’s when you get things like Apophis bites, like you’ve probably heard of Slaughter’s Disease, or of the knee where people get that bump on their shinbone. They’re aggravating the attachment of the tendon to bone, because when you’re not done growing, your tendons are a little stronger than the attachments.

In some ways.

00:48:55.920 — 00:48:57.960 · Speaker 1
Your tendons are stronger than where.

00:48:57.960 — 00:48:58.080 · Speaker 4
They.

00:48:58.080 — 00:48:59.240 · Speaker 1
Attach to the bone.

00:48:59.640 — 00:49:44.990 · Speaker 4
So you can get Apophis situs, which is just irritation of the attachment of the tendon to the growth center on the bone that it attaches to, because it’s an area of growth. So, you know, that’s when and your child will know if they’re doing too much because it’ll hurt and they’ll tell you. And it’s not. It’s just a thing that where you kind of rest as needed.

There’s no intervention other than rest as needed. But, um, you know, so sometimes too much activity can lead to Apophis. Itis in kids, but it physical activity is very good for children. There’s a you know, we have a huge obesity problem in America. Um, in general, yes. Being active is good. Not being you know, you don’t want them to be sedentary.

No. Yeah.

00:49:45.030 — 00:49:58.630 · Speaker 1
When, um, girls go through, let’s say, the no longer term for the athletes triad, the women that are over exercising under eating and they lose bone.

00:49:58.670 — 00:50:31.270 · Speaker 4
Yes. This is part of accruing bone before the age of 30. So that is a huge risk factor. Like let’s say you had what used to be called the female athlete triad. Like when you were in high school or college, you had an energy deficiency, whether it was from inadequate energy intake or just not matching your output with your intake.

That’s actually a lot of. So the reason the term is now relative to energy deficiency syndrome is not always with disordered eating. There can just actually be or not. You’re under fueled chronically, and this will be the kid that presents with the stress fracture, the cross-country runner that they don’t have.

00:50:31.470 — 00:50:37.670 · Speaker 1
And what she means by that is that, say, for example, an individual is really active and they’re just not thinking about eating and.

00:50:37.910 — 00:50:40.150 · Speaker 4
They just cannot keep up with the demands.

00:50:40.190 — 00:50:41.430 · Speaker 1
Eating a lot of food, but they’re.

00:50:41.550 — 00:50:42.550 · Speaker 4
They’re still under fueled.

00:50:42.590 — 00:50:43.150 · Speaker 1
Yeah. They’re under.

00:50:43.150 — 00:51:10.790 · Speaker 4
Fueled. Uh, so yeah. And so if you, if you tip into a state of, you know, amenorrhea or you’re not having cycles, you’re now in like an estrogen deficient estrogen deficiency, a very low body weight, you’re you’re losing bone mineral density when you’re supposed to be building up your base. Right. And so people can get to so they’ll arrive at 30 with diminished bone density.

And so you don’t want that to happen. Now let’s say you’re.

00:51:10.830 — 00:51:12.870 · Speaker 1
And what’s done about that. Do they give them a pill.

00:51:12.910 — 00:51:20.310 · Speaker 4
Well, um they’re yeah. I mean nutritional consultation and or consultation. You can use contraceptive pill.

00:51:20.350 — 00:51:22.950 · Speaker 1
Or they won’t catch up. And again, I don’t want to be negative.

00:51:22.950 — 00:51:23.590 · Speaker 4
Will tell.

00:51:23.630 — 00:51:24.110 · Speaker 1
You.

00:51:24.390 — 00:51:25.030 · Speaker 4
Um,

00:51:26.750 — 00:51:41.540 · Speaker 4
you you can but you’re It’s it. There’s some downstream effect that is not probably entirely reversible, and depends on how long it goes on for, and how many bouts of this happen to a person. Um.

00:51:42.260 — 00:51:44.460 · Speaker 1
How genetic is osteoporosis?

00:51:45.420 — 00:52:01.779 · Speaker 4
Uh, you know, I don’t know if we know the exact genetic propensity, but if that is a question when we’re assessing risk, like if you have a family history of osteoporosis, you know, that makes me more likely to send someone for a Dexa scan. No. So what I was getting at is if you arrive at, let’s say, arrive at

00:52:03.020 — 00:52:37.690 · Speaker 4
menopause and so, so menopause in and of itself is a risk for osteoporosis, as is being Caucasian, being thin or underweight. But if you also tell me, oh, I have a history of, you know, amenorrhea or an eating disorder or we didn’t call it back then when this person was young, red or whatever, like, were you where you had an added risk to not have as much bone density as you should?

Those are all adding up for you at that point. You know, these are risk factors that might mean you need to have a Dexa scan to check for osteopenia or osteoporosis sooner than is typically indicated, which is 65, which is probably too late.

00:52:37.730 — 00:52:46.810 · Speaker 1
Too late. Well, so we have a a medical practice. And we always have for baseline we have our patients. I mean they could be 40. And we want to see a Dexa.

00:52:47.210 — 00:55:00.000 · Speaker 4
Yeah. Um, now for patients under 50 of course you’re not necessarily looking at the T score. You can look at the Z score because the T score is comparing older people to younger people. And if you’re under 50 you’re kind of still younger people. But yeah, there’s there’s value in that especially with any risk factors.

And um, you know, I think the frustrating thing about the typical recommendation being to get a Dexa scan when you’re 65 is that if you get a Dexa scan, you’re 65 and you already have osteoporosis, and no one told you when you were 52 that menopausal hormone therapy can help prevent osteoporosis and prevents fractures in many people.

You know, now you’re 65 and you’re kind of. You’re kind of out of the window of time where it’s recommended to initiate menopausal hormone therapy, which is within ten years of menopause. So a lot of people are missing the boat. There are a lot of people who are seeing doctors who got their medical training, when there was a lot of misinformation about menopausal hormone therapy and don’t provide it.

And it truly is indicated for prevention of osteoporosis. So, you know, unfortunately, I think some of the most long term consequences of menopause are musculoskeletal. Um, and bone density is, you know, osteoporosis is is one of the biggest ones. So, you know, there’s just and there’s more and more of a shift in this understanding.

But again, if you just think back that initially menopausal hormone therapy or formerly called HRT was indicated for vasomotor symptoms, and that’s not even the tip of the iceberg. The long term effect, probably the one that’s most life changing, is the effect on bone density. I mean, joint pain, inflammation, arthritis, frozen shoulder.

Yes, those aren’t good things. But the the very long term consequences like it’s life altering, mobility altering. If you get osteoporosis and you get a hip fracture, it’s you know, there’s mortality and morbidity associated with that.

00:55:00.440 — 00:55:19.960 · Speaker 1
And why is that. Do you. What are some of the rates for morbidity and mortality of falls. And you know we were talking about impact training. And it seems that because I was asking these questions before that it really is about the joints or the the location that you’re loading. It’s not full body, which I think is fascinating.

Yeah.

00:55:20.160 — 00:56:03.830 · Speaker 4
Yeah. No. Um, and so if you look at what’s in these resistance exercise programs, you’ll see, yes, it does include overhead press. And I mean, again, they’re all different, but a lot of them have like an upper extremity pressing maneuver, maybe a deadlift, a squat, some impact. You’re trying to get like large muscle groups, but you’re also trying to load, you know, the upper extremities, the lower extremities, the spine.

Um, and then the impact. Yeah. Probably why it’s more likely to improve, you know, femoral neck bone density and cortical thickness is because that’s what you’re loading. You’re loading the lower extremity with that. With that impact you’re not loading so much your spine or your your arms. It’s unless you’re a gymnast and then you have good upper.

00:56:04.590 — 00:56:07.830 · Speaker 1
And it’s a side they call osteoporosis a silent disease.

00:56:07.830 — 00:56:08.910 · Speaker 4
Silent disease. Yeah.

00:56:08.950 — 00:56:10.990 · Speaker 1
Someone isn’t going to know that they have osteoporosis.

00:56:11.030 — 00:56:11.870 · Speaker 4
Until they break something.

00:56:11.870 — 00:56:13.430 · Speaker 1
Until they break something which is terrible. Yeah.

00:56:13.430 — 00:56:17.670 · Speaker 4
Or have a stress fracture. Like you could be like a masters athlete, you know, what about.

00:56:17.670 — 00:56:22.030 · Speaker 1
And if they’re younger and have a stress fracture, is that an indication that something.

00:56:22.070 — 00:56:34.950 · Speaker 4
Well, sometimes factors are part of energy deficiency syndrome. Okay. Sometimes they’re just part of, you know, bad alignment. Like, you got a high arch and your foot rolls over the sides. You’re going to get a stress fracture on your fifth metatarsal. That’s different. You know that’s an alignment issue.

00:56:34.990 — 00:56:42.870 · Speaker 1
What about tendons? Have you thought much about tendons tendon health with hormone replacement. Um loading them or is that still.

00:56:42.910 — 00:56:51.910 · Speaker 4
Yeah. So tendons also have estrogen receptors and. Yeah, definitely we see a lot more tendinitis. You know Perry, articular pain. You know, around the same time that we see increases in joint pain.

00:56:51.950 — 00:56:57.310 · Speaker 1
Do you does hormone replacement menopause replacement therapy. Uh help that.

00:56:57.950 — 00:57:32.060 · Speaker 4
Uh, I think the data is not specific enough. And that’s so, you know, again, looking back at these studies, a lot of them are just like, did you have joint pain or how severe was it? And did it get better? It’s the data isn’t as granular as it could be, which is really why orthopedic surgeons or researchers need to work with women’s health doctors, um, to get more specific information.

I started a registry with our Women’s Health department at Duke, looking at trying to sort of correlate vasomotor symptoms with musculoskeletal symptoms. So your you know.

00:57:32.100 — 00:57:37.540 · Speaker 1
These study this is um, so far you’re looking at a thousand participants. Is that.

