On this episode of the Flex Diet Podcast, I chat with Dr. Mike Roberts, a full professor at Auburn University and head of the Nutri Bolt Applied and Molecular Physiology Lab. Mike’s one of the sharpest minds in muscle science, and we go deep into the nitty-gritty of hypertrophy, including everything from rodent studies to human trials to the molecular pathways that drive muscle growth. We get into some serious geekery: ribosome biogenesis, muscle stem cells, the extracellular matrix — yeah, all the stuff happening behind the scenes when you train. Mike also shares his take on how HIIT and consistent resistance training impact muscle adaptation, and we riff on where nutrition fits into the equation. If you're into the science of muscle or you're a coach looking to better understand the mechanisms behind hypertrophy, you’ll dig this one. Tons of actionable nuggets and some fascinating research. Check it out!
On this episode of the Flex Diet Podcast, I chat with Dr. Mike Roberts, a full professor at Auburn University and head of the Nutri Bolt Applied and Molecular Physiology Lab. Mike’s one of the sharpest minds in muscle science, and we go deep into the nitty-gritty of hypertrophy, including everything from rodent studies to human trials to the molecular pathways that drive muscle growth.
We get into some serious geekery: ribosome biogenesis, muscle stem cells, the extracellular matrix — yeah, all the stuff happening behind the scenes when you train. Mike also shares his take on how HIIT and consistent resistance training impact muscle adaptation, and we riff on where nutrition fits into the equation.
If you're into the science of muscle or you're a coach looking to better understand the mechanisms behind hypertrophy, you’ll dig this one. Tons of actionable nuggets and some fascinating research.
Check it out!
Sponsors:
Available now:
Episode Chapters:
Flex Diet Podcast Episodes You May Enjoy:
Connect with Mike:
Get In Touch with Dr Mike:
Speaker: [00:00:00] Welcome back to the Flex Diet Podcast. I'm your host, Dr. Mike T. Nelson. On this podcast, we talk about all things to increase hypertrophy and muscle size performance, improve body composition, and do all of it in a flexible framework without destroying your health. Today on the podcast, we've got my buddy Dr.
Mike Roberts. He is a full professor at Auburn University, the school of kinesiology. He's also the director of the Nutri Bolt Applied and Molecular Physiology Laboratory, and he is one of my top go-to people for all things physiology and especially in the land of hypertrophy. So you may not have heard of him, but if you're definitely in the research space, then you have definitely heard of him and seen his work published.
Kind of flies under the radar a little bit and doesn't put out a lot of stuff on social media 'cause he is been [00:01:00] busy working full time in the lab and with students. He's done everything from animal research to lots of humans subject studies from exercise physiology areas to even the interventions with supplements and much more.
So I will give a warning that this podcast gets. Super nerdy and we do go really hard down some of the molecular pathways. So if you are into hypertrophy and what makes muscles bigger and then potentially stronger, I think you'll really enjoy this. It is, I wanted to do something that was a little bit different than which is good information of here's protein essential amino acids and mTOR.
I think that's super important and we'll have more. Information in another podcast on that coming up again because it is a requirement and is essential, I wanted to get a little bit more on the theoretical side of what are some other mechanisms and other things going [00:02:00] on here. Everything from the act and myosin structures themselves to other structures and organelles that might be involved.
And Dr. Roberts talks about some of the great studies his students are doing. Some of which is published or some of it will be out very soon, which may be out by the time you listen to this podcast if you're listening to it a little bit later. So it does get uber nerdy. You may have to stomp and look up a few terms here and there, but at the end we do try to make it very practical.
So if you hang in all the way to the end with what you can actually do based on some of these mechanisms. But I do like speculating. What some of the mechanisms are based on the current data that we have. The cool part about talking to Dr. Roberts is not only is his wealth of experience in this field is he also many years ago on a former life, used to work as a personal trainer.
So at the intro we talk a little bit about his academic journey and how he got to [00:03:00] where he is at now, and then we do the deep dive into the molecular underpinnings of muscular hypertrophy. And if you are interested in more great information, you can hop onto my newsletter for free. Go to mike t nelson.com.
There'll be a little button that says newsletter. We'll put a link here down below. And then also, right now, depending upon when you are listening to this podcast, we have the meet head. Cardio Level two is opened through August 12th at midnight 2025. This is the high intensity intervals, the anaerobic portion.
So everything from the Tabata protocol to 30 30, how you would set up interval work to one, both match your training. So if you are a lifting meat head, how do you do this in a way that is going to make your lifts better and potentially your competitions better? Without [00:04:00] destroying everything else in the process.
