Episode #375: The Sarcopenia Deep Dive- Why It's Not Just Muscle Loss (And How to Stop It)

25 Nov 2025 · 1 h 28 min

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In short

Barbell Medicine Podcast Episode #375: The Sarcopenia Deep Dive

Episode Summary In this episode, Dr. Jordan Feigenbaum and Dr. Austin Baraki redefine sarcopenia, emphasizing the importance of muscle strength and power over mere muscle size. They delve into the neurological underpinnings of sarcopenia, its pathophysiology involving motor neuron death, and the implications of dynapenia (the loss of muscle power). They also present evidence-based management strategies based on lifelong heavy resistance training and dispel myths surrounding aging and muscle health.

Key Takeaways

  1. Understanding Sarcopenia and Dynapenia
  2. Sarcopenia: Traditionally viewed as age-related muscle mass loss but now understood as a more complex issue focusing on muscle strength and power.
  3. Dynapenia: The significant loss of muscle strength that begins in the 40s and is attributed mainly to neurological factors, particularly the death of high-threshold motor neurons.
  1. Pathophysiology
  2. Sarcopenia is linked to the death of alpha motor neurons that innervate fast-twitch muscle fibers, leading to a selective loss of these fibers and a decline in strength.
  3. Strength declines approximately three times faster than size, highlighting the importance of strength training.
  1. Diagnosis and Screening
  2. Current diagnostic frameworks prioritize functional tests (e.g., sit-to-stand test, grip strength) over late-stage muscle mass measurements (like DEXA scans).
  3. Early functional assessments are crucial since individuals can have normal muscle size but still experience significant functional impairments.
  1. Management and Prevention Strategies
  2. Lifelong Heavy Resistance Training: Essential in slowing down motor neuron death and preserving muscle function.
  3. Resistance training should be challenging and focused on building strength and power.
  4. Walking alone is insufficient; resistance training is crucial for muscle preservation.
  • Nutritional Considerations:
  • Emphasis on high-quality protein intake (1.2 to 1.6 grams per kilogram of body weight daily) is vital, especially for those experiencing anabolic resistance.
  • Supplementation with whey protein and creatine (3-5g daily) may support muscle maintenance in individuals diagnosed with sarcopenia.
  1. Myths Debunked
  2. Myth: Walking is sufficient for maintaining muscle health.
  3. Fact: Resistance training is necessary to prevent the loss of strength and motor function.
  • Myth: Muscle turns into fat when you stop lifting.
  • Fact: Muscle and fat are distinct tissues; the muscle's quality declines with disuse, leading to issues such as fat infiltration.
  • Myth: It's unsafe to lift heavy weights past a certain age.
  • Fact: The risk of injury from lifting weights, even heavy ones, is relatively low compared to the risks of inactivity.

Episode Timestamps

  • 0:00 - Introduction: The Silent Epidemic and Dynapenia
  • 8:50 - Defining Sarcopenia: Why Size Alone is Misleading (The Green Banana Analogy)
  • 17:37 - Epidemiology and Sarcopenic Obesity
  • 23:39 - Screening Tools: SARC-F, Sit-to-Stand Test, and When to Screen
  • 40:53 - Pathophysiology: Why Sarcopenia is a Neurological Event
  • 42:28 - Motor Neuron Death and Selective Type II Fiber Loss
  • 52:33 - The Problem of Anabolic Resistance
  • 53:16 - Management and Prevention Strategies
  • 57:20 - Exercise Prescription: The "Why" and "How" of Resistance Training
  • 1:10:44 - Nutritional Strategy: Protein Boluses and Supplements
  • 1:16:21 - Sarcopenia Myths: Walking, Muscle Turning to Fat, and Safety

Conclusion Sarcopenia is primarily a neurological issue, not just a consequence of aging. Focused interventions through resistance training and proper nutrition are essential in combating sarcopenia and maintaining muscle health. Early diagnosis, through functional assessments rather than muscle mass measurements, can facilitate timely intervention.

Additional Resources For more content and resources, consider checking out the Barbell Medicine website and their various training programs and nutritional guides.

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Transcript

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0:00Welcome back to the Barbell Medicine Podcast, where we bring modern medicine to strength and and strength conditioning to modern medicine. I'm your host, Dr. Jordan Feigenbaum. And as we head into the holiday season, you're likely gonna see your parents, grandparents, or other older relatives. And if you look around the dinner table, statistically, at least one of them is likely suffering from sarcopenia, even if they look, quote, normal size. Now, we used to think this was just about muscles getting smaller, but we were wrong. It's actually much more related to the muscle becoming weaker, which is mostly related to changes in the nervous system, a process that begins decades before you notice it.

0:34And in this episode, Dr. Baraki and I will be breaking down the newest science of sarcopenia, why walking isn't enough to stop it, and what you and your loved ones should do about it. And now, on the other end of the line, is the second most handsome doctor in North America, Dr. Austin Baraki. What's going on, dude? Hey. Yeah, man. It seems like this is a topic that we've been talking about for, like, I don't know, over a decade now. But we were overdue to cover this topic in some deep detail, so here we are. Allow me to throw some shade for a second because we've been talking about this for a while.

1:04And you and I were tasked with, you know, by UpToDate to come up with strength training and primary care and like how to do it. So two articles if you're a healthcare professional and you want to see our stuff, we're on UpToDate. And we realized that UpToDate there's a gap there. There's nothing on sarcopenia on UpToDate as of this morning when I checked. and so we volunteered to like hey do you want us you want us to do the sarcopenia thing and we were told well you're not really the experts on sarcopenia and i was like quick question who actually who are the experts in this case because it seems like most people are just making stuff up and then you know they're very far into the weeds about the pathophysiology and the nomenclature and naming less into the yeah so here's what you do about it and that's i'm not throwing shade at the researchers because look, we're standing on the shoulders of giants.

1:58There are some really intelligent people in here doing great, great work. Unfortunately though, how that's being communicated to not only healthcare professionals, but also to the lay public, there's just a big gap there. And I was like, well, we do that every day. So. Yeah, I agree. I mean, I think that, you know, if you surveyed a lot of, you know, generalists or primary care folks, or even among geriatricians, they might be able to, you know, give you a sense of what this word means, even if they just draw on some context clues or think back to their like Latin roots or something like that.

2:30But taking that a step further and saying, well, how are you going to counsel your patient on this or what would you suggest for them, given that, you know, it's not necessarily easy in all contexts to just say, oh, I'm going to refer them to this practitioner because practitioners in this case are a lot of like trainers that may or may not have the, you know, level of understanding needed for the particular patient in front of them with certain medical conditions or, you know, being on certain medicines or whatever the case is. It's, there's definitely a gap there. So here we are. Yeah, look, that's a nice segue into definitions talking about sarcopenia, because if you look anywhere on the internet, you swing a dead cat anywhere.

3:08It's sarcopenia followed by age-associated loss of muscle mass and we're like, that doesn't, doesn't feel right. So, and in fact, it is not right now. This, uh, the term sarcopenia was originally coined by a Dr. Erwin Rosenberg in 1989. So relatively recent. So if you had, you know, uh, as we'll talk about, uh, sarcopenia in 1988, you actually didn't cause the term didn't exist. So I'd be very curious that maybe they just called it like frailty or like, you know, failure to thrive or something like that. I'd be very curious. But in any case, 1989, he writes this. It's not really a memoir. It's more like just a recapitulation of what happened in the medical literature.

3:53So he says, and I quote, in 1988, we convened a meeting in Albuquerque, New Mexico to look at the various measurements related to the assessment of health and nutrition in elderly populations. And I was asked to summarize some of the findings. I noted that no decline with age is as dramatic or potentially more significant than the decline in lean body mass. Hey, look, 1980s. Good observation. He goes on to say, what is sarcopenia? Is it an age-related loss of muscle mass and function or a disease or a process of normative aging? The term actually describes an important change in body composition and function.

4:30So as is typical, whenever we think we've stumbled upon something like unique or like brand new, you just actually have to go back further. Just divorce yourself from like modern history and go back even further. And you're like, oh, yeah, some of like really smart people were actually like thinking about this way before us. But why do you think from there? So that's like the term is coined. Why is it that everybody right now just calls sarcopenia age-associated loss of muscle? Like you could ask Google Gemini right now, and that's going to be the thing it spits out. And it's like, why? Yeah, I don't have a strong explanation for it.

5:08I think that some of these definitions tend to take and then they just kind of stick. And if that is the accepted definition of the term, then research using that definition will tend to look at that very outcome. In other words, it'll tend to look at muscle mass as the indicator. So it ends up being like a circular sort of thing where the studies reinforce the definition. This is a hypothesis, of course, you know, but he was seemingly ahead of his time where he included the concept of muscle function in there. And so if, you know, instead from the beginning, he had observed that muscle power was something that was, you know, plummeting with aging in these patients.

5:47And then from the very beginning, the research path was set on, you know, the loss of muscle strength and power, then maybe we'd be in a different spot. but that didn't seem to be the aspect of his line of questioning or inquiry that took as much as the loss of muscle mass. And similarly, you know, there is a little bit of a parallel. I don't think we're going to get into it in too much depth in this podcast, but I've talked about it elsewhere to where the prevalence and the development of sarcopenia, muscle mass in general, tends to track to some degree with bone mass. And so we already had this conception of, you know, osteopenia and osteoporosis relating to bone mass.

6:26And so, you know, you might intuit that, oh, sarcopenia, just muscle mass, maybe the same thing, even though it is functionally and, of course, structurally a very different tissue. Yeah. He also thought about, he said in his little memoir kind of memory thing, he's like, oh, should I have called it sarcomalacia? But at the end, like the last paragraph and all this stuff, there's a ton of references here. But in this little editorial, he was like, one question that remains, uh was it a good is it a good thing that i put a label on this basically like and he goes yeah because now people are researching it and so you know i think if around today he'd be like well i wish i would have put a bigger emphasis on this and function thing um so yeah uh as we dive into a little etymology here so where the word come from so sarcopenia means flesh poverty uh so you've heard like osteopenia for example just that means poverty and sarx is flesh or muscle tissue You could also call it myopenia.

7:23And then there's another term that we'll discuss here called dinopenia. So like strength, poverty, a loss of strength. Or it could be cradopenia, which I quite like, power, poverty, a loss of power. Now, these are the key variables in the disease that we commonly understand and talk about as sarcopenia. And it matters how we define them and the disease. So for example, muscle mass declines about 1 % per year after age 50, but strength declines about three times faster per year, and power declines even faster than that. So it can't just be muscle mass because, and I'll draw an analogy here, and this has actually been codified in the medical literature.