00:57:37.580 — 00:58:05.540 · Speaker 4
Well right now we we just opened it. We have a couple hundred people enrolled. We’re going to continue to enroll, but we’re we’re trying to look very granular at joint pain, like which joints are painful. How you know, is it bilateral? How bad is each joint? Did it get worse or better when you started hormone therapy?

Um, you know, what? Do your vasomotor symptoms mimic the severity of your joint symptoms?

00:58:05.580 — 00:58:06.900 · Speaker 1
That’s interesting. Yeah.

00:58:07.420 — 00:58:51.970 · Speaker 4
Well, we don’t know that, I don’t think. And so we’re trying to be more detailed and granular in our, in our information in that way. But so I think like the you do see this acute exacerbation of joint pain and arthritis and inflammation early on in menopause. That’s less silent. Your joints are talking to you as opposed to the osteoporosis is kind of insidiously happening in the background.

And you don’t know you have it until you get a Dexa scan or, um, you know, break a hip or your wrist or, you know, a lot of times people will be out being active in fall playing pickleball or tennis and, you know, get a distal radius fracture. You know, we tend to see some of those when people are active. We might see distal radius, proximal humerus.

Um, my neighbor just broke approximately humerus skiing, you know.

00:58:52.050 — 00:58:55.410 · Speaker 1
But she loves that she’s your neighbor, though. He just didn’t fix that.

00:58:55.650 — 00:59:07.570 · Speaker 4
But then, you know, the the the more what we typically think of as fragility fractures that happen as we get older, it’s just the same level of fall, you know, tend to be the hip fractures and the vertebral, um, fractures to.

00:59:32.450 — 00:59:44.770 · Speaker 1
The reason we are really focused on tenant apathy is because those seem to injure before a muscular injury happens. That’s right. It’s the common denominator that limits the quality of life.

00:59:44.810 — 00:59:55.450 · Speaker 2
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 of treatments.

00:59:55.490 — 00:59:56.050 · Speaker 1
Amazing.

00:59:56.090 — 01:00:19.400 · Speaker 2
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 could 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, the first thing we do is we’re going to bring in a GC. And so that’s your general contractor and.

01:00:19.560 — 01:00:20.560 · Speaker 1
What the GC oh yeah.

01:00:20.600 — 01:01:28.560 · Speaker 2
Yeah. So, um, we’re gonna you have Tina sites. So same thing in muscle. You have your myocytes and you also have your osteo sites and bone. You have these, these cells that basically look at the tendon homeostasis and they help direct traffic. And Tina’s site is a standard. It’s called a modified fibroblast cell.

So it helps to lay down collagen and also helps to direct traffic. The sites 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 tendon is actually when we put color power 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 hypothermia in a tissue. That’s already a sign that things are going in the wrong direction. Well now we say, well now you’ve aggregated this scar tissue. You’ve aggregated these other things that are there that are not that helpful. Well, we might have to bring an excavator.

And the excavator is. We have a couple of different treatments for excavation. One of our treatments is called point. So percutaneous needle tsunami, which is when under an ultrasound will actually pass a needle through the tendon several times.

01:01:28.600 — 01:01:30.000 · Speaker 1
Is that where dry needling came from?

01:01:30.040 — 01:01:31.320 · Speaker 2
It’s very similar to dryness.

01:01:31.600 — 01:01:33.720 · Speaker 1
Yeah. This came first and then dry needling was adopted.

01:01:33.760 — 01:01:43.600 · Speaker 2
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 dental path.

01:01:43.840 — 01:01:51.040 · Speaker 1
Which I just want to highlight that that takes a ton of skill. Ultrasounds are not easy to use. And, um,

01:01:52.080 — 01:02:02.480 · Speaker 1
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.

01:02:02.520 — 01:03:29.980 · Speaker 2
It’s it’s important to visualize. It’s also going to tell you whether or not there’s a tear there. You don’t want a needle a tear. Right. So a tear is a different concept. A tear is a separation. so we don’t want to excavate her 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 could be done through PMT. It could also be done through something called a ten x 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 based slightly depending on the study you’re looking at. So you have leukocyte rich so white blood cell rich platelet pipe, platelet rich plasma and leukocyte poor platelet rich plasma.

If I were treating a joint I would use leukocyte pour. I don’t need white blood cells in a joint necessarily. But when I’m 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 anatomy to, 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

01:03:31.140 — 01:05:13.850 · Speaker 2
basically stimulate the Tina sites. And another type of cell that resides in tendons called CSCS tendon stem 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 hold.

I would say it’s probably a 5050 proposition, depending on the size 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 the muscle coming towards the tendon. You have a mild tenderness 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 anthesis, 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 that’s going to heal. Where is it? How big is it. How impactful is it it to the amount of strength you can produce and 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 and um, important for people to know if you do suffer a tendon tear. There are different types from a 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.

It goes straight through from top to bottom.

01:05:13.890 — 01:05:39.770 · Speaker 1
And you usually know when you do those. Yes. That is. I have had quite a few injuries and, you know, um, when that happens, it’s not like a tendon. 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.

01:05:39.970 — 01:06:03.920 · Speaker 2
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 a sheet of paper and a punch a hole. 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.

01:06:03.960 — 01:06:08.480 · Speaker 1
That would be, for example, like a tricep tendon tear or a bicep rupture.

01:06:08.520 — 01:07:01.560 · Speaker 2
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 muscles not seeing any tension, the body prioritizes 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. Um, because that’s the most common age population to get acute Achilles tendon ruptures.

But if that occurs and that tendons not reattached or it’s not approximated, you’re putting a boot in or something like that, then foreseeable you’ll atrophy your gastro and your soleus. And that’s going to be really tough functionally to go through.

01:07:01.600 — 01:07:19.720 · Speaker 1
So essentially don’t delay. I think a lot of the patients, um, that I have and many people listening, they don’t want to stop their activity. They’ll injure themselves and they don’t want to stop. I don’t want to 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.

01:07:19.760 — 01:07:32.320 · Speaker 2
Yeah, you should be evaluated swiftly and you don’t want to see on MRI or on ultrasound. You don’t want to see those atrophic changes occur. That’s a sign that your that muscle is not going to be as functional as it originally was. And therefore your prognosis isn’t as good.

01:07:32.360 — 01:07:44.720 · Speaker 1
Again you see patients often and it’ll be daily um, either a shoulder, a knee or a hip. Do you believe that it’s because of patterning. Why are those the common injuries?

01:07:44.760 — 01:08:26.670 · Speaker 2
Yeah. Um, 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. It’s called cybercriminal impingement. So basically, you’re moving your shoulder around and the tendon gets caught underneath a 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 tendon apathy is part of a greater clinical concept known as patella ephemeral 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 in the hip.

01:08:26.670 — 01:08:30.390 · Speaker 1
So the posterior chain is actually affecting the anterior chain.

01:08:30.430 — 01:08:58.940 · Speaker 2
Yes. And posterior lateral specifically. So hallmark of patellar tendon patella femoral pain syndrome. We we commonly will look at strengthening up the gluteus medii on the side of the hip. And then the the really the whole goal there is can you get back to walking and running with stabilization at the hips.

So there’s not so much pain at the knee. Once again smoke versus fire. Your knee hurts. You do have a tendon, but mechanically speaking there’s an insufficiency of some muscles that are higher up in the kinetic chain.

01:08:58.980 — 01:09:39.140 · Speaker 1
That’s. 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 Meade and you have, I don’t know, just pick a different muscle. Sure. Are there things that individuals should all be doing? Should we you know, we wake up, we brush our teeth, we brush our hair.

Should we be getting up and doing glute activation? I don’t know. I’s, T’s and Y’s for our shoulder. Are there things that 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?

01:09:39.180 — 01:09:51.900 · Speaker 2
It’s a great question. Um, and in trying to distill what makes a lot of sense, I will give home exercise programs to patients almost to that exact effect. And they come in with a back injury. But I say, well, now’s an awful time. Good to start rehabilitating and rehabbing.

01:09:52.580 — 01:09:53.740 · Speaker 1
Is rehab a real thing?

01:09:53.940 — 01:10:00.260 · Speaker 2
Pre-op is absolutely a real thing. It’s tough because prevention is difficult to study. So it’s more.

01:10:00.300 — 01:10:01.020 · Speaker 1
A really good point.

01:10:01.020 — 01:10:48.820 · Speaker 2
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, sidelining hip abduction exercises helps stave off the onset of something. So what I see for the shoulder, a lot of times the 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 protractor.

And a really good test to see how your shoulder blades working is to do a push up with a plus. So at the top of your push up, 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 ribcage and your shoulder blade to get that to work well.

So push up with the push that I like for the hips, a single leg stance squat.

01:10:48.820 — 01:10:50.900 · Speaker 1
So would that be a pistol squat.

01:10:50.900 — 01:10:55.090 · Speaker 2
So actually I prefer this like skater skater variety. So you’re you’re.

01:10:55.090 — 01:10:55.890 · Speaker 1
You’re. I know exactly.

01:10:55.930 — 01:11:11.290 · Speaker 2
Trail leg is behind you. 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 PMR residency here.

01:11:11.570 — 01:11:19.490 · Speaker 1
So and is this standard. So do all I do. All physical medicine and rehab physicians need to learn biomechanics.

01:11:19.530 — 01:11:21.170 · Speaker 2
Yeah it’s a huge element of our training.

01:11:21.210 — 01:11:22.130 · Speaker 1
It is a part of your training.

01:11:22.130 — 01:12:34.680 · Speaker 2
And I’ll tell you why. Because unless you understand normal biomechanics through the gate cycle, you can’t rehabilitate somebody with a stroke. Once they’re Hemi, once they have a foot drop, it’s really tough. So you have to know the normal mechanical, mechanical determinants of gait to understand the dysfunctional elements of it.

So I like to see how, you know, with regards to the gate 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 Meade 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 want to have 100% stiffness, but you want to have stability.