'cause one of the downsides of high intensity interval training is it works really well for increasing VO two max, increasing anaerobic performance or what's called sometimes RSA or repeat sprint ability. So your ability to do a task and then to do that task again at high quality, which is what you're gonna need for lifting weights if you want to get bigger and stronger.
But they can add too much stress. So you have to be careful of not adding too much stress, making sure you're getting the maximum amount of adaptation. So we'll have some information there in the podcast below, but the best way to get all that information is to hop on to the newsletter. I'll have all the information out and possibly some other cool stuff there.
So go to the newsletter. We also have our sponsors element. You can check them out. For electrolytes and they're very tasty. I've been drinking the raspberry one per usual. [00:05:00] If you're looking for ketones to help potentially with cognition under fatigue or just cognition later during the day, I've been using them during more, I'd say grip lifting sessions, some lower rep, higher CNS activity stuff, and my little air quotes here.
And it definitely seems to help. Dose I usually find is about two cans, which is about 20 grams of a ketone Esther. So check out our friend's, Teton below. I do some work with 'em, and I'm also an ambassador for them. So full disclosure. And then one of the other parts we talked about in the show is are there some benefits to doing maybe concentric only, or eccentrics or isometric testing and things of that nature.
And we've got more information on that through Beyond Power, the Vulture one device. So you can click the link down below here. I was talking to Dr. Robertson, the podcast. His lab actually has a couple of the devices, which is super [00:06:00] cool. I am an affiliate for them, so full disclosure, I have a device at home.
I absolutely love it. I actually like it much better than I thought I would. And one of the things I really like about it is the automatic changing from concentric to eccentric. So for example, if I'm doing a seated row, I can pull the concentric portion. So pulling back with a hundred pounds, then I can add whatever I want on the eccentric.
So I've been working up to even 50% eccentrics for four to six rep count all some of the phasic training from Cal Dietz and myself. We wrote the Phasic two training book. So on the ecentric, the lowering or the handle being pulled back to the device, I can go up to 150 pounds. So it'll do that automatically.
Just program it on the screen. You don't need an app or anything else. They do have an app, but you don't need to run it and it'll automatically detect the end range of motion. It'll add to 50 extra pounds, [00:07:00] and it's pretty cool. I've actually really enjoyed it. So if you have any questions on that, hit me up.
There's a link below if you are interested. I'd highly recommend you check that out. So those are our sponsors. Thank you so much for listening. And here is the podcast with Dr. Mike Roberts, all about muscular mechanisms of hypertrophy.
Dr Mike Roberts: i'm a professor here at Auburn University. I've been here since 2013. I've overseen the training of 25 graduate students. Nice. And I've graduated 17, about to be 18 in December. Most of our research has focused on the effects of exercise nutrition aging mainly on skeletal muscle physiology.
Although at times our research questions may be more generic, just body composition changes. But yeah. Yeah. My love is skeletal muscle [00:08:00] physiology and we do take a molecular approach. And so that does involve us usually getting skeletal muscle biopsies from our participants. And with that once we get biopsies.
We can look at a variety of different things ranging from, fiber type specific cross-sectional area changes with training. For instance, we can look at muscle stem cell content. We can look at ribosome content and muscle. We can look at signaling pathways at trigger protein synthesis. We can look at markers of proteolysis, we can look at mitochondrial markers.
And so we really do have a variety of options breaking the skin and getting down to that tissue level with our interventions.
Dr Mike T Nelson: That's great. What made you study muscle in particular?
Dr Mike Roberts: Yeah. I've always, growing up I was, as a [00:09:00] young kid, I was a little bit into athletics, but I didn't do.
Athletics in high school, nor did I do athletics in college, with the exception of walking on and then walking right back off of the Baylor football team. So, that unto itself is a story. My, my roommate in college was a scholarship guy and he thought I was good enough to, at least try out.
And I was on the team like formally for
Speaker 2: whatever, there you go. Eight weeks.
Dr Mike Roberts: So, yeah. But anyways, one thing I always did do though was lift weights. That practice was instilled onto me by my parents. They were avid weightlifters my dad more so than my mom. My mom was doing it more for the, quote unquote toning aspect.
And she was really into doing walking and jogging and and that sort of thing. But they both were routinely exercising. And yeah that really during my formative years just stuck with me, lifting weights, you can see strength [00:10:00] changes, you can see physique changes. I started doing it very regularly in high school ninth, 10th grade.
And then you graduate looking into sports nutrition, like, how can you optimize your weight training in the gym? And that's when I started trying supplements such as h and b and creatine. I remember, trying glutamine glutamine yeah and things of that nature back in the 1990s.