8:06It's called the green banana relationship here. So a green banana and a ripe banana might be the same size, but their chemical composition and firmness are totally different. So old muscle, to draw a parallel, can look full on an MRI due to fat or water or other things, but have zero or reduced contractile quality. So you can't just go on size alone. So I'll ask this question to you again, Dr. Baraki, but in a different way, and maybe you'll have a better answer. For a long time, the medical community was obsessed with measuring muscle mass. So even as far back as 2010, the European Working Group on Sarcopenia in older people, well, their guidelines said that small muscle basically equals disease.

8:49That's sarcopenia. But then we saw this paradox in the data where you had people with, quote, normal-sized muscles, but they were still falling and fracturing their hips. So can you walk us through why the guidelines have shifted now as late as 2019 to prioritize strength and function over just muscle mass alone? Yeah, it's been an important and interesting evolution. And like many kind of fields of study in medicine and theories, it tends to get refined over time as we learn more. I remember writing some original articles for Barbell Medicine over a decade ago on the website and referencing the European Working Group on sarcopenia and older people, the original version before the second version that you are citing here from 2019.

9:31And that's where there kind of started to be this more formalized shift in the way we thought about sarcopenia instead of focusing on the mass aspect to explicitly state that sarcopenia is more probable when low muscle strength is detected. So shifting a little bit somewhat away from mass and more towards function, although the definition and the way we conceptualized it still tended to envelop both. But I think that marked a time when there started to be a bit more emphasis on the strength component. And these guidelines looked at sarcopenia across the lifespan and emphasized that they kind of viewed it as a muscle disease that started earlier in life.

10:13and you would kind of accumulate these hits across the lifespan in various ways due to what we call secondary causes, meaning like if somebody is accumulating certain diseases or they are progressively more inactive or one area that I observe on a day-to-day basis is each time one of my patients gets admitted to the hospital, there's some literature that these have been termed, quote-unquote, catabolic crisis. For example, each time somebody with COPD gets admitted to the hospital or somebody with heart failure gets admitted to the hospital, every time, you know, they end up getting sick, they get inflammation, they spend most of their time in bed, they get put on certain medicines like corticosteroids and things like that, that accelerate the process of catabolism and muscle breakdown.

10:55And so each one of these episodes contributes to the accumulation of these hits kind of across the lifespan. And so they looked at the concept of sarcopenia and they said, well, it's probable if the person has some low muscle strength. and if you combine that and they also have low muscle quantity or this concept of muscle quality that you alluded to where it might appear that they have a decent amount of muscle mass but it is of such poor quality that it doesn't work very well that was essentially confirmatory of a diagnosis of sarcopenia and then if on top of that you layered on that this person had kind of what we call objectively poor physical performance or low physical performance as assessed by certain you know, uh, tests that have been studied that we'll get to a little bit later that would qualify as more severe sarcopenia.

11:40Yeah. Yeah. And the, and the key thing here is that, you know, with the old, just muscle mass centric or muscle centric, um, you know, definition and diagnosis, it just, it didn't correlate very well as far as like, it wasn't very predictive of like, oh, these people are going to do worse. They're going to fall more fracture, get more fractures, uh, not be able to live independently, or mortality, for example. And so you're like, well, why do we have this disease? And we're going to harangue ourselves to like diagnose it when it's not that great as far as predicting these things. But if you actually change the definition, instead of it just being muscle mass only to actually you need some poor muscle function and here's how we're going to define that, well, it gets much, much better.

12:23And we have good data on that now that continues to emerge. And actually it looks like the pendulum has swung the other way rather than it being like muscle mass centric. It's more muscle strength, muscle force production centric. I just had an interesting thought, and let me run this by you and see what you think of it. One of the common things that we talk about all the time that we hear is critiques of BMI. I was just, okay. Where people say that BMI, we're on the same page here. BMI as a tool to assess body fatness or adipose tissue is not ideal in certain circumstances because it fails to account for how much muscle somebody might have as part of that calculation.

12:59and what you're suggesting here, what we've been talking about as far as muscle quality goes or quantity goes is that even if you are to assess the size of someone's muscle, it's almost in some ways like BMI because just the sheer size of it does not tell you much about the quality in terms of how much fat is actually in the muscle that is that useful. It's kind of like going in the other direction. Do you think that that holds water? Yeah, I think it does and I just imagine people, again, if there was just this outrage like the European working group on sarcopene and older people People have no idea.

13:30This test is just about muscle size and not muscle strength. Right, right. I also think that, and we'll get to this, that the hand grip strength is just one of the tests that you can do in the office. It doesn't require a lot of skill. Like, whatever. I understand why it's used, but I don't love it, and we'll get into reasons why. But I think that's like the BMI test also. It's just like, if you want to be upset about things, be upset about BMI and hand grip strength and then whatever. Yeah, yeah. All right. But anyway, the whole point is when you shift away from a mass only sort of definition of sarcopenia and you include strength or even just have strength alone, power alone, it does much better predicting falls, mortality, so on and so forth.

14:05And we've linked a ton of data showing that from the sarcopenia definitions and outcomes consortium. There's just too many acronyms here, I think. So now to add one tiny addition to my prior comments, I think much like BMI, though, muscle mass quantitation, if you wanted to measure it, is probably still quite useful at the extremes. So in the same way that I can tell you, if somebody's BMI is, you know, 17, I know that they are extremely underweight and I can kind of visualize them when I see them. Or if their BMI is 42, I know that they are 100 percent confident that they are carrying too much muscle mass, whereas there is a range in between where it gets a little.

14:41sorry, excuse me, fat mass. There's a range in between where it's a little bit hazier, kind of similar with muscle mass, right? It's very unlikely that somebody with just overwhelming amounts of muscle mass on them is likely to have insufficient muscle function to be able to live a generally healthy life from a functional standpoint, although there might be other issues to speak of with respect to how such muscle mass was acquired. But at the same time, when I think about some of the thinnest and most frail patients that I see, it's like I can just tell by the sheer, you know, how little muscle mass they have when I can essentially see their skeleton.

15:18I'm like, yeah, there's no way you're like extremely functional with this. So at the extremes, that quantity is still useful, but there's a broad range of kind of less certainty, not unlike what we've described with BMI, where you need additional data to kind of adjudicate that. Yeah, although this is a nice segue into our next little talking point here, because there's a distinct situation where a person is likely to actually be carrying either a normal amount of lean body mass or like even elevated amount of lean body mass but have poor function and they also have a significant amount of fat mass and that's called sarcopenic obesity.

15:53Generally speaking, individuals with obesity or individuals with overweight tend to carry more lean body mass than lean individuals. That's just, you know, kind of how the disease develops. People just don't gain 100 % fat mass. Despite that, individuals with sarcopenic obesity, as Dr. Baraki will tell us about, also have poor muscle function despite having a significant size of their muscles. So Dr. Baraki, what's up with sarcopenic obesity? What is it? And like, why is it even that much more dangerous than just run-of-the-mill sarcopenia? Yeah, it's essentially a second hit to their physiology and to their health risk.

16:32So it is a kind of a next level up in terms of risk because it combines all of the risks of sarcopenia where the person might have insufficient muscle mass but more likely has some impaired muscle function leading to the consequences of that. But on top of that, they have the additional risk from the excess body fat, which we have talked about at length over the years on this podcast, from the levels of inflammatory signaling molecules called adipokines coming from muscle, the effects of fat physically infiltrating into the muscles, that's called myosteatosis, and it causes this toxicity within the muscles that's called lipotoxicity and leads the muscles to become insulin resistant, meaning they don't take up glucose as well.

17:14They have impaired metabolism. People's resting lactate levels will be abnormally high in those situations just because their metabolism is not functioning very well at the level of the muscle. And so this ends up being a pretty harmful and negative physiologic or pathologic feedback loop, I would say, in people because they have kind of both impairments on the muscle side and on the fat side because both are going in the wrong direction. Yeah. Yeah. Now, when we try to figure out how many people actually have sarcopenia, because of all the problems with definitions that have almost only recently kind of been resolved, although there's still some active work being done, it's very challenging to come up with a confident, like, hey, this is how many people have it.

17:55But right now, based on the best estimates and the best data that we have, about 5 % to 13 % of community-dwelling adults age 60 to 70 have sarcopenia, and that goes up to almost 50 % for those over the age of 80. Now, I suspect with these new definitions, these new frameworks coming into play, that that prevalence is actually going to increase, but we'll need some more data to feel confident about that. There's an interesting nuance here, though, that there are different types of sarcopenia. We talked about sarcopenic obesity, but broadly speaking, you can really differentiate sarcopenia into two types, a primary and secondary.

18:34Primary being mostly age-related, meaning that there's no other specific cause that's evident of this, except for aging itself. And this is really a diagnosis of exclusion. So there are intrinsic biological clocks, not to get too fancy, but there are the little nuclei in your muscle cells. These are responsible for making proteins, right, maintaining a particular area of the muscle, making sure everything's working well. Well, you get some DNA damage that accumulates there as we age. We can't really reverse that totally anyway. You have mitochondrial dysfunction. There are some hormonal changes, not necessarily the ones you might think about.

19:11Everyone just immediately jumps to testosterone, but I'm thinking more about the hormones produced by the muscle, like myokines, for example, also hormones produced by the fat tissue, adipokines, and there's some other signaling stuff. All of this is in flux and father time is undefeated. Now that said, despite those negatives, muscles are still very responsive to activity. We've got evidence that people even in their 90s can get stronger, which I think is awesome. But as far as like can we completely reverse aging? No. So that's primary sarcopenia, which to my mind, and we don't have evidence on this yet, but I would suspect that is a very like rare or a minority of individuals with sarcopenia.

19:55To me, it's kind of analogous to when we look at obesity. People say, oh, they're addicted to sugar or they have food addiction. I'm like, well, that is a very narrow subset of individuals with obesity, but it does not represent the majority of individuals with obesity. So primary sarcopenia certainly does happen, but it's a minority of individuals with sarcopenia. Now, secondary sarcopenia occurs when there's one or more distinct causal factors that act in concert together to basically age the muscle faster. It's like an accelerant. You're pouring an accelerant on a fire here. So disuse is one of these.

20:27That's what I would suspect is the primary one, particularly in otherwise healthy individuals or mostly healthy individuals, but also chronic medical conditions that people tend to accumulate as they age. Now, that includes stuff like rheumatoid arthritis, COPD, as you mentioned, chronic kidney disease, heart failure, type 2 diabetes, the list goes on. There's a lot of inflammation goes on there. You can get these, like you said, catabolic crises, particularly if they're admitted to the hospital and taking other agents to treat why they're in the hospital for that catabolism. It could also be nutrition-related, whether it's a person who has difficulty accessing food, so food insecurity.

21:02Or as individuals age, their appetite tends to go down. um protein intake tends to drop so there can be some nutritional element here as well is that how you understand the kind of differences between primary and secondary sarcopenia yeah for sure i don't think that at least in my you know type of clinical work that i would ever confidently diagnose a case of just primary sarcopenia almost exclusively you know even if the person tells me that they have no medical problems yet they somehow meet that criteria it's often going to be attributable to insufficient physical activity and as you mentioned disuse but my patient population that I tend to work with a bit more, at least outside of the barbell medicine context, where we select for people who generally don't have sarcopenia because they're here because they train, are going to be those hospitalized patients who have all those medical conditions that you described.