If you have a lot of hip movement when you’re walking, it’s oftentimes an indicator. Well, it’s not as not 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 my I always encourage young athletes. I’m like, if you have to focus on a couple things, it would be 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.

01:12:34.680 — 01:12:37.080 · Speaker 1
So all athletes are made in the legs?

01:12:37.120 — 01:13:31.360 · Speaker 2
Yes. And I believe that very strongly great pitchers have a good set of legs. They know how to really drive off. Um, 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’re going to be 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 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 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.

01:13:31.400 — 01:13:35.560 · Speaker 1
Do you think that everybody should continue to sprint or never lose that ability?

01:13:35.560 — 01:13:49.520 · Speaker 2
I would love for everybody to sprint. I think sprinting is 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.

01:13:49.630 — 01:14:06.109 · Speaker 1
And to be clear, actually, I evolved my hamstring doing a long stride sprint. Would you recommend people listening to this or thinking, because we’re going to cover zone two cardio and training because you and I really see eye to eye. Excuse me. Sure. About

01:14:07.950 — 01:14:44.190 · Speaker 1
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. Um, 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?

01:14:44.230 — 01:14:45.390 · Speaker 2
It’s absolutely fair to say.

01:14:45.430 — 01:14:56.629 · Speaker 1
Can we talk a little bit about, Um, well, I mean, let’s tie up the rest of Tennant because I’m curious about some

01:14:57.830 — 01:15:07.190 · Speaker 1
risk factors, which in my mind would include medication. Yeah. Common medications that may affect tendon health.

01:15:07.230 — 01:15:52.500 · Speaker 2
Yes. The first one that comes to mind is fluoroquinolones. So that’s like ciprofloxacin level fluoxetine. That’s a whole class of medications. Those are antibiotics. Um fluoroquinolones are very strongly linked with tendon problems and tendon rupture. Um 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, um, 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 Thelma’s 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.

01:15:52.500 — 01:15:54.900 · Speaker 1
But if they have.

01:15:54.940 — 01:15:55.220 · Speaker 2
If they.

01:15:55.220 — 01:15:59.940 · Speaker 1
Had that familial hypercholesterolemia. That’s right. But not if they just have high cholesterol.

01:15:59.980 — 01:16:25.900 · Speaker 2
It’s tough to say. It’s tough to say because hypercholesterolemia, diabetes, um, gout, these are gout, hyperglycemia are all risk factors for tendon apathy 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.

01:16:26.700 — 01:16:40.020 · Speaker 1
Um, 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.

01:16:40.060 — 01:17:17.210 · Speaker 2
Diabetes patients will rehabilitate more slowly than non-diabetic patients, and partly because tissue healing is slower. So as an excellent textbook that I came across that actually looks at all the metabolic influences on tendon empathy. 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 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 is is not as quick as it could be, or as as comprehensive as it could be in one tissue, there’s no reason to suggest that it’s going to be better than another.

01:17:17.210 — 01:17:21.810 · Speaker 1
So fluoroquinolones, yes, can cause a risk of tendon rupture.

01:17:21.850 — 01:17:22.330 · Speaker 2
Yes.

01:17:22.370 — 01:17:39.730 · Speaker 1
Which it’s really important that physicians educate their patients. Don’t go sprinting. Don’t go running when you’re on these statins. Statin may have a positive effect depending on the person. Yes. Um anything else that is known to affect tendon corticosteroids.

01:17:39.730 — 01:18:05.490 · Speaker 2
So corticosteroids if I had a great, um, a great attending while I was in residency. He said, if you 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, um, you know, your skin changes color and texture. Um, 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.

01:18:05.810 — 01:18:08.690 · Speaker 1
And also it’s important to point out its standard of care.

01:18:08.730 — 01:19:02.320 · Speaker 2
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 tendon and they’re getting a corticosteroid injection, that injection should be guided. It should be into the adjacent versa. You don’t want to put corticosteroid into a tendon. That’s not going to help anybody.

But if you’re putting in the adjacent Bursa, there’s theory that perhaps you’re going to anesthetize and kind of decrease the pain signals coming from those little nerve inlets that have actually grown into the into the tendon themselves. And if I get you some short term pain relief for three months, which is on average what we we cancel people for corticosteroids.

If I get you some short term pain relief and you can 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 rheumatology conditions.

01:19:02.360 — 01:19:04.760 · Speaker 1
And we’re talking about a prednisone a whole dose back.

01:19:04.800 — 01:20:20.430 · Speaker 2
That’s exactly right. Um, 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, um, and we can’t get them through PT because they’re in such a bad spot. We’ll use a medical dose pack.

Now medical itself is going to be absorbed by the body. The body. Your body does not know exactly where to disperse this medication. It’s going to be absorbed. It’s going to impact hormone production. It’s going to suppress natural production of things like testosterone and sex hormones. It’s going to 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 if you’re susceptible and you have a pre-dating injury and you go through a medical dose back and you go exert yourself, there is a potential that you can injure yourself. Now once again, risk benefit ratio in everything we do.

Um, 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 tendon, it’s been recalcitrant and 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.

01:20:20.470 — 01:20:21.910 · Speaker 1
Is pain worse at night?

01:20:21.950 — 01:20:33.630 · Speaker 2
Um, 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. So.

01:20:33.670 — 01:20:36.870 · Speaker 1
And is it because cortisol is lower? Why is why does that happen.

01:20:36.870 — 01:20:58.790 · Speaker 2
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 delt wakes up really sore.

And that’s because you’re compressing a tendon. Tendons like load. They don’t like compression.

01:20:59.070 — 01:21:01.430 · Speaker 1
Tendons like load. They don’t like compression.

01:21:01.430 — 01:21:03.950 · Speaker 2
That’s right. So same thing.

01:21:04.270 — 01:21:06.430 · Speaker 1
We’re learning a lot of really good one liners.

01:21:06.630 — 01:21:06.870 · Speaker 2
Over.

01:21:06.870 — 01:21:08.430 · Speaker 1
Here. Really really great.

01:21:08.470 — 01:21:29.390 · Speaker 2
There’s a um same thing. Somebody has a gluteal attendant on the side of the hip. Lying on that side will be very painful at nighttime. Extended compression on a tissue that’s irritated. You’re going to know about it. Um, somebody has an Achilles tendon problem. Shoe fits. Not correct. Or they. They tried say they were in the first time in cleats for a while, that they weren’t in cleats before.

You might inflame that area.

01:21:30.030 — 01:21:32.710 · Speaker 1
Um, any other medications that can be harmful?

01:21:33.190 — 01:21:35.070 · Speaker 2
Um, there’s perhaps more as well.

01:21:35.150 — 01:21:36.380 · Speaker 1
Um, but these are the big ones.

01:21:36.420 — 01:21:42.420 · Speaker 2
Those are the big ones. I think more about the in some circumstances, some of the hormone replacement. That’s helpful.

01:21:42.420 — 01:21:51.780 · Speaker 1
I was going to ask you I was going to ask you on the flip side of this, are there potentially oral agents or injectable agents that could be beneficial for tenant health?

01:21:52.100 — 01:22:07.020 · Speaker 2
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. Um, leucine? No surprise there has has been. I’m sure Lucien’s been on this podcast before.

01:22:07.060 — 01:22:07.980 · Speaker 1
No, never heard of it.

01:22:08.020 — 01:22:23.660 · Speaker 2
Yeah, right. So, um, leucine is is actually a component of a proteoglycan around tendons called Dickerson, 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.

01:22:23.660 — 01:22:29.420 · Speaker 1
Circuits good for muscle it’s probably good for tendon. I love this because we have really left tendon out of the conversation.

01:22:29.700 — 01:22:53.290 · Speaker 2
We’re back. We’re back to your to your neck of the woods and muscle. But the the interesting thing is we know that to some degree it’s a substrate driven issue. You do need adequate protein intake. It is a calamitous structure. Whether you absolutely need collagen because your college is going to 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 three intake has been associated with decrease in tendon.

01:22:53.650 — 01:23:00.330 · Speaker 1
And is that because of its impact. You know I always think okay, well what would the mechanism of action would that be an inflammatory perspective?

01:23:00.370 — 01:23:44.570 · Speaker 2
I think it’s the low grade anti-inflammatory aspect of the resolving pathway. Yep. So I think that that’s it. Now, um, and for that reason it’s important to point out a hallmark of tendon is expression of prostaglandin E2. And so for people who don’t know E2 is something that is present in acute inflammatory processes.

It’s why a lot of anti-inflammatory medications work. So megas act on the same aspect without a lot of the potential downsides. So I will counsel patients to take omega three 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. Vitamin.

01:23:44.610 — 01:23:46.330 · Speaker 1
Are there doses that we know of?

01:23:46.370 — 01:23:54.170 · Speaker 2
You know I’d have to 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.

01:23:54.210 — 01:24:02.970 · Speaker 1
And have you heard of I don’t know if you ever use these in clinic, but ESPN’s the specialized pro resolving mediators orally.

01:24:03.010 — 01:24:05.130 · Speaker 2
I’ve not used them. What is a.

01:24:05.170 — 01:24:19.290 · Speaker 1
Yeah I, I am not so sure on the data, but um, we’ve used them. Some of my colleagues have used them a lot with operators. Okay. But you and I will have to look at some of the, the actual data. But I am curious.

01:24:19.330 — 01:24:59.600 · Speaker 2
Yeah. And vitamin D can be helpful as well. So vitamin D has been proven to be helpful in tendon as well. Can help decrease some of the pain. Vitamin D, vitamin C and vitamin D deficient rats have decreased rotator cuff healing after 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 you came 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 tendon,

01:25:00.920 — 01:26:45.550 · Speaker 2
which is fascinating. Yes. Um, thyroid hormones, basically T3 and T4 play a role of stopping apoptosis or programed cell death in tendons in teno sites. So in your general contractors that are overseeing work on your tendon. So if you have insufficient thyroid hormone stimulating your 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. Um, the sex hormones are also interesting too. So, um, estrogen is the interplay of female sex hormones and what these deeply collegiate structures, like tendon and ligaments, is the subject of fascination for a whole body of literature.