Then you start reading things like Muscle and Fitness and Flex Magazine. And to me that, that was really, I think remarkable. I remember going to the grocery store in high school. I didn't have much of a life in high school. I didn't go party, I didn't go out and like, hang out with friends or cow tip or any of that stuff that people No cow Tipping to Texas.
Yeah. Growing up in Texas, that's what the kids did. But I would go to the grocery store with my parents on Friday night, man. That's how boring my, my life was. But I loved it. I loved my parents. They were great parents. And while they would, do their grocery shopping or whatever, I'd go [00:11:00] straight to the magazine aisle and I would like sit down on the grocery store floor and just read flex magazines.
That was what I did in high school. So, I'm sure your comment section would be, man, what a loser that guy was. But yeah, no, I remember that to me, I think marked my love for working out and wanting to look like folks like Jay Cutler, Ronnie Coleman, flex Wheeler, Dexter Jackson.
And so then I went to college and I was a biology major. And I think the intent originally was to be get into dentistry, like pre-dent stuff.
And I, I just didn't, I'd shadowed a dentist or two. I just didn't enjoy it. And so I took another year as a senior and was trying to figure out what I wanted to do.
My mom of all people like, emailed me and said, Hey, I heard there's a new professor at Baylor that just showed up and he's setting up an exercise physiology laboratory. You gotta go check that out. I said, okay, yeah, sure. So I went over to [00:12:00] the kinesiology building at Bailey University. And the new professor was Rick Kreer, who had shown up from the University of Memphis.
And so I knocked on his door and he. He said, can I help you? And I said yeah. I'm an undergrad and I just, I want to see what you're, setting up here and what you do. And he showed me around that laboratory and I was pretty amazed at the time. I didn't even know people like researched exercise or sports nutrition for a living.
I didn't know professors did that. I had an idea that professors research things, but that wasn't one of the things I had thought that they did. So I said, do you mind if I shadow? And Rick was very generous. He said yeah. Just start, coming in and helping out with projects and that sort of thing.
So I had shadowed and volunteered for his laboratory for my last senior year at Baylor University. And then I thought, well, I'd like to get a master's. This seems [00:13:00] pretty interesting. And I at, to continue on and study under the. The tutelage of Rick that'd be great to get a master's degree.
And I did that during my second year at Baylor. Rick had recruited Darren Willoughby to set up a wet laboratory, and that's the first time I saw muscle biopsies. And that to me was fascinating that, that really, at that point on that memory, I thought, wow, I can integrate my biology training from undergraduate studies to, human physiology as human participants in these studies, or either supplementing with things that are supposed to alter bioenergetics or enhance hypertrophy.
Or I can study, muscle in the context of aging and how exercise can help mitigate, the aging defects that we see in muscle. And so that's when I truly got [00:14:00] bit by the bug and knew from that moment on I'm getting a PhD, and then I'm, I figured after the PhD I can become a professor, but then I soon realized you can also do postdoctoral work so you can become a postdoctoral fellow before you then become a professor.
And I said I absolutely wanna do that. I want to take this as far as I possibly can in terms of learning all of the nuance in regard to studying human skeletal muscle with this biopsy technique. And so, yeah, I went on to do my PhD at the University of Oklahoma. So Chad Ick was my mentor. And and I also, I was involved with projects with Jeff Stout and Joel Kramer. So a lot of my influence. Between Masters and PhD work, were a lot of the folks that are involved in the ISSN, right? Nutritional supplementation when you talk about Rick Ryder, Darren Willoughby, Chad [00:15:00] and Jeff Stout. And I really enjoyed that. There was nothing against that. I wanted to go mechanistic and the one thing I didn't learn during my master's or my PhD was rodent work or doing cell culture projects.
Meaning studying muscle cells in a p petri dish, be it via microscopy or you can even do gene manipulation studies pretty easily in a Petri dish as you can and in rodents two. But I didn't have any of that experience throughout my master's or PhD training. So I looked around the country and there were two labs that stuck out.
One was Karen Esser. She was at the time at the University of Kentucky. At their medical school and then Frank Booth, and Frank was at the University of Missouri in their vet school. So I got offers from both of those laboratories to do my postdoc work. And it was an incredibly hard decision because Karen is just an [00:16:00] absolute saint, great mentor.
And at the time she was really innovative and frankly, this is nothing against Frank. He's like a father figure to me. But I felt like Karen was a little bit more innovative on the hypertrophy side of things. When doing the mechanistic rodent work. She was the one that pretty much identified that the mTOR signaling pathway is responsible for promoting muscle growth when implement mechanical overload.