21:48Advanced end-stage organ system diseases affecting the lungs, the heart, the kidneys, the liver, all of those can lead to chronic inflammatory states, changes in appetite, changes in nutritional status. Among the worst of them tends to be cirrhosis in particular, where I think it's a very, very common and under-recognized issue because a lot of patients with cirrhosis for a long time, they also tend to just retain a lot of water in various areas and they tend to be swollen. And so they don't physically look as thin and frail, at least until the much later stages. And then you combine that with various other aspects of that disease and it can be particularly catastrophic for them.

22:23So most of the people that I see have some combination of insufficient activity, multimorbidity, which is a fancy term to say they have multiple medical conditions, and sometimes even the drugs used to treat these conditions can have negative impacts on muscle. So like, for example, the frequency that people with COPD are put on prednisone, which is a catabolic steroid that can impact their amount of muscle mass over time, and then poor nutrition or insufficient nutrition in general kind of conspire to increase the prevalence of sarcopenia in my patient population in particular. Yeah, yeah. So to summarize before we move on to diagnosis, sarcopenia, which is size loss, dynopenia, strength loss, and cratopenia, power loss, well, they're all different.

23:03Because strength declines about three times faster than muscle size, and it correlates better to actual clinical outcomes like falls, fractures, mortality, et cetera, the modern guidelines on sarcopenia prioritize function and strength for diagnosis over size loss alone, as muscle can be normal-sized in sarcopenia, but still dysfunctional. That's a nice segue into diagnosing sarcopenia, so how do you know you have it or a loved one has it? This is where things get kind of tricky because even when you look at the guidelines, it's not exactly clear like, hey, do this. It's based on awesome evidence, so just do this.

23:36Like there's no like clinical practice guidelines, a bunch of consensus statements out there. But one of the things that you'll see if you dig into the literature or if you're working in the space is this idea of lead off with the questionnaire, this SARC-F questionnaire, which stands for strength, assistance with walking, rise from a chair, climb stairs and falls, which kind of tells you what's in this questionnaire. The problem with this, and this is almost like a direct analogy to BMI, it has a very high specificity in that if somebody has a positive test for a SARC-F questionnaire, I'm feeling pretty confident that they likely do have sarcopenia.

24:14But if they don't meet criteria, which is a score of greater than 4, I'm not sure that they actually don't have it. So it's not very sensitive. It misses almost half of the people that do have sarcopenia even if they take this test. So if you lower the threshold to a score of two or one, well, yeah, the sensitivity actually improves. And some authors, some researchers have suggested, well, yeah, it improves sensitivity and it actually is not an unacceptable loss of specificity. And I suspect that's because in individuals being administered this questionnaire, the pretest probability of having sarcopenia is so high that it's like we're not getting these questionnaires, you and I personally.

24:56But like older individuals, generally speaking, because it's likely way underdiagnosed, far more common than we think, that, yeah, you just end up capturing a lot more people. Does that kind of jive with your understanding of this? Yeah, my thoughts on this, I think I've been kind of making some consistent arguments for many years about this at this point. Basically starting out from the concept of what is a diagnostic label and what is the point of giving somebody a diagnosis? And from the patient perspective, of course, I understand that it can provide some sense of certainty, some closure, things like that.

25:31That's actually not what I'm talking about here. From the clinical and management standpoint, what is the point of giving somebody a diagnosis? It is because that diagnosis should ideally inform some degree of our understanding about prognosis and ideally should impact our management plan, what we do with the person. And so this is a situation where I actually I'll start out with a different type of scenario to illustrate the point. It is important for me to make a specific diagnosis of cancer in somebody to rule in cancer or to rule out cancer if I'm considering potentially administering them chemotherapy, because I would not want to give chemotherapy to somebody who does not have cancer.

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26:13And it might, it may be appropriate for somebody who does have cancer, right? In the context of sarcopenia at the present time, we're jumping briefly ahead to like treatment. We are not routinely administering these patients' toxic drug therapies. We're not giving them ultra high doses of oral anabolic steroids or something like that. Speak for yourself. Yeah. But rather the management of sarcopenia, the optimal management, at least at present, involves kind of aggressive disease modification for the conditions they already have to improve health from that standpoint, increasing physical activity, training, nutritional support, things like that.

26:52none of these things carry with them such a disproportionate risk that I, at least at present, have a great deal of concern about the risk of potential overdiagnosis here. Now, it might not make somebody feel good to have a diagnosis like this if they don't, in fact, have the condition, but if ultimately what I'm going to do, or if ultimately what I would like for this label to do, especially as it gains attention among clinicians in practice, be it primary care, hospital medicine, et cetera, is that it prompts a more dedicated discussion, potential referral to resources for more aggressive physical training interventions, nutrition interventions, things like that.

27:29I'm kind of okay with that at this point, with the caveat being that, hey, to the extent that those resources might be limited, then yeah, you don't want to like insanely overdiagnose people. But clinicians ought to be addressing this with patients, especially those who are at risk anyway. And so, yeah, if you ask somebody about their strength or if they're needing assistance with walking or if they're having difficulty rising from a chair or climbing stairs, if they're falling, yeah, any one of those is enough to get me concerned. So in my mind, in my practice, if I'm asking those questions, yeah, a score of one is enough to get me concerned about this person.

28:02It might not be the most severe phenotype or the most severe manifestation of sarcopenia where we need to just pull out all the stops. But, you know, not unlike our discussions around cardiovascular disease and cholesterol management, it's this kind of cumulative lifelong thing. I'd rather catch you earlier on before you fall and you fracture your hip. And then I have to, you know, deal with the rehab on the back end of that, which is a much, you know, harder, harder lift than, than addressing this a little bit earlier. So if I hear that somebody has any of the impairments in that questionnaire, that's already my first tip off that somebody ought to be, something ought to be done to kind of alter this patient's trajectory.

28:37All right. Well, let me, let me play devil's advocate here then. All right. So we have the SARC F questionnaire, and I just imagine all of the obstacles for somebody to actually administer that in practice. They're like, I got to download it. I got to ask the questions properly. I got to record it, the EMR, whatever. Yeah. Let's just say in the bizarro world, this alternate reality that we now live in, that look, anybody past the age of, let's say, 45, automatically, like as soon as your first visit, encounter with the clinician, at risk for sarcopenia pops up. And so at that point, it prompts the physician to basically counsel them on, hey, resistance training is going to be super important for you.

29:14eating enough protein is going to be super important for you. You have these medical conditions. We should really try to optimize these because these are all things that you should be doing anyway, to be clear. And the reason why that time point is so important as, again, we're jumping ahead a little bit, that the pathophysiology of sarcopenia, like when you get down to the level of muscle, this stuff starts in your 40s or even before that a little bit. So the idea is like let's catch it early. Let's have a large strength span or muscle span, whatever term you want to use. And so if we agree that this sort of like push, screw the Sark-F, everybody's going to get this counseling because that would likely increase uptake.

29:52You know? I don't know. That's a big assumption that, you know, counseling more people in the doctor's office would help more people exercise. I think there's some evidence I could argue. It's not very strong, but like it's there. I don't know. What do you think about that? Yeah. Yeah, I think I'm generally prickly about the idea of instituting more things for primary care doctors to do. There's, you know, they already have so many things that are like mandated in some things that are actually far dumber that are mandated for them to have to do. Totally. And I wish that, you know, for me, like in my practice, yeah, I don't actually use this questionnaire because I'm like having a conversation with the person and I'm observing them.

30:32And I am very consciously attuned to this person's like functional status and getting a sense of what is their life like and I watch them move and I try to get them up and walk them around the hospital room or something like that and you know those things just tell me what I need to know even without meeting like checkbox kind of criteria that take up you know that that level of time but I also understand that not all clinicians are like that and so you know there's this fine line to walk between what do we like mandate in clinical encounters and electronic medical records and things like that and like make people make doctors pull their hair out compared with just like getting to their patient and having a conversation that's individualized to them, but also knowing that, hey, not everybody even does that.

31:08So it's a tough thing. I don't have a great answer for it. Yeah, man, I just think, look, the colonoscopy pops up at a particular age. I think this pops up at a certain age. You get more counseling about it. Maybe there's more uptake. Maybe there's more motivation or levers to pull during motivational interviewing. Anyway. Okay, so that's the SARCF. That's a questionnaire. Now, there are other better metrics that if you really wanted to dive into, like, hey, how's the muscle actually functioning? And so grip strength, for example is one of them uh studies indicate that grip strength values of less than 36 kilograms for men and less than 23 kilograms for women may identify better identify probable sarcopenia than lower thresholds um and so theoretically if you had this hand grip dynamometer which if you've never done one of these things you just squeeze it real real hard and it comes up with the number um there's a bunch of interesting stuff on these tests like which ones are better than others like it matters how textured the material is the leverage how big someone's hand is the handedness the person had all sorts of stuff the weird thing is it doesn't correlate super well with actual like improvements in dynamic strength so like austin your squat you know has gone from with 285 to you know over 600 pounds and i don't know that your hand grip strength has actually gone up that much i know that your hand grip asymmetry strength asymmetry has gone down which anyway that's for another podcast perhaps but i'm just waiting for apple to come out with the iphone 18 Pro Max that actually has like a pressure transducer built into the case.

32:32And so you have people just squeeze the phone case and it tells you like, oh, you're at risk for sarcopenia. You know, look, they already got VO2 max. Why not have like a grip strength built into the case or built into the phone? Do you, are you using grip strength at all? Like when you're going around seeing patients? No, I don't like it. I don't use it. It does require like a, you know, a calibrated or validated device and things like that. And that's just added complexity for little, you know, gain compared with just using a simple functional test as well as like talking to a person. Yeah. So you could use like a sit to stand test like and this if you're look, if you're going home for Thanksgiving, you're going to see your loved ones for Thanksgiving.

33:06This is something you can do. You don't even need to tell them it's a test or if you know, if you do want to tell them it's a test, that's fine, too. Maybe they'll try harder, which is ideal, you know, to get a more accurate sort of depiction of their functional status. So, hey, can you stand up from a chair five times as fast as you can? Don't use your arms. And so you just do this at home. basically you start your stopwatch and if they do it in under 15 seconds you can feel a little bit better about their sarcopenia risk and if it takes them longer than that or they have to use their arms maybe you can say hey why don't you come to the gym with me tomorrow that would be the best case scenario rather than saying you should work out it's like well yeah duh they already knew that how do you break that barrier there are other tests like appendicular skeletal muscle mass which is a fancy way of saying how much muscle are you carrying you can measure that with x-rays so it's a DEXA scan or MRI or CT.