So I don’t want to do them a disservice 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. And, um, in adolescent females who are are in the developing stage there and engaging in sport, that perhaps you could have a 2 to 6 times increased risk of ACL injury during specific phases.

And then we know in the postmenopausal population that tend to these tend to develop. So the absence of estrogen appears to be a problem. Um, same thing goes for a testosterone. Now testosterone there is a clear um, in that same postmenopausal puzzle population, the testosterone is going to decrease as well.

So testosterone appears to be beneficial for tendon where the where the conversation gets very interesting is are the testosterone analogs. Are the synthetic analogs detrimental.

01:26:45.990 — 01:26:56.870 · Speaker 1
And that’s a really good question. So basically what he’s saying is the use of certain anabolic steroids, um, going to injure tendons. I think it’s a really good question.

01:26:56.910 — 01:28:02.900 · Speaker 2
And the answer is they appear to be clearly do the use of them. The muscular 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 let’s say somebody starts on anabolic steroid regimen and they’re drastically increasing their muscle size.

Well the athletic adaptation curve does not change. You might not 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 does it or can it be something else? The from 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?

01:28:32.660 — 01:28:55.740 · Speaker 1
So there’s a great paper here. So this is this is titled is hormone replacing therapy associated with reduced risk of adhesive capsular itis in menopausal women a single center analysis. This came out 2023. And um I just think it’s so fascinating that, you know, there’s this domain of sports injury, and then there’s this domain of life.

01:28:55.740 — 01:28:57.260 · Speaker 4
What happens to women, what happens.

01:28:57.260 — 01:29:05.540 · Speaker 1
To women, life injury. And, um, you talk here about, uh, frozen shoulder and that typically hits women between 40.

01:29:05.580 — 01:29:05.980 · Speaker 4
40 and.

01:29:05.980 — 01:29:06.580 · Speaker 1
60.

01:29:06.620 — 01:29:34.810 · Speaker 4
Yeah. So I love the topic of frozen shoulder. It is definitely not sexy in the world of orthopedics. People like, have a woman coming in with frozen shoulder like, oh, I’m gonna see this person forever, or they’re going to be in pain. They’re not going to need surgery. But I love helping people with this problem.

Uh, you really can help people a lot. And actually just validating what’s going on with them is helpful. But, uh, so, yeah, typically occurs in women age 40 to 60. It was labeled as idiopathic forever. And you know what idiopathic means. It means we just don’t know.

01:29:34.810 — 01:29:36.210 · Speaker 1
What causes it. No. We’re idiots.

01:29:36.250 — 01:30:05.810 · Speaker 4
But how can it be idiopathic if this happens mostly in women and not in men? And in fact, if it happens in men, it’s almost always in someone with really poorly controlled diabetes. So that’s that’s a different situation. And of course diabetes is associated with high levels of inflammation. But so, you know, a low estrogen state is associated with high levels of inflammation.

And there are some really, you know, interesting animal studies that show, um, that, you know, the presence of these estrogen receptors in the synovial, um, you know, say, of the shoulder and that, um,

01:30:07.330 — 01:30:33.280 · Speaker 4
uh, applying estrogen, uh, to the the tissue of the lining of the shoulder can reduce levels of inflammation and reduce the fibrosis. And there’s an actual pathway. In a recent study, uh, looking at mice, showing how basically fibroblasts are activated without estrogen. And this is kind of probably what contributes to the the thickening and the scarring of the tissue around the shoulder joint.

01:30:33.880 — 01:30:37.720 · Speaker 1
But I say the shoulder right, as opposed to say, the hand or the wrist.

01:30:37.760 — 01:31:29.040 · Speaker 4
I have wondered about that. I don’t know if the shoulder joint perhaps has like an increased density of, um, you know, estrogen receptors or something. And it’s not always bilateral. But I will tell you, I have many patients that it hits one side. And then, you know, year later they’re back with the other.

But the good thing is, when it comes on the second side, they know right away. And if you’re developing a frozen shoulder, what happens is at first it’s really painful and not stiff. And then it gets stiff and painful and then it just gets stiff. And a lot of times what happens is people wait to come see you until it’s just super stiff and they’ve kind of suffered through the painful phase.

And at that point it’s a little bit hard to get rid of. You know, it kind of thaws out over a year. But if we catch you when you’re still painful and not stiff or painful and stiffening, Thing. It’ll respond really well to a steroid injection and kind of try to, you know, reverse or shorten the process. And usually when women have it on one side, they know right away when it’s happening on the the other side, how.

01:31:29.080 — 01:31:36.920 · Speaker 1
So someone listening to this and they just hit 40 and they’re thinking, oh my gosh, I do not want to get frozen shoulder. What are they. What are the signs.

01:31:37.520 — 01:31:56.880 · Speaker 4
It starts with usually no trauma. Um, sometimes people will call. This is, I would say, one of the more common things I was walking my dog and my dog really pulls on my arm. But it’s not anything you would think would like, you know, cause a trauma. And they often wake up just with pain. The pain is usually okay when you’re sitting, but it’s painful at the end range of motion.

01:31:56.920 — 01:31:59.320 · Speaker 1
Everyone’s sitting in your chair. Go ahead. Yeah.

01:31:59.560 — 01:32:34.910 · Speaker 4
And and, you know, look down. Move side to side. Do you have the same motion on each side? Uh, so the pain isn’t usually mid arc, but it’s kind of at the end of the arc. And like a classic sign of adhesive, capsular itis or frozen shoulder is pain and range of external rotation at the side. There’s really almost nothing else that causes that specific pain with that very minor motion.

Um, so then the other motion people will start to lose is they’ll say, well, it’s hard to reach across my body, like shaving under your opposite armpit or fastening a bra or tucking in a shirt. Those are the functional things people start to notice. But I’m always amazed that people don’t notice. I would lose notice if I lost like five degrees of motion.

01:32:35.070 — 01:32:42.150 · Speaker 1
But let’s be fair, what people don’t know is your Division one former Division one athlete and married to an orthopedic surgeon with five children.

01:32:42.190 — 01:32:43.190 · Speaker 4
And I’m an orthopedic surgeon.

01:32:43.350 — 01:32:43.470 · Speaker 1
Yeah.

01:32:43.670 — 01:33:20.100 · Speaker 4
So? So they don’t they don’t notice. But by the time they come in, they’ve usually lost the motion and they’re painful. Um, the other weird symptom people will say is, oh, my fingers feel tingly. Not like cervical, ridiculously pinched nerve down into my hand, but they’ll just have the vague sense that there’s this tingling sensation in their hand.

And then some people will have like also like lateral epicondyle itis because they’re basically what’s what they’re doing is now they’re just using their arm like, um, like T-Rex arms, like you’re just using everything from the arm down. So there’s probably some positioning. There’s probably some inflammation of the capsule around the shoulder, and maybe that spills over a little.

Bit to the plexus of nerves that go down your arm.

01:33:20.300 — 01:33:20.740 · Speaker 1
Wow.

01:33:20.780 — 01:33:36.460 · Speaker 4
But if you inject their shoulder, usually within three months of symptoms, um, things reverse really nicely. I can’t take credit for it, but the tingling feeling in the hand will go away. Usually the range of motion goes back, and occasionally you have to, like, inject them one other time.

01:33:36.460 — 01:33:38.940 · Speaker 1
But it is a full resolution.

01:33:39.220 — 01:33:55.660 · Speaker 4
Yeah. Pretty much if you catch it early. Um, it is, I would say, in all things orthopedic for use of a steroid injection. A glenohumeral joint injection with steroid is the best indication for steroid injection. I know people are afraid of steroids, but it can really save you.

01:33:55.740 — 01:33:56.500 · Speaker 1
Not this crowd.

01:33:56.620 — 01:34:02.420 · Speaker 4
Well, yeah, it could save you. Yeah, it can save you a couple of years of, you know, thawing out. No, I.

01:34:02.420 — 01:34:15.340 · Speaker 1
Have I have a question. Um, you said that one of the reasons is because there’s a decrease in estrogen and you treat it not with injectable estrogen. right? Well but.

01:34:15.420 — 01:34:38.460 · Speaker 4
Yeah, I would I would love to do a study of let me see that the study I would love to do is apply an estrogen patch right here. But that is very off label use of transdermal estrogen. So estrogen, you know, menopausal hormone therapy including transdermal estrogen is FDA approved for symptoms, you know, vasomotor symptoms of menopause and for prevention of osteoporosis.

01:34:38.500 — 01:36:08.970 · Speaker 1
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01:36:19.880 — 01:36:32.800 · Speaker 1
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01:36:33.120 — 01:36:49.880 · Speaker 4
Uh, luckily, I’m so glad it’s approved for that because it’s very helpful with that. But it’s not approved for my allergies. Um, joint inflammation, you know, poly arthralgia. Um, even though there’s mounting evidence that there’s so much inflammation associated with menopause. Joint pain.

01:36:49.920 — 01:36:51.280 · Speaker 1
Do you know anyone that’s doing it?

01:36:51.320 — 01:36:52.520 · Speaker 4
Um, well.

01:36:52.520 — 01:36:54.160 · Speaker 1
I enter articular.

01:36:54.200 — 01:37:06.000 · Speaker 4
Will not enter articular, but I will tell you, I have a very close working relationship with my colleague, Doctor Anne Ford. At Duke Women’s Health, we are literally across the hall from each other. And.

01:37:06.000 — 01:37:08.120 · Speaker 1
And did you inject our shoulder with estrogen?

01:37:08.560 — 01:38:09.910 · Speaker 4
Knight and injection. We’ve definitely helped each other. She’s had an early round of frozen shoulder and eye. She came right over and I injected her shoulder and I. This is unbelievable. As someone who studies adhesive capsule itis. I mean, I’m an almost 47 year old female orthopedic surgeon, but I, um, a few weeks ago, I had adhesive capsule itis.