Right. So. Karen was doing that. She was doing exciting micro RNA work. And she was the first to determine that with mechanical overload. And by the way, mechanical overload just means weight training if you're gonna keep it simple, some
Dr Mike T Nelson: form of tension on the muscle.
Dr Mike Roberts: It's a form of tension on the muscle.
You can't necessarily weight train rodents, although I take that back because you actually can wait train rodents. Troy Hornberger is doing this right now.
Dr Mike T Nelson: Yeah. So squatting mouse apparatus and some interesting things they have.
Dr Mike Roberts: They are. [00:17:00] They are. But Troy is actually doing a ramp protocol where it's resisted, loaded and Oh, adaptations across several different muscles are looking like you would see with human resistance training.
Huh, interesting. An increase in hypertrophy. Yeah. So Troy is just front and center. Him and Ja, Jamie Hier the postdoc in his lab. Where was I going with that? So, yeah no. I say mechanical overload. That's just a little bit more appropriate when you talk about like synergist ablation, which yep.
Is a surgical induction of hypertrophy and a rodent. So Karen was, doing eem acute bouts showing mTOR signaling was operative with hypertrophy. She was also showing with synergist ablation that microRNAs are expressed in skeletal muscle. And again, this is back in the sort of mid to late two thousands.
So these are revolutionary findings. We take some of these findings for granted now, but Karen was really crafting the [00:18:00] narrative around these topics. But with Frank, I went and I think with Frank, I was just sold on he's been innovative on a lot of different fronts, meaning like.
Frank was the first to look at global mRNA expression and muscle in response to disuse atrophy. And this was in rodents. Frank was the first to measure mRNA in, in muscle tissue period. Him and Pete Watson did that in the early 1980s. Frank with some of his work with John Halsey showed that with exercise you can increase mitochondrial biogenesis.
And in addition to that, with disuse, you see this rapid and exponential decline in, in skeletal muscle, mitochondrial content. And so, I think I leveraged my decision on just saying with Frank, he's always been at the forefront. Karen was a little bit younger and was really focusing on hypertrophy.
And so I thought, [00:19:00] Frank just based on that, like I, I chose Frank. I don't regret that, but I always had wondered and what if I went with Karen, because she is just extraordinarily innovative in her own right and regarding mechanisms surrounding skeletal muscle hypertrophy.
I would frankly say that Karen Esser is like front and center, like the George Washington of that Mount Rushmore. And that's my own personal opinion. But yeah that's how I got into muscle. And then after my postdoc here at Auburn University, I accepted a assistant professor position.
And I thought initially I would continue on with doing heavy rodent research. I set up my laboratory to where I can do human training. I could do some rodent stuff. It wouldn't be in this laboratory. It'd be across campus in their vivarium. And I also could do cell culture. So I can look at muscle cells and petri dishes, and you can put different things [00:20:00] on them.
You can put amino acid, you can put creatine, you can put novel ingredients on these muscle cells to see, if there's an anabolic response. So I had the three-pronged approach to where I can do cells, I can do rodents, I can do, I could do humans. We started with rodents and we worked with a great and dear friend Chris Lockwood.
When I first started here at Auburn on some rodent research. But then I got approved to do muscle biopsies on campus with the medical with the physician on the IRB. And so once I got, approved to do that. I just didn't look back. People tend to appreciate the human exercise findings more so than the rodent findings, even though I will make the argument that the rodent researchers have driven the innovation in our field.
My job I view right now is being [00:21:00] as innovative as I can on the human side of things. So, we as examples, current projects, right, we're interested in why older participants don't gain as much muscle when doing 10 to 12 weeks of resistance training compared to college age participants.
And so we have a, an older cohort, we have a younger cohort, around 15 participants each we have pre-intervention biopsies, we have biopsies following. At the last training bout, that'd be 72 hours post what we showed phenotypically right, is that the VASIs lateralis muscle and older participants gained about 50% hypertrophy relative to the younger participants.
And then looking at whole body dexa lean tissue, which would, represent skeletal muscle mass changes. We [00:22:00] see the same thing. There's this 50% reduction in muscle mass gained after 10 to 12 weeks of resistance training. So now we have the biopsies and we have a collaborator on campus where we're gonna be looking globally at the proteomic changes in terms of all of the proteins that are changing in the younger participants pre to post training.
All of the proteins that are changing pre to post training in the older participants. Then we can do some machine learning and bioinformatics to say, what do all of these collective changes mean? Right. Are there certain biological pathways that are predicted to be operative in terms of explaining why older participants cannot hypertrophy as well when compared to the younger participants?