33:54I was impressed to learn that there's also another measure of a specific muscle group's size, the lumbar muscle mass. And I'm just saying, I'm never getting sarcopenia if they measure my lumbar erectors. There has been some interesting evidence recently. This is a little bit of a side tangent, but on the use of essentially AI looking at scans that people are already getting, for example, to estimate their bone density, because if people are already getting CT scans, there are algorithms to calculate their bone density based off their ct scans and it's like maybe you would be screening way broad way more broadly and it's using data that we're already collecting if you did that and so i suspect that for people anybody who's getting an abdomen pelvis ct scan for example yeah there is uh there is you know a slice that you could take of their kind of maximum i don't know which of the spinal erector muscles or the you know the iliopsoas muscle cross-sectional area that they're using in these types of studies, that you could collect that data based on what you're already scanning.

34:54Of course, the caveat here is that these imaging tools, again, are looking at muscle quantity or cross-sectional area size and not assessing function. You know, the example that you previously gave, the sit to stand, that's like my favorite because I leverage it not just from a diagnostic standpoint to assess the person's function, but hey, I turn it into their exercise program of like, hey, okay, cool. Here's what we're going actually do is sets of this to strengthen your you know hip girdle and musculature and things like that yeah uh you can also test somebody's gait speed so like a four meter walk test or even a 400 meter walk there's like can you do that um so yeah and other things other things you can do at home so basically there are a bunch of different tests um that you can do now uh you've kind of already we're not really burying the lead here just just talking but how do you diagnose sarcopenia in practice?

35:41Is it mostly just the sit to stand? And further, who gets screened and what, if any, confirmatory tests are needed after? Are you following the European working group specifically to the letter, or are you just kind of a cowboy out and do your own thing here? No, I'm not actually following those. And this isn't to throw shade at them or to speak negatively about them, but it's rather that I'm very kind of attuned to this as an issue, point a and then b is i have a patient population that is highly enriched for those with this diagnosis meaning like my pre what i'll call my pre-test probability or like before i even walk in the hospital room what's the likelihood that the person i'm about to see has this condition and it is far higher compared with the general population just because of where i work in an acute care hospital setting dealing with mostly you know older older multimorbid types of patients And then my sense of comfort with this involves, A, like looking at the person, because at the extremes, it is easy to diagnose.

36:39When I see somebody who's thin and frail, skin and bones, and I can see their ribs and their temporal bones and things like that, then, yeah, I am very likely to have made the diagnosis almost on site. and then through a conversation with them, depending on the nature of what brought them into the hospital, what their life is like at home, if they need help with accomplishing their activities of daily living, things like that, that'll further strengthen my case. And then if I get them up out of bed and walk them around, or sometimes I've done five times sit to stand in a hospital room and seen how they can do.

37:08And more often of the time, they're either unable to get up even once without using their arms or they might need to use their arms, but it's still very slow. And obviously that'll prompt not only inpatient physical therapy consultation, but it might prompt a conversation once the patient is ready for that about, you know, the path forward in terms of what can be done. It's not always appropriate to have that conversation in the hospital setting, depending on the context. And, you know, if the person is in active respiratory failure or if they're, you know, impending, they're going to die soon, then I might not be having these conversations every single time.

37:39But, you know, like I said, given just how common it is in my population, I can, you know, look at the person, talk to the person, and then watch the person try to get up out of a chair. And that's my like more pragmatic sequence of events that doesn't involve carrying around a hand grip dynamometer and like following a European working group algorithm or something like that. Yeah, not everybody needs the DEXA scan. Definitely not. So potentially, you know, look, if it affects up to 50 % of people over the age of 80 and if it's maybe 5 to 13%, probably closer to 20 % of the general population between like 60 and 70 or something like that, should more clinicians be doing what you're doing?

38:17What about fitness professionals? And, you know, I just go back to your previous point, like, look, if we identify this more, how does it change what we do? But I guess if people are looking for it, maybe they're going to do something about it rather than just, well, they're just getting older, you know? Yeah, I think so, especially when it's paired with, you know, more trained or skilled or effective behavioral kind of interviewing, motivational interviewing. You know, I do think that clinicians should be doing it more often. But when I say doing it, again, I don't want to convey the idea that, oh, I'm just like stacking more requirements onto your plate because what I'm doing does not feel like, oh, I'm like checking off this additional box or it's this additional burden on me.

38:57Because again, I'm like walking in the room and like A, looking at the person, B, talking to them about their life and what it looks like at home and their ability to do the things that they want to be able to do, which is like part of normal, you know, history taking anyway. and then standing them up. And that's also part of a routine kind of exam. So it's almost built, it's almost like when we talked about, hey, let's like use AI to like analyze these measures that we're already getting off a CT scan. This is just me like paying attention during the history and physical that I'm already doing.

39:26So it's not actually adding a ton in terms of clinical burden, but rather if I'm able to identify the issue and tie it to something meaningful to the person, right, then that is my kind of my lead point to get into the motivational interviewing aspect, right? If they want to be able to do something and they can't right now, and it's like, well, I just noticed that you had a hard time standing up out of that chair. You know, do you think that if we were able to do something to get you being able to pop up out of that chair more quickly and robustly that you'd be able to do these things that you want to be able to do?

39:55Oh yeah, sure. Okay, let's talk about some strategies that we could use to kind of get you there. So it is kind of baked into what I'm already doing. And again, just the context of where you are can impact this. So if somebody is a fitness professional and you have somebody who like strolls into your gym and wants to get started with personal training, yeah, like they're already like addressing this if they have it, but they probably don't have it in the first place or at least they're less likely. My person who I'm seeing in the hospital for a hip fracture, 100 % chance nearly that they already have it because they fell and they very likely have osteoporosis and so they probably also have sarcopenia.

40:26And so I'm like, my case is already closed before I even walk in the room in most of those situations. So that's kind of the spectrum that we're talking about here. Yeah, yeah, good advice. All right, so we know that with poor muscle function as evidenced by reduced strength, power, and overall performance, the risk of losing independence skyrockets. But we want to catch people way before they are at the cliff. So we're going to talk about the physiology because this is where barbell medicine differs from everyone else saying that sarcopenia is just age-related muscle loss. This isn't just atrophy.

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41:55You get 15 % off your first order at wearfigs.com with code FIGSRX. That's wearfigs.com, code FIGSRX. All right, we're back here on the Barbell Medicine Podcast. We're talking about sarcopenia. Now we're into the physiology. We're going to go into why does sarcopenia occur in the first place? I think the overarching sort of paradigm here is that muscle quality decreases. And what is muscle quality? Well, that's a specific term relating to the amount of strength or power. Really, it's force production created per unit mass. Okay, so muscle quality can be measured as the amount of strength, power, force production produced per unit mass.

42:37And this goes down in sarcopenia. So the mass may stay the same or decrease a little bit, but the loss of strength, power, and ultimately force production far outpaces that. But why does this happen? So first up, we're going to talk about motor neurons, or as my neuroanatomy professor said, motor neurons. And if that is the correct pronunciation, like shout out to Dr. Tolbert, because I've just ignored that you said that for an entire year. Do you think it's like umbilicus versus umbilicus? Yeah, it's somebody that probably said it that way with him way back in the day, and it stuck. Or like, do you say duodenum or do you say duodenum?

43:17Duodenum. Yeah, okay, same. But like in anatomy, when I was doing my anatomy masters, they were like, it's not that. And I'm like, okay, well, I'm just going to be an idiot the rest of my life. In any case, motor neurons, motor neurons, what these are, these are nerves that go from your spinal cord to your muscles, your skeletal muscles. And so specifically what happens as people age is that these alpha motor neurons, these specifically the ones that innervate or connect to your high threshold, fast twitch or type two muscle fibers, these things die. And when these neurons die, a nearby slow neuron tends to sprout a branch to try to go rescue this abandoned muscle fiber.

44:02So the muscle fiber itself, if it's connected by one of these sprouts, one of these branches, the muscle fiber typically survives, but then it's converted to a slow twitch or type 1 muscle fiber. So you lose your high gear from these type 2 muscle fibers, which is why you lose power first. You lose this riding reflex, the ability to catch yourself when you trip or rising quickly from a chair. And so that's why people fall and ultimately can fracture hip, for example. This selective loss of type 2 muscle fibers explains why muscle power declines so much faster than strength and why strength declines so much faster than muscle size and that's why falls are common with aging.

44:41This kind of leads into this reversibility sort of question, like can we reverse sarcopenia? Well, you can't regrow a dead motor neuron. You can only strengthen the ones that are left, and this is why prevention tends to be superior to treatment. And so we've got tons of evidence on this. If you take a muscle biopsy of an individual with sarcopenia and you look at it under a microscope, you see a dramatic shrinking of the type 2 muscle fibers by up to 50%, while type 1 muscle fiber size tends to be the same. And at age 70, an individual may lose 25 % to 50 % of their alpha motor neurons compared to what they had when they were age 20.

45:20And so the next question then becomes, well, why? Why does this happen? Well, these type 2 muscle fibers, these fast twitch muscle fibers, they cost a lot. The metabolic demand of these muscle fibers is higher. They also require a lot of signaling from the environment to maintain them. So mechanotransduction, loading them, being active with them compared to type 1 muscle fibers that are just like postural, for example, and you're going to use them regardless of if you exercise or not. And ultimately with this disuse, not only do the muscle fibers like not have any reason to stick around, but the actual satellite cells or stem cells for the muscles that we call satellite cells basically become unresponsive.

46:04And so you lose not only the muscle fiber, right, it changes its morphology and the motor, the nerve also kind of goes away, but also the machinery you had to repair the muscle fiber when it gets damaged also goes away. and it's mostly from disuse, although, again, we can't completely stop this aging, this biological clock. Interestingly, though, with training, again, you can't stop the aging process entirely, but strength training is kind of like a firewall here. It doesn't just build muscle, but it changes the survival rate of these type 2, these fast-twitch muscle fibers that are typically destined to die.

46:41Now, the activity, engaging in resistance training, sends a signal back to the nerve cell that says, hey, look, I'm still needed. Please don't kill me. I need me around. And this is evidenced by master's athletes, specifically those who engage in resistance training. Because you see master's athletes that are endurance athletes. Previously talked about Natalie Grabo, that 80-something-year-old who completed the Ironman, which also amazing. But if you look at older runners, they generally show high levels of what's called fiber-type grouping. Now, normally under a microscope, your muscle looks like a mosaic.

47:14You've got fast twitch, slow twitch, and it looks like a mosaic. But when you get this fiber-type grouping, that's evidence that your type 2 muscle fibers have kind of gone away, and they just have a bunch of type 1 muscle fibers. So endurance performance is great, but they're not doing much with that type of training for these type 2 fast-twitch muscle fibers. Resistance training, on the other hand, is different. Lifelong strength athletes often show less type 2 fiber loss and a fiber distribution pattern that looks more like a young person's. So heavy resistance training doesn't just help slow the loss of neurons.