Of course, you know, I diagnosed myself, but it was classic pain and range of motion. Then I couldn’t reach across my back. It was front to back, deep in my joint. And, you know, I called her right away, and I was like, well, number one, I had my glenohumeral joint injected. Number two, I was like, it’s time for me to go on transdermal estrogen because I’m perimenopausal and I don’t want to bottom out.

So I’m. Yeah. So we joke around. It’s it’s definitely an off label use. And I’m not saying that every single person that gets frozen shoulder should go ask for an estrogen patch, but but, um, we know the basic science of estrogen receptors in synovial.

01:38:10.150 — 01:38:12.190 · Speaker 1
We know it’s a fascinating conversation.

01:38:12.230 — 01:39:30.860 · Speaker 4
I mean, even like the Women’s Health Initiative studies, they showed that estrogen. So so they had a study where 77% of menopausal women in their study had joint pain. And when treated with menopausal hormone therapy with estrogen, there was significant decrease in joint pain, a number of joints that were painful and severity of joint pain.

And when the therapy was stopped, there was, um, you know, some some there’s some increase in the pain. So, you know, there are studies that are not new that that show this, you know, ameliorating effect of estrogen on joint pain. Um, and we know that women are disproportionately, again, affected by arthritis.

It’s kind of like a geometric proof. It’s a matter of putting all these things together. But it’s definitely not an FDA approved indication. But there’s a, you know, a lot of menopausal women will present with, um, with joint pain. So, yeah, I’m now I have my transdermal estrogen patch and I’m hoping to stay on that.

I’m on the moderate dose. And then you go into menopause and then you, you know, go up on your dose. But I just I don’t want to get osteoporosis and I don’t want to get frozen shoulder.

01:39:31.660 — 01:39:33.420 · Speaker 1
Come on. You gotta be you gotta operate.

01:39:33.460 — 01:40:06.300 · Speaker 4
But so sometimes I’ll have a patient. Let me tell you, sometimes I have a patient who’s recalcitrant to things like they’ve had a steroid injection and it’s still hurting. Um, and they’re also telling me I have night sweats and I’m depressed and I can’t sleep, and so they need to go see a women’s health doctor anyway.

But one of their other symptoms is they have a frozen shoulder and I send them to an and then she, you know, treats them. But um, so yeah, I’m not and I Caveat I’m not a women’s health doctor. I’m an orthopedic surgeon.

01:40:06.340 — 01:40:12.180 · Speaker 1
Yes, yes. But you’re a very progressive, forward thinking orthopedic surgeon. Um,

01:40:13.420 — 01:40:26.940 · Speaker 1
the estrogen and arthritis. We talked about adhesive capsular itis, which is kind of this inflammation, this shoulder. Right? Yeah. Doesn’t seem to happen to men, if nearly at all. I mean, unless.

01:40:26.940 — 01:40:28.260 · Speaker 4
They have poorly controlled diabetes.

01:40:28.500 — 01:40:32.660 · Speaker 1
Typically, which is, uh, a good portion of the population.

01:40:32.700 — 01:40:32.940 · Speaker 4
Right?

01:40:33.500 — 01:40:54.740 · Speaker 1
Right. We have to say, uh, say that, um, but is there a level someone comes in and they don’t know that there are menopause? Maybe they’re not up to date with their blood work or they’re not tracking their periods. Or maybe they are on an oral contraceptive or have a Marina or something so they’re not aware.

Yeah. They present with frozen shoulder.

01:40:54.900 — 01:40:55.340 · Speaker 6
Mhm.

01:40:56.300 — 01:41:11.730 · Speaker 1
The individual figures out that they need hormone replacement. Is there a particular. Okay, so I understand that you’re a surgeon, but I’m just curious if someone were like, okay, well, what would be the number that we shoot for in the blood? Or is it just. Oh, blood.

01:41:11.730 — 01:41:37.530 · Speaker 4
Work? Yeah, the blood work is, um, again from my work with my women’s health partners, as I understand it is not a great tool because it’s so, um, the, the issue with hormone levels and perimenopause is that they’re actually kind of changing and irregular and, you know, they’re chaotic. And so really, they they rely heavily on symptoms, not not blood levels.

Yeah. Yeah.

01:41:37.570 — 01:41:42.130 · Speaker 1
Which is interesting because for men there’s a total testosterone a free testosterone, right.

01:41:42.410 — 01:41:42.970 · Speaker 4
Every guy.

01:41:44.090 — 01:41:44.490 · Speaker 4
Yeah. Yeah.

01:41:44.530 — 01:41:49.850 · Speaker 1
Every guy I know is, you know, my husband’s like, where’s my testosterone? What’s 900? What’s what’s my free testosterone?

01:41:49.850 — 01:41:53.050 · Speaker 4
The range is so broad and yeah I know. Yeah. So yeah.

01:41:53.090 — 01:42:47.210 · Speaker 1
You know, as we try to draw correlations to set up a paradigm of thinking, right. This framework of thinking about Out. Musculoskeletal issues with menopause. Metabolic issues with menopause. And, yeah, um, you know, really begs the question. What I find fascinating is that, you know, I worked on some of the early studies of postmenopausal women and body composition changes, and we corrected for diet and exercise, and we saw amazing resolution of body fat.

And when I say resolution, they lost weight. They were able to maintain lean muscle mass. And I think within the traditional nutritional science world, people, um, when when diet and exercise are corrected for we see that body composition can be managed. However, when we really begin to think outside the box, the influence of these hormones, because women are saying over and over again that they go through menopause and their body composition changes.

01:42:47.250 — 01:42:47.530 · Speaker 6
Yeah.

01:42:47.570 — 01:42:52.050 · Speaker 1
And that they’re having joint pain and they’re having all of these other symptoms.

01:42:52.050 — 01:42:54.090 · Speaker 4
Right. Increased visceral fat. Exactly.

01:42:54.290 — 01:43:07.280 · Speaker 1
And so it just it just begs the question, do we, You know, what is it that we know? And how can we redefine our treatment protocols for people? Um, um, you know, obviously we’re not there yet.

01:43:07.320 — 01:43:09.160 · Speaker 6
Yeah, it’s it’s really fast.

01:43:09.200 — 01:43:47.000 · Speaker 4
And we’re learning more and more about fat, body fat as being inflammatory, like, you know, um, fat has, uh, lipo genes, which are basically, you know, a, uh, something that stimulates, um, inflammation and elevates inflammatory markers. And in obese patients, we know that they’re, you know, more likely to have arthritis, but not just in weight bearing joints.

So, um, so, so patients who have obesity, you would think, oh, this is just mechanical overload of the cartilage. That’s why they’re getting more arthritis. And we know that’s true.

01:43:47.000 — 01:43:47.720 · Speaker 6
Definitely what.

01:43:47.720 — 01:43:48.040 · Speaker 1
We would.

01:43:48.040 — 01:43:49.120 · Speaker 6
Think. Yeah.

01:43:49.120 — 01:43:53.160 · Speaker 4
But they also have more arthritis and non weight bearing joints.

01:43:53.600 — 01:44:03.790 · Speaker 1
Um tell us what arthritis is. And the number one question we get is not that we get, but one of the questions that we get is does running really cause arthritis we talked about or is that a myth?

01:44:03.830 — 01:44:12.030 · Speaker 4
Yeah. So what is arthritis? And actually explain this in my book because I think people just don’t understand what arthritis is.

01:44:12.070 — 01:44:13.630 · Speaker 1
What’s the name of your book? Will you share it for us?

01:44:13.670 — 01:44:15.550 · Speaker 4
Yeah. The complete bone and joint health plan.

01:44:15.590 — 01:44:18.350 · Speaker 1
And when does that book come out? And where is my copy?

01:44:18.710 — 01:44:21.670 · Speaker 4
Oh, yeah. They should send you one. I’ll get you. Yeah. I want to get you.

01:44:21.670 — 01:44:23.590 · Speaker 1
A signed copy, please. Okay.

01:44:23.630 — 01:44:35.670 · Speaker 4
All right. Um, so, uh, and also I want to add coauthored with my lifelong friend and colleague Sidney Gorski, who is, um, a dietician, but. So.

01:44:35.710 — 01:44:36.710 · Speaker 1
So we got to have her on.

01:44:36.750 — 01:45:11.390 · Speaker 4
Yeah, I know we’re gonna have to come back with her. You would love her, but. But, um. Yeah. So what arthritis is, is, uh, basically gradual loss of the cartilage, which is the smooth gliding surface of joints. And over time, the cartilage gets thinner. Um, the body forms bone spurs called ostia. Fights along, you know, the edges of the joint.

You get inflammation and thickening of the lining of the joint called the synovial. Then you get like some stiffness, loss of range of motion. Um, usually.

01:45:11.390 — 01:45:13.790 · Speaker 1
The cartilage changes because it doesn’t glide as well.

01:45:13.830 — 01:45:40.430 · Speaker 4
Well, no, it’s probably so this is very confusing. It’s multifactorial. So then also there’s different types of arthritis. So osteoarthritis we think of as wear and tear or arthritis that you just develop over time as you age. And that even has multiple components. Some of it is loading like biomechanical um, and some people are just built badly.

Like if you’re really bow legged or knock kneed or whatever, you’re going to overload parts of your joint and they’re going to wear out sooner.

01:45:41.030 — 01:45:42.110 · Speaker 1
Or if you have hip dysplasia.

01:45:42.150 — 01:45:46.030 · Speaker 4
Or you could have a badly shaped joint. Thanks, dad.

01:45:46.070 — 01:45:46.550 · Speaker 1
Yeah.

01:45:46.590 — 01:46:01.020 · Speaker 4
But, um, and there’s a little bit of a biochemical factor. So even in osteoarthritis, which is, considered wear and tear. We see these elevated inflammatory cytokines in joints like interleukin one six tumor necrosis factor alpha.

01:46:01.020 — 01:46:02.260 · Speaker 1
Within the joints.

01:46:02.300 — 01:46:02.900 · Speaker 4
Yeah, like.

01:46:02.900 — 01:46:03.620 · Speaker 1
Systemically.

01:46:03.660 — 01:46:58.090 · Speaker 4
Systemically and in the joints. Um, and there are different cell types that are activated. And there’s like a kind of a cascade of reactions that leads to breakdown of the, um, cartilage and also, um, cell death of the condor sites, which are the cells in cartilage. Um, but so in osteoarthritis is probably a combination of biomechanical and, and a little bit inflammatory.

But then on the other extreme, you have entirely inflammatory arthritis like rheumatoid arthritis or psoriatic arthritis, where these these people have very high levels of inflammation. It’s autoimmune. The same, um, bad acting cytokines are in their joints and affecting their cartilage, but they’re at much higher levels like the same IL one and six and TNF alpha.

And then somewhere in between you’ve got probably like what? Menopause. Arthritis is where you have.

01:46:58.170 — 01:46:59.050 · Speaker 1
Is that a thing?

01:46:59.210 — 01:47:28.569 · Speaker 4
Well, I think it’s a thing, but maybe not everybody thinks it’s a thing, but it’s basically where you have now. You have a combination of yes, you’re over 50. Um, but there’s an acceleration of the inflammation, higher inflammatory markers and, and, um, more signaling of that pathway that leads to cartilage breakdown, um, you know, faster loss of the thickness of the cartilage over time, you know, differences between men and women.

So

01:47:29.610 — 01:47:37.930 · Speaker 4
there’s probably an interplay between inflammation and then, you know, the biomechanics of aging in women that’s different than in men.

01:47:38.530 — 01:47:44.370 · Speaker 1
Uh, so men get arthritis. What percent less than women?

01:47:44.890 — 01:48:21.050 · Speaker 4
Uh, women are 30% more likely than men to have arthritis. And that doesn’t even up again until we reach age 80. Women are more likely to need a knee replacement than men. Also, women are more likely. This may not surprise you to present farther into the disease process than men, so we’re probably actually underestimating the sex based difference so women don’t come in for their knee arthritis until it’s like, much worse.

You know, the x ray looks worse. They have more symptoms. Um, so they’ve been like kind of delaying treatment. So we’re probably underestimating the difference.

01:48:51.320 — 01:48:56.840 · Speaker 1
So as the listener is thinking, well, how do I know if I have a tenant? Should I go get an x ray? You would not go get an x ray.

01:48:56.880 — 01:49:53.990 · Speaker 2
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 going to 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 going to help me formulate a therapeutic exercise routine for this person. On the topic of you know, not if it’s when it’s it’s a it’s a tough pill to swallow.

01:49:53.990 — 01:49:55.390 · Speaker 1
I know, and I hate to say it.

01:49:55.430 — 01:50:02.150 · Speaker 2
It’s and I hate to say it as well, because I do believe I’m one of those people. It’s like in the ideal circumstance, could we avoid it?

01:50:02.190 — 01:50:07.150 · Speaker 1
Yes. If you didn’t do anything you absolutely could avoid.

01:50:07.350 — 01:50:21.590 · Speaker 2
But but in that case, you’re going to 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 loading, I think we can do a lot for injury prevention.

01:50:21.590 — 01:50:31.350 · Speaker 1
And we know what normal mechanics are, despite the fact that everyone has different arm lengths and different leg lengths. Yes, there are standards of mechanics.

01:50:31.390 — 01:51:15.070 · Speaker 2
There is. 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 like. And these are all these are all Gaussian distributions, bell curves. So you’re going to 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 rotation, 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.

01:51:15.070 — 01:51:19.190 · Speaker 1
For example, um, raise your arm up.

01:51:19.190 — 01:51:19.790 · Speaker 2
Yeah.

01:51:20.030 — 01:51:22.830 · Speaker 1
Like is this strong? Can you push it against.

01:51:22.870 — 01:51:37.070 · Speaker 2
Exactly. And what I, what I like to look at is, um, say I’m examining somebody’s hip and I’m going to 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.

01:51:37.790 — 01:51:39.990 · Speaker 1
Weak versus strong. Mobile versus stiff.

01:51:40.030 — 01:52:15.020 · Speaker 2
Yeah. So to give you an for for instance of who kind of fits in each category. So for our elderly patients who have unfortunately accommodated a lot of a lot of time, and where they are most often stiff and weak, so joint ranges of motion decreased with time, you get calcification of soft tissues. Your joint capsules harden a little bit.

We 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.

01:52:15.420 — 01:52:17.900 · Speaker 1
You hear a lot about that. People are very hyper mobile.

01:52:17.940 — 01:52:18.580 · Speaker 2
Yes.

01:52:18.980 — 01:52:22.220 · Speaker 1
And it’s interesting to hear. But as they age that they would stiffen.

01:52:22.260 — 01:52:42.050 · Speaker 2
Yeah, just about everybody’s stiffness 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 hyper mobile a patient. So hypermobility does come.

It doesn’t. It’s not always a dedicated Ehlers-Danlos diagnosis. We have something called the Biton score.

01:52:42.090 — 01:53:00.490 · Speaker 1
That you should mention Ehlers-Danlos, because there 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.

01:53:00.490 — 01:53:15.130 · Speaker 2
So there is a good evidence based score. It’s called the bite and score that can actually be, um, that can be performed in the office to test for hypermobility. And what we look at is can you bend down to the floor, touch your palms on the floor, can you bend your pinky back and then greater than 90 degrees.

01:53:15.170 — 01:53:17.210 · Speaker 1
Everyone’s gonna be trying it. Yeah. Go ahead Mia.

01:53:17.250 — 01:53:27.410 · Speaker 2
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 um, so when we think about.

01:53:27.570 — 01:53:28.610 · Speaker 1
It’s not treatable. Correct.

01:53:29.250 — 01:53:33.810 · Speaker 2
To the degree. Yeah. So it can be treatable with modifiable with exercises. And I’ll explain that in.

01:53:33.810 — 01:53:34.010 · Speaker 1
A more.

01:53:34.050 — 01:53:41.730 · Speaker 2
Wonderful. But you know these are things these are relative not absolutes. So you’re mobile and weak patients are most commonly hyper mobile.

01:53:42.450 — 01:53:44.450 · Speaker 1
The mobile and weak.

01:53:44.490 — 01:54:09.210 · Speaker 2
Yeah. So on the on the two by two. Stiff and weak is elderly your mobile and weak or hyper mobile. Now stiff and strong or stiffer and strong is like an offensive lineman. If you examine an offensive lineman tips, they’re not going to rotate a whole bunch, but they’re as strong as heck and they can put the power down.

So that’s stiff and strong. Stiff and strong is not a bad place to be. Um, then your mobile and strong, those are your Michael Jordan’s.

01:54:09.290 — 01:54:10.530 · Speaker 1
Those are the people and strong.

01:54:10.570 — 01:55:11.000 · Speaker 2
That’s that’s the that’s the grail. 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 actively activate muscles to protect my body in that range of motion. It’s just range of motion for range of motion sake.

Not all mobility is uniformly beneficial, in my opinion. I believe that if you’re going to 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 is 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 and play much more of a role there. So whether you’re hyper mobile 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 going to influence.

01:55:11.120 — 01:55:12.320 · Speaker 1
I didn’t know that. Yeah.

01:55:12.360 — 01:55:13.600 · Speaker 2
Just broadly.

01:55:13.600 — 01:55:14.520 · Speaker 1
Speaking okay.

01:55:14.560 — 01:55:17.200 · Speaker 2
Broadly speaking. Um, so these are,

01:55:18.520 — 01:56:22.440 · Speaker 2
these are these are some determinants that are going to predict some of the soft tissue extensibility and then the the mobility aspect and really how stable you are, a huge element of that is that that same neuro kinetic 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 is 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 you’re 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 to achieve everyday life. And that’s why the the concept of stretching is a very interesting conversation to have.

What we’re achieving with stretching is a very interesting conversation to have.

01:56:22.480 — 01:56:36.030 · Speaker 1
Should we do it? This is going to bring me to the yes or no section. Oh dear. Okay. So you’re not going to like this because you’re very academic. But I’m going. You can only answer yes or no. Okay. Pilates.

01:56:36.070 — 01:56:36.710 · Speaker 2
Yes.

01:56:36.750 — 01:56:38.110 · Speaker 1
Steroid injections.

01:56:38.150 — 01:56:38.710 · Speaker 2
Yes.

01:56:38.750 — 01:56:39.670 · Speaker 1
Zone two.

01:56:40.110 — 01:56:40.790 · Speaker 2
Sure.

01:56:42.710 — 01:56:46.790 · Speaker 1
We’ve never had a guest answer. Sure. Ever.

01:56:46.830 — 01:56:48.870 · Speaker 2
I think it’s beneficial. I think it’s a question.

01:56:48.910 — 01:56:49.110 · Speaker 1
Not.

01:56:49.150 — 01:56:52.150 · Speaker 2
Not the question. Is the dose, the type and the what?

01:56:52.270 — 01:56:53.630 · Speaker 1
This is very difficult for people.

01:56:53.670 — 01:57:00.350 · Speaker 2
I always this is why. This is why I’m not on the hill. Okay. If I wanted to. If I wanted yes or no. I’d be a politician. Fair.

01:57:00.670 — 01:57:01.390 · Speaker 1
Yoga.

01:57:01.750 — 01:57:05.310 · Speaker 2
Um. Mhm. Whoa! Yeah.

01:57:05.470 — 01:57:08.710 · Speaker 1
I love this section of the podcast. Yeah. Is that a yes or no?

01:57:08.750 — 01:57:15.550 · Speaker 2
I’m not, I’m not. No. And I’m not. Yes I’m gonna bow out of that one. I’m going to use my fifth amendment on that one.