47:49It prevented the death of them in the first place. And this is evidenced by some interesting data in powerlifters. So shout out to powerlifters because I know that the person, the author of the study had to be a powerlifter to look at powerlifters. There's no way anybody else is interested. The typical general population sees a strength decline of about 1 % per year after middle-aged, accelerating significantly after the age of 60 due to, again, this loss of alpha motor neurons. Strength athletes do much better. In this study on powerlifters, men over the age of 69 showed a decline of only 0.35 % per year, and women over the age of 59 actually displayed a 2.5 % to 5 % improvement in strength if they kept participating in powerlifting.

48:34So this neurogenic atrophy or neuron cell death that kills type 2 muscle fibers in the general population is slowed in lifelong lifters by like 300%. Really, the difference is 0.35 % to 1%, which I think is pretty awesome. Yeah, that's an awesome finding. Very cool, nice find. Everybody should be a power lifter, I think, is the takeaway. We just end the podcast. Yeah. But there's another factor. So that's the story with motor neurons, all right? But there's another factor. It's not just one thing, that one weird trick. There's another thing going on here. Anabolic resistance tends to become much more prevalent.

49:09So Dr. Baraki, what is anabolic resistance and why is it so important here? Yeah, it is a concept, another one that we've been talking about for a long time, and we're kind of more formally addressing here. It's this idea that when you deliver what we'll call a dose of anabolic stimulus to somebody, and those anabolic stimuli tend to be most potently physical training or mechanical stimulus to the body, to the muscles, and secondarily to that, a dose of, say, dietary protein, amino acids, for example, different people will have a different anabolic response to that dose. So some people might mount a very large anabolic response, a lot of muscle protein synthesis, and others might display a more blunted anabolic response or a lesser degree of muscle protein synthesis.

49:55And in this situation that we're calling anabolic resistance, it is kind of the term used to describe that more blunted response to an anabolic stimulus. We tend to see it more often in older folks, although again, I kind of hesitate to ascribe it to aging alone, just like when we hesitated to ascribe sarcopenia to aging alone. Anabolic resistance, we know, is more common in the context of that, what I call multimorbidity, or when people have multiple, you know, concomitant medical conditions, especially in the, like, very acute setting. So for example, if somebody is admitted to the ICU with a raging, you know, illness or bad case of, you know, sepsis, multi-organ failure, or something like that, we know that they tend to be very, very anabolically resistant, not to mention that they're generally, you know, laid up in bed nearly 24 hours a day, things like that.

50:42But even outside of this condition with, you know, complex medical conditions, acute conditions, and chronic conditions, those who tend to be less physically active or have more sedentary behavior in general, that tends to be a significant contributor, especially as folks get older as well. Now, we know that this phenomenon of anabolic resistance is not destiny. It is not permanent. It is something that can be overcome if we adjust that dose of stimulus that we deliver to the person. So this has also been studied to where, for example, in exercise contexts, increasing the volume and or the intensity of activity that is being delivered to the person can restore a degree of sensitivity to that anabolic stimulus meaning that whereas somebody who is generally sedentary and not moving around, and then they might do a set or two sets or something of an exercise might get a lesser anabolic response, if we increase that to three sets or four sets or push the intensity a little bit higher of their conditioning activity, we tend to see a more significant muscular response to that activity.

51:47And similarly, when we give them a dose of 10 or 15 or 20 grams of dietary protein, including in particular the amino acid leucine where it might be a gram or two of that in that dose of protein of up to say 20 grams they might have a lesser response in terms of their muscle protein synthesis but if you increase that to you know 30 grams of protein or even 40 grams of protein you might restore that anabolic response i think that this has been taken um maybe because it's telling some people what they what they want to hear based on their bias of uh we'll call it protein maxing these days to where they think that, oh, if this is, you know, as people get older, they just need to have, you know, more and more massive amounts of protein and that'll solve this issue.

52:30But this has also been looked at and just increasing protein intake does not meaningfully impact outcomes in these types of situations. It is supportive of, you know, adaptation and recovery and things like that to the training. But on its own, you are unlikely to build a significant degree more muscle just by increasing the dietary protein alone. And so for that reason, both of us, I think, tend to emphasize way more importantly the idea of the physical activity, the training, as well as addressing any reversible underlying health factors that you can actually address to restore that degree of sensitivity.

53:03We even know that if you take folks and they do a little bit of activity prior to the protein meal, that they can be more sensitive to that lower dose again. so you know it's almost like your post-workout you know protein bolus from a shake or from a meal or something like that they're more likely to have some evidence of restored sensitivity to that when it's taken after physical activity you know a brisk walk or an actual lift or or some interval training whatever you're able to get them to do that sensitivity improves rather than somebody tending to remain insufficiently active and just like taking more protein shakes throughout the day is not going to meaningfully impact their trajectory here yeah and further uh even like when people are in the hospital and they're on like a steady a drip of just like you know protein and feeding yeah yeah they become very anabolic resistant now some of that is due to the disease process that got them in the hospital the first time but that food situation is not helping them not that the hospital food in and of itself is like anabolically resistant just the frequency at which it's being administrated which is continuous is a is a problem all right well Well, now that we know why sarcopenia occurs, let's talk about what to do about it.

54:10Now, Austin, how do you normally speak to your patients with sarcopenia about management? You did the assessment, you got them up out of bed, you had them do the sit to stand maybe, and you're like, dang, this person is much weaker than they should be. How do you talk to them about this? Yeah, much like conversations around nonspecific low back pain, where I never use the term nonspecific low back pain, in these situations I also never really tend to use the term sarcopenia. I basically do the assessment and I, again, try to get a sense of what the person's day-to-day life and function are like and what their goals might be to improve that function if they have those goals or what their general health goals are.

54:46And I basically try to find an in into the conversation in real time where I can tie what are going to be my recommendations for managing sarcopenia to something meaningful to the person, right? So it's kind of like when we have conversations about back pain or osteoarthritis or whatever condition might be ailing them. What do you want to be able to do? And then are you open to negotiating a plan that might help you get to that goal? So making it meaningful to the person. And so it's the same thing here. If the person has no goals or interest or aspiration in improving their health or function, then I can talk to them all day about sarcopenia or that it's increasing their risk of all sorts of things, and I'm going to not make any meaningful progress.

55:25But if I can get a sense of what the person's life is like, what they want to be able to do that they can't do now, or if they have a particular health goal and tie it to the very demonstrable impaired function that I just showed them by virtue of the fact that they were unable to get up out of a chair, then I might be able to kind of weave a narrative that makes sense to them to where they, you know, by working on that and improving that ability, they will then regain or build the ability to achieve the goal that they had in mind, the meaningful activity, or improve their health in the way that mattered to them most.

55:58So I know that was a very high level kind of general description, but that's really the approach that I take. There's not a formula to this. It's one of those things where having more experience with having these conversations and the process of motivational interviewing, you end up getting more comfortable listening to people, and you can kind of in real time hear these little threads that they're offering up to you that, oh, I might tug on that a little bit and see if that ends up being a useful lead point into this process of, you know, here's a way that we can intervene or something that we can negotiate a plan that ties into something that you care about and that you're willing to, you know, have some buy-in.

56:33And if I have a family member there or a spouse there or a sibling or a child, somebody who is able to kind of be present as well to listen to this conversation, maybe to, you know, contribute to the conversation, maybe to offer to join into this process, that's another way that I sometimes do this in practice. And this applies to general exercise counseling as well. I remember recently having a gentleman in the hospital for new onset atrial fibrillation, and he had obesity and he drank too much alcohol and he had just some metabolic syndrome and various risk factors for developing a fib. And I had this whole conversation and he was unaware that any of those things contributed to his atrial fibrillation.

57:11And he really wanted to address it because of various life circumstances that I'll leave out for now, but his wife was there as well and she was all about it. And they were both willing to leave the hospital and act on this, especially knowing that by intervening on these things, it would impact something meaningful to them while also reducing his risk of recurrent atrial fibrillation. So that's kind of the key method that I would apply. And so recommendations for people who are wanting to get into it really has to do with getting some experience and practice with motivational interviewing. And then if you have the really solid understanding of the condition that you're trying to intervene on, then you can kind of weave those things together in real time much more effectively.

57:51Yeah. Yeah. That to me is where the fund of knowledge stuff, where you know the pathophysiology, you know what the person, uh, you know, the risk factors and so on and so forth. You can take that with your fund of knowledge with respect to exercise prescription, weave them together and bada bing, bada boom. Yeah. That's a hundred percent success rate. That's how that works. We, we wish, um, when I think about management here, I think about two distinct sort of like use cases. One is going to be prevention and the other one is going to be, well, what do after someone has received a diagnosis of either sarcopenia or like, you know, at risk for sarcopenia.

58:24So let's start with prevention. In both cases, exercise is going to be one of the biggest lever that we can pull as far as why. Well, we know that we retain muscle plasticity, whether we have sarcopenia or not, but even in old age, you can get stronger even into the 90s. We have good evidence of that. And we know that exercise, specifically resistance training, reduces the loss of those motor neurons, so you don't lose the type 2 muscle fiber, so you don't lose the strength and the power, so you don't have the fall, so you don't break your hip, so you don't end up seeing Dr. Baraki. There are easier ways to see Dr.

58:56Baraki than breaking your hip in the state of Texas. We know we have good evidence from master's athletes showing that it slows down aging and also preserves muscle mass and other interesting things within the muscle, the muscle capillarization. So how many blood capillaries do you have? Which is important for amino acids to make their way to the muscles, for sugar to make its way to the muscles, all these sorts of things. So that's the why. As far as how, the physical activity guidelines are fine. Resistance train twice a week. Do at least 150 minutes of moderate to vigorous intensity cardio.

59:28That would be like steady state stuff. Or you can do 75 minutes at least of vigorous intensity. Conditions would be a little harder where you can't really speak in short sentences. for example, that's like the minimum. I'd probably prefer something close to like double that because I think there are additional benefits afterwards, not only on function and performance, but also in like reducing risk of sarcopenia later on. Basically, you get to build this big base of physical development. Your 401k, your physical 401k is fully funded. And should you need to make a withdrawal later, well, you got some in reserve.

1:00:00And also you can be aggressive, more aggressive with respect to actually delivering that training load to an individual mostly because these people are starting with a higher level of fitness, generally because they have less medical comorbidities. There's been less sort of disuse over the years, and so you can be a little more aggressive as far as working up to that. You should still be gradual, but you don't have to take special care because the population you're dealing with is less frail, less risky. So that's the exercise situation. From a nutrition standpoint, we'd still recommend getting about 1.2 to 1.6 grams of protein per total kilogram body weight.