01:57:15.590 — 01:57:17.590 · Speaker 1
This then leads me to stretching.

01:57:17.910 — 01:57:24.550 · Speaker 2
Um, stretching can be beneficial. Okay. So it’s not uniformly beneficial. The question is what you’re trying to achieve with it.

01:57:24.550 — 01:57:53.500 · Speaker 1
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 Hamada. He’s my coach and my sister said, you know, we are done working out. We should stretch. I’m like, for what are we stretching?

Why are we doing this? And then I said, I’m going to talk to Doctor 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.

01:57:53.540 — 01:58:14.140 · Speaker 2
Oh, well, let’s let’s see. So there is this is one of those topics that I, 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 going to give it a shot for you. So stretching, proactivity, decrease neuromuscular firing, decrease stability. Not beneficial for power athletes.

01:58:14.700 — 01:58:16.340 · Speaker 1
And can we define power athletes.

01:58:16.340 — 01:58:32.660 · Speaker 2
So uh pitcher pitcher um shot putter um elite power lifter. Um, you could even throw fighters in there. That’s a powerful sport. So you’re producing power is force over time. So you’re going to produce a force over a very short period of time. So

01:58:34.100 — 01:58:37.700 · Speaker 2
static stretching. Probably not beneficial for anything.

01:58:37.740 — 01:58:38.860 · Speaker 1
Or just we’re talking about power.

01:58:39.140 — 01:59:07.180 · Speaker 2
Pre pre pre exercise for power generation now. Stretching. There are different categories. There’s static stretching. So I’m going to hold a pose for a while. Typically 20s or more and hopes to elongate the tissue. Now you’re not just stretching the 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.

01:59:07.220 — 01:59:09.860 · Speaker 1
Are these the Golgi spindle virus?

01:59:09.900 — 01:59:11.540 · Speaker 2
Yeah. So Golgi, just curious.

01:59:12.380 — 01:59:13.220 · Speaker 1
If I remembered anything.

01:59:13.260 — 01:59:41.450 · Speaker 2
Yeah. So the Golgi is interesting. Um, you know, the the other apparatus are also interesting, but the 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 even like with an isometric or let’s say you’re going to do a heel drop and just hold it there, that could have some benefit now.

01:59:42.210 — 01:59:44.490 · Speaker 7
For power or for.

01:59:44.690 — 01:59:46.090 · Speaker 2
For recovery, for recovery.

01:59:46.130 — 01:59:46.930 · Speaker 1
For recovery.

01:59:46.970 — 01:59:59.570 · Speaker 2
Yeah. Now I say a lot of I’m going to heavily wait the May here. Okay. Because I think it may help. But I’m also going to tell you from a personal aspect I don’t do it. So I think it’s important to note that I don’t.

01:59:59.570 — 02:00:02.010 · Speaker 1
Neither does my husband. I’ve never seen that guy stretch.

02:00:02.050 — 02:00:23.130 · Speaker 2
He’s he’s a smart man. So. So, um, now if you’re going to if you’re going to stretch with a hope to teach your muscles how to engage at a larger range of motion than you do, so proprioceptive neuromuscular facilitation. And the answer for that is CNF.

02:00:23.410 — 02:00:27.800 · Speaker 1
PNF, proprioception, neuromuscular facilitation.

02:00:28.080 — 02:00:53.760 · Speaker 2
So PNF is a process by which okay, so I’m going to um, I’m going to stretch say my hamstring and somebody’s going to push against my leg, and I’m going to actually try to contract my hamstring at a larger length than than I did pre stretch. And then I’m going to stretch from there. And so there’s typically these on off cycles like a ten second isometric at a one length ten second stretch at another.

And you can do that now.

02:00:54.080 — 02:00:55.760 · Speaker 1
And the benefit of that is.

02:00:55.760 — 02:01:05.760 · Speaker 2
The benefit of that is you are you’re teaching somewhat that the muscle can relax at a larger length. Okay. So whether pre pre exercise or post exercise I’m not clear on.

02:01:05.760 — 02:01:11.399 · Speaker 1
And this seems to work with a lot of people do it with pain. Is that so is

02:01:12.680 — 02:01:13.200 · Speaker 1
used.

02:01:13.200 — 02:01:13.840 · Speaker 7
For.

02:01:14.000 — 02:01:16.720 · Speaker 1
Mitigation of pain to a muscle or.

02:01:17.040 — 02:01:49.800 · Speaker 2
Yeah it’s used it’s used in rehab. So it’s used by uh physical therapists and Atkins and other people who um who will rehabilitate patients. so it’s definitely part of it. When I design a physical therapy protocols for patients, I like eccentrics for lengthening. So once again, eccentrics. Your muscle is contracting periodically or mitigating that 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. We are also gliding the facial layers. So here’s another.

02:01:49.800 — 02:01:50.840 · Speaker 7
Way that you brought this up.

02:01:50.840 — 02:01:52.600 · Speaker 2
So here’s here’s fascia from another.

02:01:52.640 — 02:01:55.080 · Speaker 1
That’s it. Would you consider that an organ system.

02:01:55.160 — 02:02:01.280 · Speaker 2
Uh it’s interesting. It’s part of the musculoskeletal system, but it’s so richly innervated. It’s so large, it could be its own category.

02:02:01.320 — 02:02:02.480 · Speaker 1
What is fascia?

02:02:02.560 — 02:02:06.920 · Speaker 2
Fascia is interconnected connective tissue that can run the entire length of the body.

02:02:06.960 — 02:02:07.760 · Speaker 7
Incredible.

02:02:07.800 — 02:02:12.320 · Speaker 2
Here’s why we don’t get taught about fascia as much as we could. We should be.

02:02:14.040 — 02:02:20.399 · Speaker 2
A lot of it is almost as if we during the process of medical school, when we dissect

02:02:21.880 — 02:02:22.720 · Speaker 2
cadavers.

02:02:23.630 — 02:02:24.670 · Speaker 1
It’s gross.

02:02:24.670 — 02:02:26.070 · Speaker 2
It’s necessary.

02:02:26.110 — 02:02:27.870 · Speaker 1
And it’s absolutely disgusting.

02:02:27.870 — 02:02:34.670 · Speaker 2
It’s also, um, important. It’s important. Yeah. And thank you to everybody who donates their who donates their bodies to science.

02:02:34.670 — 02:02:37.590 · Speaker 1
It’s incredible that people are willing to do that.

02:02:37.630 — 02:02:51.310 · Speaker 2
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.

02:02:51.790 — 02:02:52.510 · Speaker 7
You did.

02:02:52.710 — 02:02:53.510 · Speaker 1
You were just.

02:02:53.550 — 02:02:55.390 · Speaker 2
Hey, and I wasn’t in Italy. It just happened.

02:02:55.430 — 02:02:56.310 · Speaker 1
You were just thinking.

02:02:56.350 — 02:02:56.950 · Speaker 7
I spoke to.

02:02:56.950 — 02:03:24.540 · Speaker 2
So I spoke to somebody. Um, basically, because ultrasound is one of the main ways to evaluate fascia in the living specimen. So there is specific cadaveric preservation techniques for preserving fascia. But one of the reasons we don’t really understand it or appreciates 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 ritually integrated structures in the body. That means the most nerves.

02:03:24.580 — 02:03:26.580 · Speaker 1
Does it have pain? So does it feel you feel pain?

02:03:26.660 — 02:03:40.540 · Speaker 2
People feel myofascial pain. I believe it is a it’s part of the diagnostic spectrum of pain. So you have a muscle that hurts. You can have a tendon. It hurts. You have a joint that hurts. You could have a ligament that hurts. And fascia also can hurt. In my opinion.

02:03:40.540 — 02:03:46.220 · Speaker 1
I feel it. If someone were to say, would that have anything to do with, um, fibromyalgia?

02:03:46.460 — 02:06:51.759 · Speaker 2
It’s interesting. Yeah. So the the concept around fibro is um, I think it’s part of it. The fascia is part of the issue. Um, but we also see myofascial pain and people who don’t have fibro, you know, and so we see myofascial pain and overuse syndromes, a very common myofascial pain that perhaps some people will experience is if if they have a pretty large asymmetry in their hips, how their hips move and function, they feel a lot of myofascial pain in like 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.

So. And he the foreword was written by Stu McGill. So it talks about facial 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 in pain? How much of 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 neuro kinetic level there. There’s changes at the muscle level there. Presumably there are some changes at the facial 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 towards a specific goal because on some level or another, your entire body is adapting to that stressor. So you always have to keep that in mind of when you’re training an athlete, you can’t all be treated the same, not any exercises uniformly, the perfect one for everybody, for their specific needs.

You have to you have to do an individual needs assessment for that patient. So fascia is very interesting. Um, we do visualize it on and specifically where fascia are, where the small nerves like say for instance, the nerves that talk to the the muscles of the back fascia are the facial 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, um, 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 in tendons. So

02:06:52.960 — 02:07:11.280 · Speaker 2
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. My 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.

02:07:12.840 — 02:08:20.470 · Speaker 1
Really? Well said. I’m learning just so much. 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 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 3 to 4 days a week. There’s 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 going to leave that for you to take it wherever that you’d like to.

02:08:20.510 — 02:09:01.149 · Speaker 2
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

02:09:02.270 — 02:10:04.070 · Speaker 2
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 max muscle mass help predict how they do. And we know that quality of life, mortality and morbidity.

The more fit you are from a cardiorespiratory 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 going to 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 suboptimal VO2 max, but it’s their first time doing a certain athletic activity.

They’re never going to be you’re going to be gassed. If if I even if even if I’m a marathon runner, if you throw me into a boxing ring, I’m going to be gas in two rounds, because.

02:10:04.110 — 02:10:06.390 · Speaker 1
You might be amazing, but not a normal person.