1:00:41That's kilogram body weight. So if you want to think 0.6 to 0.8 grams per pound, that's fine per day. But there's no micromanagement here, meaning like I'm not worried about where you're getting the protein from. I'm not worried about how much protein is in each meal, anything like that. Just at the end of the day, are you getting about this much protein? And that's all well and good. Check the box. Supplements in this case would be per preference for individuals who want a protein supplement because they otherwise aren't getting enough protein or it's easier for them or they're using it as a meal replacement to displace other foods.

1:01:12That's all fine. They want to take creatine. That's fine, modest effect. But I don't really feel strongly that a person needs supplements outside of personal preferences. Yeah, and I would want to point out here regarding the dietary protein sources. I mean, if you listen to a lot of folks in this space, they will, you know, aggressively harp on the need for all of the protein to be animal derived for like optimal efficiency and bioavailability and things like that. Nah. And we have talked about this before, that when studies have looked at actual outcomes of muscle gain and strength gain, when people are consuming enough protein in the doses that we're recommending, it actually doesn't matter whether it comes from animal or plant derived sources.

1:01:53and we can make an argument that for when people tend to bias it more in that plant-derived direction, they also will tend to derive a number of additional health benefits as well. And so, you know, to the extent that somebody, if I have somebody with cardiovascular disease or chronic kidney disease and they're asking me, should I, you know, continue or you're telling me I need protein, should I be consuming, you know, a couple of ribeyes a day or should I consume a variety of protein sources from, you know, beans and legumes and lentils and tofu and various other sorts of plant-derived sources, I would say, you know, I'm not strictly in opposition to animal-derived protein sources, but I definitely encourage the consumption of many of those plant derived sources as well because those will also stand to benefit your underlying medical conditions to a greater degree, your cardiovascular disease, your chronic kidney disease, your, you know, things like that, especially when consumed in sufficient doses.

1:02:45There's a lot of other benefits to be had from the other plant-derived compounds, the polyphenols, the fiber content, the differences in fat composition and impact on lipids and all sorts of other things. So yeah, I want to strongly distinguish our recommendations here for nutrition compared with what folks might hear in many other conversations around sarcopenia in this space that aggressively narrow in on it has to be animal-derived for bioavailability reasons or some other nonsense like that. Yeah, not an evidence-based take. And further, if you're like, well, look, whey is animal derived. I should replace my whey protein with soy protein.

1:03:22And then boom, more plant-based. That's what they said. That's probably not going to make a difference. In fact, I feel strongly that it's not. But instead, if you're getting more protein instead of it being steak or, you know, other sort of protein like that, and instead of you're getting it from plant-based sources, whether it's tofu or something similar, that's what we're talking about. More vegetable matter, more plant matter, generally speaking, it tends to displace foods that are high in calories, not very filling, low in fiber, and may have other sort of things that you really want to limit to some degree, like saturated fats from animal sources, for example.

1:03:57But yeah, just swapping like a whey protein shake for a soy protein shake is not going to do anything. All right. So that's the story with preventing sarcopenia to the extent that we can. And then from a health perspective under that umbrella, look, try to avoid obviously any chronic medical condition. And the ones that you do have, try to optimize them. Address them. Don't just say later when I'm older because all of these things can certainly contribute to developing secondary sarcopenia like we mentioned earlier. Now, so that's the first kind of umbrella or bucket that I kind of think about.

1:04:29The second one is individuals who have been diagnosed with sarcopenia or who are at high risk for sarcopenia. the first lever we're trying to try to pull here is exercise again. And why? Well, we can't regain the motor neurons that we've already lost, but we can still get stronger both in low velocity sort of applications. So traditional resistance training, but also high velocity stuff. So more power, which is better for avoiding falls, which is better for avoiding that hip fracture as a secondary to that fall. So you can improve performance. All that is well and good. Now, when you look at the evidence on actual training outcomes, those things readily improve.

1:05:07Strength, low and high velocities, that's power, readily improve and improve performance on whatever performance battery you want to give somebody. Improving muscle mass seems to be a little more challenging, but I'm kind of okay with that. Look, I want folks to get jacked too, but if they don't gain a bunch of muscle mass but gain a bunch of function, that's better for sure. And we can also then preserve existing muscle and improve its function, ultimately better quality of life. So that's the why. Easy sell for most folks, especially if they already have a diagnosis of sarcopenia. As far as how, well, this is where it starts to get a little different.

1:05:40So we want people to get at least to these physical activity guidelines and ultimately beyond. But because they're more vulnerable, likely due to long-term chronic disuse, right, so insufficient activity and being ultimately undertrained, they're a little more vulnerable to the dosing right out of the gate. So starting a little bit lower than you otherwise would is reasonable advice. But in saying that, I also must speak out of the other side of my mouth that I have a lot of concerns about underloading and undertraining this population. Yeah, you want to avoid injury risk, for example, but you also want to avoid spinning your wheels and just saying, yeah, this is good enough, like just walking, for example, or lifting very, very light weights that aren't anywhere close to failure or intentionally slow tempos for some particular reason.

1:06:29All of these things would be less likely to provide benefits. So you're kind of riding a fine line here, and ultimately you would want an experienced individual to be at the helm. But, yeah, we are offering some resources for this. So I just redid our beginner program. Now, previously this was mostly for younger individuals or other folks who kind of made their way to barbell medicine, and they're like, what do you do? I'm just starting out. What do I do? This is more public-facing, but there's going to be a number of different programs in there. One is an express sort of program. It's two days a week.

1:07:05It's completely based on machines and dumbbells. Whether or not this is more accessible to the general public, I suspect yes, just because it's like, look, I can do a leg press all day, but you want me to squat with a bar on my back? I'm not going to do it. While I'd like to unpack that later, I can't do that in an article, at least not to my satisfaction. So that's going to be one of the included templates. It might be perceived as less intimidating, ultimately easier to increase participation. And there'll be a version of that that's aimed at individuals who are either at risk for sarcopenia or who have sarcopenia.

1:07:36So it's going to be a slightly lower dose. So you get those two templates, a more three-day traditional type template for folks who are like, look, I'm 25 years old. I've never lifted weights before, but I want to be serious about it. What do? So you get all of that. That's coming out this week, so stay tuned to the Barbo Medicine channels. You'll check that out. Now, existing data on optimal programming appears very weak for individuals with sarcopenia. And I suspect it's either AI generated or some sort of English second language type thing because this is like the latest meta-analysis on this.

1:08:09And I'm going to read a direct quote from this. Okay. A recommended 19-week program includes three sessions per week at 49 % of a 1RM, featuring 15 exercises per set, six sets, and 16 repetitions per exercise, totaling up to 1 ,400 reps weekly. This is a quote? That is a direct quote. This is the worst AI hallucination I've ever heard. Either that or the worst coach I've ever heard. 100%, yeah. So, yeah, unfortunately, there's not great guidelines here for optimal sort of programming metrics. Now, just the way I think about programming in general, one of the acronyms that's used here frequently is FITVP, where that stands for frequency, intensity, time, type, volume, and progression, right?

1:08:55Now, frequency is mostly a tool that we can leverage to distribute the exercise over the course of generally a week based on a person's preferences. It doesn't really matter how you split it up, provided a person can do it, all right? So that's mostly a personal preference thing. Intensity, on the other hand, is not really negotiable here. We need the individual to be lifting weights with a rep range somewhere between like 3 to 20 reps. And most of those sets should be fairly challenging but not maximal. So depending on the rep scheme that you pick, that's going to determine the absolute load on the bar, the machine, the dumbbell, whatever.

1:09:30But it should be pretty challenging. So that's the intensity bit. You can't mail that in. It has to be somewhat challenging, and they should try to move each rep with intention quickly if possible. They try to get those fast-twitch muscle fibers to stick around. Time, this is mostly related to conditioning, but they should be doing conditioning as well because this appears to combat not only anabolic resistance, it improves the mitochondrial dysfunction that is prevalent in individuals with sarcopenia, and concurrent training is not a problem, plus all of the other sarcopenia-independent-type benefits of cardiorespiratory fitness improvement.

1:10:07So that's time. As far as type, exercise selection is really up to the individual, what they're willing to do. If you want machines, that's fine. You want dumbbells, that's fine. You want free weights, like barbell-based, that's fine too. Kettlebells, I don't care. You just have to do it. I do think there are some unique benefits with freestanding exercise from like a balance perspective and like moving the body in space. case perhaps uh that would be useful to an individual who's worried about falls for example but on the other hand a person who's already worried about falls ask them to walk out of weight and be challenging and perhaps that would limit the load that they can use ultimately compromising their outcomes in that case a leg press might be a better quote strengthening exercise to start whereas the squat training like a freestanding squat would be more like skill practice at first And then volume, again, I said it's going to be a little lower than you would otherwise want, but gradually increasing over time.

1:11:02And progression is the same as we've always described, progressive loading. As somebody's fitness improves, as their training tolerance improves, as they get stronger, they are required to put more weight on the bar, the machine, the dumbbell, whatever, to match their newfound fitness. That's the story on programming. You'll see that reflected in the new sarcopenia version of the Express Beginner Program. That'll be up on the website. It'll be freely available, so your parents won't have to download the Barbell Medicine app to get a free program. But yeah, we'll have that. So that's the training story.

1:11:37Nutrition story is much the same, but with some additional nuances. So the same protein target, 1.2 to 1.6 grams of protein per kilogram body weight per day, or like 0.6 to 0.8 grams per pound. But there is some micromanagement here because I do really want each meal to contain a significant protein bolus, meaning that I don't want them to have all of their protein at one meal. And I don't want all of the protein to be from sources that don't contain all the essential amino acids or a high concentration of them. Doesn't mean they should avoid plant-based proteins entirely, but paying some additional attention to this can be important for two reasons.

1:12:19One, anabolic resistance is prevalent, but the big issue, I'm less concerned about that, particularly in an active population. I'm more concerned with these folks, their appetite tends to be low. They tend not to eat a lot of protein in general anyway. And so if they're just like, oh, I get more protein from beans. And you're like, well, that's true. And I like the fiber and I like all the other stuff, but I really want something that has more essential amino acids in it. So a whey protein supplement can be pretty useful here, particularly for individuals who struggle meeting their protein target.

1:12:51I also feel maybe slightly more optimistic about how creatine could positively affect somebody's life. There does seem to be some good data here on it improving lean mass outcomes and improve sit-to-stand performance compared to individuals receiving a placebo. You don't need to take 20 grams a day like that idiot Rhonda Patrick said. You can take three to five grams per day. That's the dose. If somebody wants, that's fine. There are other sort of supplement recommendations that have very weak evidence and would not routinely recommend. So like vitamin D, it has some evidence around reduced fall risk and improved bone health.