02:10:06.590 — 02:11:16.290 · Speaker 2
But, um, the truth is, I would be gassed guest and the. It’s because I’m not familiar with the movements. It’s the way that I should be. So it’s important. That’s an important caveat. Don’t get down in 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 a familiarity with the movement.

If you’re on a bike. There are so many determinants of how your performance on a bike. Absolutely. Your positioning, your familiarity with it, what muscles you’re activating your shoe angle with, with, with, with the actual pedal. And I’m out of my league there. I know that that’s that 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 I think.

02:11:16.330 — 02:11:20.050 · Speaker 1
And you have two children and a beautiful wife and a full practice.

02:11:20.090 — 02:13:00.530 · Speaker 2
Yes. And time is tough. So I, I don’t engage in a ton of zone to myself. If I had more time in the week, perhaps I would. But then high intensity, high intensity interval training appears to be as beneficial for VO2 max as 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, right? You’re just you’re getting better at pushing it higher. But the the 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 1 or 2 times a year, they’re in really good shape. So same principle applies to weight training.

So or should we or could we be going to neuromuscular failure if our goal is muscle hypertrophy. Should we be focusing on just muscle hypertrophy and specific muscle segments or generalized strength instability. I think these are good questions, but the I, 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.

Um, most of the time it’s in one hand, and that by nature destabilizes you and you’re not going to get destabilization if you’re working only with barbells. So if.

02:13:00.530 — 02:13:03.770 · Speaker 1
You’re not going to get destabilization working with barbells.

02:13:03.810 — 02:14:01.440 · Speaker 2
Only, you know as it relates. Right. As it relates to the frontal and the transverse plane. So you’ll be 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 like things would hurt and I’d be like, well, well that’s interesting. You know, 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 the work from the strong first organization and and Dan John online in his own endeavors have done a great job elucidating the cardiorespiratory benefits of kettlebells that you can get strength and conditioning. And so I try to follow that I, I also do something and we spoke about this, this term exercise snacks, which I don’t particularly love, but.

02:14:01.440 — 02:14:03.270 · Speaker 1
I don’t either I but I can’t think of it.

02:14:03.310 — 02:14:05.590 · Speaker 2
We’ll find a way to rebrand it. But, um.

02:14:05.590 — 02:14:06.270 · Speaker 1
Definitely.

02:14:06.310 — 02:14:50.350 · Speaker 2
Yeah. Um, I call it farmhand strength. So, like, if you’re working on an outdoor, let’s say you’re not a farmhand. Let’s say you’re just somebody mulch in your yard. You’re not going to, um, basically go to the point where you’re falling down every single time. You’re going to leave a little bit on the table, you’re going to come back to it, you’re going to go to a different activity for a short period of time, and then you’re going to come back to it.

And so what I’ll do, what I’ll do is I’ll intermix like some sets of kettlebell swings throughout the day. I might do a set at 9 a.m. and do a set at 1030. I’m not looking to build a sweat, I’m just looking to get better at the movement. So I’m really stressing that neuro kinetic element. Am I getting more? 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, you know, a skin ripping pump out of it.

02:14:50.350 — 02:14:53.030 · Speaker 1
But potentially you could build a workout like that.

02:14:53.110 — 02:15:50.710 · Speaker 2
Yeah, there’s a, there are. You know, when we look at some of the really good people who are training, and what they do, and a lot of the rehabilitation from injury. Sometimes it’s three, five, ten minute rests, you know? And so the question becomes I think in there is do you want to be really. Do you want to be super proficient with the 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 23.5 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, and their jobs can do that, and some people unfortunately can’t do that. Um, but I like, like, you know, I saw you both do a set of push ups before as its own little stimulant prior to the podcast.

02:15:50.750 — 02:15:55.229 · Speaker 1
That’s our, um, pre-game push up. There you go. We do a

02:15:56.550 — 02:15:57.790 · Speaker 1
now podcast ritual.

02:15:57.830 — 02:16:01.900 · Speaker 2
Now, is is that not helpful? Because you only did one set? No. Of course it’s.

02:16:01.900 — 02:16:03.700 · Speaker 1
Helpful. You do know that we’re doing some after this?

02:16:03.740 — 02:17:08.570 · Speaker 2
Well, I’m happy to do it. Um, but you did. 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 shopper, and that has something to do with it, too. So I think the coming back to the concept around zone two, it’s if you were to train, I think the the probably what makes sense from a metabolic corollary for with weight training is like if you’re going to neuromuscular failure, your muscles are on fire.

You’re not in zone two, right? I think we can comfortably say that. Right? Yes. So you’re probably in zone five or 4 or 5. So you’re really getting there. Now if you train and you say you do ten 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 the 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.

So I can’t.

02:17:08.570 — 02:17:09.410 · Speaker 1
Read learning.

02:17:09.530 — 02:17:59.490 · Speaker 2
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 hit training or powerlifting or whatever it might be. I 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, you know, casual powerlifting. I tried to be, you know, a crappy bodybuilder for a period of time, and it wasn’t great at it. But and then on top of that, you know, I might not have I mean, I might not be running a marathon like Shane in a couple of weeks, but I did run a half.

And you learned so much going through those, 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.

02:17:59.530 — 02:18:19.170 · Speaker 1
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, um, in your practice. How do you incorporate some of these things? So you practice in. Um, where are you in practice right now?

02:18:19.210 — 02:18:21.490 · Speaker 2
I’m in Florham Park, new Jersey. I work for Summit Health.

02:18:21.530 — 02:18:23.089 · Speaker 1
Okay. And

02:18:24.490 — 02:18:57.880 · Speaker 1
people could make an appointment with you if they would like to. I 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 Doctor 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 trained?

02:18:57.920 — 02:18:58.639 · Speaker 2
Yes.

02:18:58.719 — 02:19:04.440 · Speaker 1
I’d love for you to expound upon your training and just your individual practice.

02:19:04.480 — 02:19:09.719 · Speaker 2
So my my practice is a sports and spine practice. I did a sports and spine fellowship at the hospital for Special Surgery.

02:19:09.719 — 02:19:15.080 · Speaker 1
Which, by the way, is one of the best in the country, if not one of the best places in the world.

02:19:15.120 — 02:20:05.590 · Speaker 2
Yeah, it’s a great place to train, a great place to be. I have been, 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. That’s how 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 a later stage career people, and I also have mentors who are non-clinical or not even doctors, you know, who are out 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, and 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.

02:20:05.630 — 02:20:06.390 · Speaker 1
Amazing.

02:20:06.390 — 02:21:30.310 · Speaker 2
Now, from my perspective, from from my practice. My practice focuses heavily on the biomechanical determinants of pain. And when the 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 time frame, 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 and 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 Taleb book, which is one of four books in the concerto which are very difficult and fun to read. I love.

02:21:30.910 — 02:21:31.990 · Speaker 1
Very thick.

02:21:31.990 — 02:23:03.460 · Speaker 2
Books. Yes very thick. There are 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 stretcher is adequate, the Stressor is adequate.

The the structure can actually get stronger. So I branded myself antifragile 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, small 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 going to run a marathon in a couple of 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, we’ll extrapolate based upon the knowledge of my biological foundations. So but I my practice is a sports and spine practice. So I see a lot of hip pain, back pain, shoulder pain, neck pain to a limited extent elbow.

And then of course, um, knee and some ankle. Ankle. Foot as well. And the two main, 3 or 4 main conditions I treat are back. Specifically low back pain, tendon options around the body and then a lot of neck pain. And you’ll find that patients who have low back pain have tendon problems as well. And you’ll find.

02:23:03.500 — 02:23:07.500 · Speaker 1
In the shoulder it’s it’s a whole sling essentially.

02:23:07.500 — 02:23:43.100 · Speaker 2
So the whole whole sling can have problems. But I think it’s you’ll find specifically that there are there are insufficiency in the, 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, etc. and it matches up with a good physical exam. Well now we have clarity of diagnosis. Then the treatment, everything we provide from a treatment aspect there out is much more beneficial.

02:23:43.380 — 02:24:09.770 · Speaker 1
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?

02:24:10.050 — 02:24:32.890 · Speaker 2
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. Um, you know, we spoke about the athletic accommodation curve. There’s also the, you know, the innovation curve of companies and products. And I’m instead of like being on the absolute first phase of stuff, I’m probably one phase delayed.

02:24:32.890 — 02:24:39.850 · Speaker 1
I, I feel the same way. We have to make sure that things are safe. Effective? Yes. Worthwhile for patients to spend their money? Yes.

02:24:39.890 — 02:24:43.490 · Speaker 2
Agreed. Um, and first rule of medicine is do no harm.

02:24:43.490 — 02:24:45.520 · Speaker 1
That’s right. So do no.

02:24:45.520 — 02:26:29.080 · Speaker 2
Harm. Anything we do, we want to understand what we’re doing. We want to put it in the right place. Um, so I think there’s some very interesting work that’s going on from a stem cell aspect. Um, 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 understand a little bit more about mechanics other than just isolated joint range of motion and whole body movement. Um, I think that the it takes a lot of interest in that and study to do it.

But I think we’re getting there. And I think the, The Last Frontier is in a lot of ways the first, most important, which is prevention. And an ounce of prevention is worth a pound of cure. And how can we prevent these injuries? Or, you know, you see this word circulate online bullet proofing like we’re going to bulletproof your shoulders.

Bulletproof your knees. NIS. Um, 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 I hope we study more of that. And then of course, predictive predictive analytics around who who’s going to 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 in the we’re starting, I think, to in a greater 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, you know, like we said, are the exercises we can engage in.

I’m certainly going to do my best to find out and and to and to figure out what is the most effective ones. I think that the question becomes minimally effective dose of everything.

02:26:29.080 — 02:26:31.600 · Speaker 1
Yes. Of training, medication?

02:26:31.640 — 02:26:41.240 · Speaker 2
Yes. How much is too much? And are we overtraining tissues. And that’s why we’re seeing so many musculoskeletal problems. Or are we just inefficiently training?