1:13:31So if an individual has osteoporosis, they're gonna be on vitamin D or have been recommended to take vitamin D anyway. But I don't think it changes anything with respect to sarcopenia proper. Same thing about fish oil. and I saw HMB in one of these papers and I was like, we know that HMB doesn't do anything. So I would not recommend those two routinely. Vitamin D, I'm kind of whatever. Do you feel differently about vitamin D since you're the vitamin D whisperer? Right. No, no. I mean, I agree that this population, similar to how I described how my hospital population is enriched for those with sarcopenia, those with sarcopenia most often due to the collection of medical conditions that they have are also, I'll say, enriched for having vitamin D deficiency.

1:14:12That if the person is willing to take a supplement to improve that, then that's fine. But similar to creatine, I'm not pitching it as a game changer and certainly not as getting equal emphasis in our conversation compared with training. Yep. Yep. Biggest lever to pull for sure is going to be training, for sure. And lastly, about medicine. So individuals with sarcopenia tend to have multiple medical problems, and so optimizing this chronic disease management from a medical standpoint would be useful, like obesity, for example. We'll talk a little bit more about this in about 180 seconds. If somebody has testosterone deficiency, that would be a good time to potentially investigate that.

1:14:52It does, if you have an individual with testosterone deficiency, and then they are placed on testosterone replacement therapy, TRT, they do see an increase in muscle mass, but improvements in gait speed or like physical battery tests don't necessarily go up if a person is not actually exercising. Just again, showing that mechanotransduction is the ruler of all these things. You have to exercise. Yep. A hundred percent. And other things, if somebody has got an autoimmune disease, inflammatory condition, other sort of primary disease that should be optimized as well. And then also something that may kind of be last on your list of things to do, it's last on our outline here, is a sort of medication reconciliation.

1:15:35So beta blockers, for example, or glucocorticoids or other medications that either promote anabolic resistance or otherwise lead to decreased exercise or reduced exercise intensity or all of these things. That's tough. I would not recommend just coming off these things just because you're listening to this podcast. Don't go pour grandma's medications down the toilet. That's not what we're saying. But these are things to have conversations about the risks and benefits, especially because sarcopenia and decreased sort of function can compromise somebody's ability to live independently. Yeah, these are things that are, I think, underrated in terms of their importance to talk about.

1:16:15And unfortunately, in the same way that not all clinicians are going to be as facile and comfortable with the types of conversations that I described earlier with patients around this. Many clinicians get out of date or lazy with their use of medicines in this space. So like routine use of beta blockers for blood pressure management. And there are other situations where beta blockers have historically been used that now we're learning are probably not ideal uses. So in certain forms of heart failure, we thought maybe it would help. And now we're using less of it in, again, certain types of heart failure or in certain other contexts where there are some types of beta blockers that are better than others.

1:16:50And then And certainly with glucocorticoids or the medicines like prednisone, especially when they're prescribed all the time for like bouts of back pain and things like that, not ideal. Of course, that's usually for a relatively short, short course, but repeated short courses over time can be problematic if they're potentially avoidable. And then if certainly if somebody is on long-term prednisone, that's more often like for a reason. But if it's being done by a wise clinician, they should also have in the back of their mind, hey, what methods can I use to try to get this person on the lowest dose possible or on a steroid sparing agent to get them off of the glucocorticoid or the prednisone altogether because that is almost always preferable to somebody being on long-term prednisone therapy as an example.

1:17:29Yep. All right. Now we're going to transition to the last part of this podcast, lightning round. Quick answers to some common internet comments surrounding sarcopenia. First off, and this is one of the things that maybe initiated the development of barbell medicine. Walking is enough. Just walk more. Walking has had kind of a glow up. Hot girl walks. I don't know if there's an analogous hot dude walks, but if anything, I'm trying to do that. Walking is enough. Decidedly, no, in this case. We have good evidence from endurance athletes who, by the way, are doing way more than just walking. Much more intensity.

1:18:11But they still do not avoid that type 2 muscle fiber loss. So, no. Not going to be enough. have to do resistance training. It has to be challenging enough to force those type two muscle fibers, those motor neurons or motor neurons, depending on how you say it, to stick around non-negotiable. Walking is not enough. Walking is great. You got to lift some weights too. Yeah, I agree. And I think, you know, to put a firmer point on this, you mentioned a little bit of a distinction between those in whom we're trying to prevent sarcopenia versus those who already have it and in whom we're trying to treat it.

1:18:46And it kind of reminds me to some extent of our discussions around like cardiovascular disease for example where given that it's a lifelong process if you start way earlier in life you don't necessarily have to be quite as aggressive right you can do some just like you know relatively low level run-of-the-mill activity do a little bit of lifting here and there and even though it might not be enough to maximize your strength or conditioning it may well be enough to prevent you from developing significant sarcopenia in older age if you're consistent with it across your entire lifespan similar to you know reasonable control of your blood pressure, your blood lipids throughout your life is probably enough to avert the risk of a cardiovascular event pretty significantly.

1:19:22On the other hand, after somebody has a heart attack, as an example of a cardiovascular event, we have to like turn up the dial to 11 on our control of their risk factors, get their blood pressure as well controlled as we can, get their lipids as tightly controlled as we can. We get very aggressive very fast after one of those types of events. And in the same way, if somebody does have what we'll call clinical sarcopenia, or certainly a complication from it. Like if they have a significant fall with consequences with or without a fracture, for example, suddenly I'm like, you know, wanting to be much more aggressive and particular with all of these things.

1:19:54Now, it might not be the same way where I'm able to immediately institute maximum dose strength and conditioning training, but it's much more essential that they do it and that we progress it, you know, as aggressively as their physiology and recovery will tolerate if we want to reduce the risk of further complications down the line. So the stakes get higher. The intensity of your intervention has to get higher as well. Is the Pilates craze going to contribute to an increase in sarcopenia prevalence in about 20 years from now? I don't know that it's going to increase in prevalence, but it's probably not going to significantly decrease the prevalence.

1:20:26Not helping. Not helping. That's for sure. Also, excellent spinal tap reference. All right. Lightning round question number two. Well, isn't it true that if I stop lifting, a muscle is going to turn into fat? No. There are two distinct tissues. Thing one. So it's not like just the muscle that you have is going to like turn into fat and just like the fat that you have is not going to turn into muscle. That said, as Austin talked about earlier, my osteotosis and lipotoxicity is real. You get this lipid overflow of excess fat and it gets deposited in the muscle cells. Now this does all sorts of weird stuff.

1:21:01One, it exacerbates insulin resistance so the muscle is less responsive to all sorts of cool stuff like protein, like glucose, like mechanotransduction. And it also damages the mitochondria in the muscles themselves, so it makes it work. They don't work quite as well. Still, the biggest change that happens between these two compartments, muscle and fat, as people age, they tend to lose strength, which outpaces the muscle size loss, and fat mass also tends to grow. But they're not transitioning to one or the other. So that doesn't work. Okay, Austin, take on this. the third lightning round question.

1:21:37It's unsafe to lift heavy after 60. Old people can't lift heavy. What's up with that? Yeah, my admittedly anecdotal evidence on this that I'll share with you is that I'm thinking back over my past, say, decade seeing people in an emergency department and hospital setting, and I have admitted probably zero patients in the 60-plus demographic to the hospital for a complication of lifting. They certainly might show up for, you know, a tweak or a strain or a sprain or, you know, some, some ache or pain or routine musculoskeletal injury that are, as we have talked about before, they tend to be non-catastrophic.

1:22:15Whereas I have admitted presumably probably hundreds and hundreds and hundreds of folks whose conditions may well have been mitigated or prevented altogether if they had been lifting across the lifespan, even if there was some degree of trade-off or, you know, some, you know, nominal increase in musculoskeletal ache, pain, or injury risk, which in my mind would be acceptable to me compared with the risk of complications that I observe in terms of their cardiometabolic health, you know, falls, fractures, injuries, all sorts of other things that are more significant. So if I were seeing, you know, septuagenarians coming into the hospital left and right for, you know, deadlift complications, then we'd be having a different conversation, but ain't the case.

1:22:57So my argument is that it is much riskier to not lift in this demographic than it is to lift. Yeah, life is not a risk-free endeavor, and you have a risk of injury even if you don't exercise. And fortunately, the risk of lifting weights, even heavy weights, even if you don't do it with, quote, perfect form, is relatively low. The best data on this is about two to four injuries per thousand participation hours, which is not dissimilar from like cycling or, you know, recreational walking, particularly if you include motor vehicle accidents that happen there. But that's a separate podcast. In this population, lifting is also very safe.

1:23:37There's not like an influx of just injuries, even when they're doing power training, like plyometrics, which I probably wouldn't exactly have folks do, but sure, maybe. So, yeah, relatively safe. and the risk of not exercising far outweighs the risk from lifting heavy. Most injuries that do occur are not catastrophic. They resolve on their own within about two weeks. They don't require specialized medical attention. So, yeah, you should lift. Last lightning round question. Well, Dr. Baraki, look, man, all these GLP-1 agonists, Ozempic, Wigovie, Zepbound, et cetera, aren't they just causing sarcopenia?

1:24:15They are definitely not in general. Now, I will say that there have been some situations where, for example, I have seen maybe a patient who had advanced cancer, and they also had diabetes, and they were on one of these medicines for their diabetes. And maybe they started cancer treatment, and they had no appetite, and they're losing weight. And I'm like, okay, well, maybe this isn't the best medicine for you. Those cases are few and far between. As we will discuss on another upcoming podcast discussing GLP-1 agonists in very great degree of detail, these medicines are very useful. And despite the hysteria around them reducing quote-unquote lean body mass, we'll talk about in that episode, there's differences between impacts on lean body mass versus on muscle mass.

1:25:00Those are not the same thing. and additionally as we have made the case this entire podcast muscle mass is not the primary variable of interest here because we know that it's possible to have more muscle mass but poorer muscle quality if there's a whole bunch of fat in it and so based on some other very interesting recent evidence there's you know based on certain diagnostic criteria for sarcopenia the semeline study that you have cited and that we'll talk about there as well actually showed that it reduced the incidence of sarcopenia because as people lost weight their physical function improved as you address their obesity, their physical function was able to get better, which actually led more people to no longer meet criteria for sarcopenia.

1:25:37So, you know, I think that obviously clinicians need to use their brain when they're prescribing these medicines. So if somebody's, you know, coming in with a, you know, starting BMI of, you know, 20, probably not the best patient to start on, you know, a high dose of a GLP-1. Although, depending on how this class of drugs evolves in the future, there may be some that have maybe a more deliberate, less impact on body weight and appetite and more impact on maybe substance use tendencies or various other things. That's a TBD, but this is not a great source of concern for me at the moment. And none of this obviates the need for people to just train.

1:26:11So even if you are on one of these, you need to be training regardless. That's our strongest recommendation. Yep. Agreed. Yeah. For all the, as you said, hysteria surrounding the potential of excessive muscle loss, show me the data. show me the data and until then i would not say that confidently or with like a lot of panic uh surrounding the message but it's a reasonable hypothesis and we want to be risk averse but like where's the data yeah all right let's wrap this up sarcopenia is not a disease of the elderly but rather it is a process that begins much earlier in life when an individual can build their physiological reserve or fund their physical 401k if you like finance analogies First, we must move away from the focus on muscle mass, and especially conflating it with lean body mass in general.

1:27:02The real enemy is dynopenia, the loss of force and power. A large muscle that cannot generate force is a liability, not an asset. Second, regarding diagnosis. If you wait for a DEXA scan or for your doctor to tell you that you're sarcopenic, you're too late. Functional tests like gait speed, sit-to-stand tests, and similar are early warning signs that you or a loved one might have sarcopenia. Third, on reversibility. We cannot regrow dead motor neurons. However, we can still intervene with exercise and make sure the remaining fibers are preserved and functioning well. For the healthy individual, the goal is to fund your physical 401k as much as possible.

1:27:39Build strength and proficiency across a wide variety of different exercises, rep range, and tasks. Generally speaking, get as fit as possible. Future you will thank you. For the person who has or is at risk of sarcopenia, the time to act is now. Start with relatively low volume training and gradually increase from there, making sure that they're pushing themselves, lifting relatively challenging weights and moving the loads as fast as they can. The risk of under-training and under-loading a person with sarcopenia far outweighs the relatively small risk of injury in this population. Finally, nutrition.

1:28:12Most individuals would benefit from eating an additional serving of two of high-quality protein each day. But this becomes even more important for those with sarcopenia, where appetite is relatively low and the likelihood of anabolic resistance is high. Making sure each meal has a good dose of high quality protein is likely to be beneficial. Supplementing with a whey protein that's third-party tested can be useful, especially for those who struggle to eat enough. However, eating more protein alone will not significantly improve sarcopenia absent of physical training. Don't wait until you or a loved one is weak.

1:28:43The time to start investing in yourself is now. And with that, that is a wrap on the Barbell Medicine podcast on sarcopenia. Special shout out to Dr. Austin Baraki for joining us and sharing his expertise. Before you guys go anywhere, please leave us a five-star rating and a review. It really helps drive traffic to our podcast so we can keep bringing you all the latest nuance in health and fitness. From everyone here at Parable Medicine, I'm Dr. Jordan Feigenbaum. We'll catch you next week and every week right here on the Parable Medicine Podcast.

From the publisher

Episode Summary: Dynapenia, Motor Neurons, and the Firewall


In this episode, Dr. Jordan Feigenbaum and Dr. Austin Baraki redefine sarcopenia, shifting the focus from simple age-related muscle size loss (atrophy) to the more critical loss of muscle strength and power (dynapenia), a process that starts in the 40s. They explain the profound pathophysiology: sarcopenia is primarily a neurological event caused by the death of high-threshold motor neurons, leading to the selective loss of fast-twitch (Type II) muscle fibers. This explains why strength declines 3x faster than size.


The hosts detail the modern diagnostic framework—prioritizing functional tests like the sit-to-stand test over late-stage mass measurements. They provide the definitive, evidence-based management plan: lifelong heavy resistance training is non-negotiable as it acts as a firewall against motor neuron death. The episode concludes with a debunking of common myths (e.g., "walking is enough," "muscle turns to fat," "lifting heavy is unsafe for the elderly") and practical advice on optimizing protein and creatine use to combat anabolic resistance.


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Key Takeaways

  • Sarcopenia is a Neurological Problem: The primary cause is the death of high-threshold alpha motor neurons, leading to the selective loss of fast-twitch (Type II) muscle fibers—the fibers responsible for power, speed, and fall prevention. This explains why strength (dynapenia) declines 3x faster than muscle size.
  • Diagnosis Must Be Functional: Waiting for a doctor to diagnose sarcopenia via a muscle mass measurement (like a DEXA scan) is too late. Modern guidelines prioritize functional tests like grip strength and the sit-to-stand test as early warning signs, as muscle can be normal-sized but still dysfunctional.
  • Resistance Training is the Firewall: Lifelong heavy resistance training slows motor neuron loss by 300% compared to the general population. Walking is not enough; only challenging resistance work sends the necessary signals (mechanotransduction) to preserve these critical motor neurons and Type II fibers.
  • Nutrition for Treatment: For individuals diagnosed with sarcopenia, managing anabolic resistance is key. This requires attention to protein timing: consume a good dose of high-quality protein (rich in essential amino acids) at each meal. Supplementing with a third-party tested whey protein and 3-5g of creatine daily may be beneficial.
  • Safety & Risk: The risk of injury from lifting weights, even heavy weights, in the elderly population is relatively low (2-4 injuries per 1,000 participation hours) and is greatly outweighed by the risk of immobility, falls, and subsequent complications.


Episode Timestamps

  • 0:00 Introduction: The Silent Epidemic and Dynapenia
  • 8:50 Defining Sarcopenia: Why Size Alone is Misleading (The Green Banana Analogy)
  • 17:37 Epidemiology and Sarcopenic Obesity
  • 23:39 Screening Tools: SARC-F, Sit-to-Stand Test, and When to Screen
  • 40:53 Pathophysiology: Why Sarcopenia is a Neurological Event
  • 42:28 Motor Neuron Death and Selective Type II Fiber Loss
  • 52:33 The Problem of Anabolic Resistance
  • 53:16 Management and Prevention Strategies
  • 57:20 Exercise Prescription (The "Why" and "How" of Resistance Training)
  • 1:10:44 Nutritional Strategy (Protein Boluses and Supplements)
  • 1:16:21 Sarcopenia Myths: Walking, Muscle Turning to Fat, and SafetySection I: Sarcopenia Redefined—A Failure of the Nervous System

Dynapenia and the Shift in Diagnostic Focus


The episode establishes that sarcopenia must be understood as a problem of dynapenia (loss of strength and power) first, not just muscle size. Historically, the term, coined in 1989, focused on flesh poverty (Sarc-o-penia), but data quickly revealed that strength declines 3x faster than muscle mass. Old guidelines prioritized size, leading to a paradox: people with normal-sized muscles were still experiencing falls and fractures.

The modern framework, driven by groups like the European Working Group, prioritizes functional outcomes. Waiting for a diagnosis via muscle size (like a DEXA scan measurement) means intervention is often too late. Muscle quality—the force produced per unit mass—declines dramatically due to neurological and cellular changes, even if the muscle maintains its volume through fat or water infiltration.


The Pathophysiology: Alpha Motor Neuron Death

The root cause of dynapenia is primarily neurogenic atrophy.

  • Motor Neuron Loss: As individuals age, the high-threshold alpha motor neurons that innervate fast-twitch (Type II) muscle fibers begin to die (a process that can start in the 40s).
  • Fiber Type Conversion: When a high-threshold neuron dies, a neighboring low-threshold (slow-twitch) neuron attempts to rescue the abandoned Type II muscle fiber. The fiber survives but is converted into a slow-twitch (Type I) fiber.
  • Loss of Power: Since Type II fibers are responsible for rapid force production, the selective loss and conversion of these fibers means the individual loses speed and power, severely compromising the ability to perform activities like quickly rising from a chair or catching oneself during a trip (the righting reflex). This is why falls and subsequent hip fractures become common.


Sarcopenic Obesity

A particularly dangerous presentation is sarcopenic obesity, where a person carries both a significant amount of fat mass and poor muscle function. While individuals with obesity generally carry more lean mass, the fat infiltration (lipotoxicity) into the muscle tissue exacerbates anabolic resistance and insulin resistance, making the muscle dysfunctional and resistant to training and nutritional signals. This combination significantly compounds the risks of immobility and mortality.

Section II: Management, Prevention, and Training Prescription

Resistance Training is the Firewall

The primary goal of intervention is prevention, as lost motor neurons cannot be regrown. Resistance training acts as a firewall against further motor neuron death.

  • Mechanotransduction: Challenging resistance work sends necessary signals back to the motor neurons, signaling that the muscle fibers are still needed, slowing the rate of death.
  • Evidence: Lifelong lifters show a neurogenic decline of only 0.35% per year, compared to the general population's decline of 1% per year—a 300% slower rate of loss. Walking is not enough to achieve this protective effect, as endurance athletes still show evidence of Type II fiber loss.

Exercise Prescription: The Physical 401K

For prevention, the goal is to fully fund the "physical 401K." This means exceeding the minimum physical activity guidelines:

  • Resistance Training: At least twice a week, training all major muscle groups.
  • Cardio: Aim for double the minimum (e.g., 300 minutes of moderate-to-vigorous activity per week).
  • Progression: Individuals should build a big base of fitness, allowing them to be more aggressive with training load and resilient against co-morbidities later in life.

For individuals with a diagnosis of sarcopenia (secondary prevention/treatment), the training emphasis shifts:


  • Intensity is Non-Negotiable: Lifts must be challenging and performed with the intent of moving the load quickly to stimulate remaining Type II fibers.
  • Start Lower, Progress Gradually: The population is more vulnerable to over-dosing due to chronic disuse. Start with a lower total volume but ensure progression is gradual and consistent.
  • Type: While barbells are fine, machine-based training (e.g., leg press) may be a less intimidating entry point and can allow for higher training loads by mitigating the balance/fall risk of free weights.

Section III: Nutrition, Supplements, and Myths

Combating Anabolic Resistance with Protein

Anabolic resistance—the reduced responsiveness of muscle to nutritional signals—is prevalent in sarcopenia. To overcome this, the focus should be on protein timing and quality:

  • Total Intake: Aim for 1.2 to 1.6 grams of protein per kilogram of body weight per day (0.6 to 0.8g per pound).
  • Protein Bolus: Ensure each meal contains a significant bolus of high-quality protein, rich in essential amino acids, to maximize the anabolic signal. This is critical for individuals whose appetite is often low.
  • Supplements: A third-party tested whey protein supplement can be a useful tool for those who struggle to meet targets. Creatine (3-5g/day) is also strongly advised due to data supporting its benefit in improving lean mass and functional outcomes like the sit-to-stand test.

Sarcopenia Myths Debunked (The Safety of Lifting)

  • Myth: Walking is enough. Fact: No. Walking does not provide the challenging stimulus required to save high-threshold motor neurons and Type II fibers.
  • Myth: Muscle turns to fat. Fact: No. Muscle and fat are distinct tissues. However, chronic disuse leads to fat infiltration into the muscle (lipotoxicity), which impairs function.
  • Myth: It's unsafe to lift heavy after 60. Fact: The risk of injury from lifting weights in the elderly is relatively low (2-4 injuries per 1,000 participation hours) and is greatly outweighed by the high risk of immobility, falls, and subsequent complications caused by inactivity.
  • Myth: GLP-1 agonists (Ozempic/Wegovy) cause sarcopenia. Fact: This is hysteria. Data does not support excessive muscle loss, and the benefit of reducing obesity-related risks far outweighs the low risk of muscle loss when coupled with resistance training.


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