And we already have some clues from some of our prior data that indeed there are probably there is some dysfunction with muscle aging. And so when you lift weights, [00:23:00] you may be working against the grain, especially if you've never lifted weights in your life. We, we do have some insight there.
So this gets molecular and bear with me, but one thing that we consistently have seen in older participants, granted these aren't large studies. These are, I would say what we have so far is preliminary data, but what we have seen. Is that there seems to be dysfunctional gene splicing events.
Which is to say that there is more machinery in the nuclei of muscle cells in older participants that lead to RNA splicing, which can lead to different protein isoforms being expressed in muscle tissue. And it's hard to determine, okay, is there a functional consequence here that, with that dysfunction?
But I think our argument has been, [00:24:00] well, in younger people you don't see those splicing events, right? So this is either coinciding with muscle aging or it could be a contributing factor. Another thing that we have seen in older rodents, and I'm looking up in the air thinking if we have the human data on this.
Yeah, we do. So in older rodents and in older human participants, we see an increased presence of long non-coding. RNA in particular, this transcript is called line one or L one, and people have said, Hey this L one gene is, it should be repressed in the healthy state, well, in skeletal muscle.
In older participants, we do seem to see some higher levels of this L one transcript, which implicates that you have nuclear instability [00:25:00] or otherwise thought of as when you have DNA that's compact in the nucleus of a younger participant. As you age, you may have the loosening of that chromatin.
That can lead to dysfunctional transcriptional events like increased L one. So with aging, I think there is some nuclear instability that occurs in skeletal muscle. And now we, what we're becoming more interested in is okay if short-term resistance training can't reverse that, what about training for years to decades?
Can I continue to train me personally? And by the time I hit 60, my muscle still at the molecular level resembles a younger person. Meaning I have less L one transcript floating around, right? I have less chromatin loosening in my muscle cells. I have less splicing events in [00:26:00] my muscle cells.
And then does that coincide or cause. My muscle cells to be relatively healthy and rejuvenated. So that's probably one of our main focuses right now. But we have a lot of other projects going on. So one student, his name is Daniel Plotkin. We just finished static collection on his project, but he is very interested and he's driving this.
This is all his idea. I just help support him to give him the resources to do this. And I took the biopsies, but he's interested in length and contractions whether or not length and contractions can promote more hypertrophy versus conventional full range of motion resistance training. So we had a really cool study design there.
It was within subject where 15 trained resistance trained college aged men had one leg assigned to doing lengthened partials. And then the other leg assigned to do full range [00:27:00] of motion training. They train two days per week for eight weeks. Prior to and following that intervention, we obtained biopsies from both legs and we did MRI scans on both legs.
And so we're gonna have a lot of data as it relates to, Hey, does the M MRI say that lengthened partials are a better way to train for hypertrophy versus, full range of motion. And in addition to that, with the biopsies, right, we can look at fiber type specific muscle cell size changes. We can look at ribosome changes because there's a body of literature to suggest that your hypertrophic potential is really high if your muscle cells can upregulate ribosome content with resistance training.
Same thing with satellite cells. So we're gonna look at muscle stem cells. See if lengthened partials increase muscle stem cell content. And again [00:28:00] if, lengthened partials do that more so than the conventional training, the implication is well, with longer term lengthened partial training, more muscle stem cells will lead to probably heightened or more hypertrophic potential.
So yeah, Danny's doing a great job with with that project in our laboratory. Do you
Dr Mike T Nelson: know when the results of that may be out?
Dr Mike Roberts: Yeah I would estimate he's doing the histology right now. Oh, okay. And so, he's, we're probably thinking that by mid to late fall, we'll at least get a preprint Oh, nice.
Bio archived and then we're gonna decide as to where to submit that. I have another student who is looking. Very elegantly at disuse atrophy and then whether or not recovery resistance training can bring back the muscle that was lost. The twist on that is we [00:29:00] had two groups in that study.
One group had pretty robust training history in terms of resistance training. The other group was untrained and so anyways, trained untrained, you get biopsies, you get the ultrasound of the vl the leg muscle. We do some strength testing and then we put a leg brace on for two weeks.
Both groups. After that two week period, we take off the leg brace and we get a biopsy. We do the ultrasound, we do the strength assessments, and then you resistance train for eight weeks as a recovery. Strategy. And at the end of that eight week period is when you do the last testing battery. Right? So you do the biopsy, the ultrasound, the strength testing.
So we already did and published the preliminary findings from that study. That's in the Journal of Applied Physiology, but Oh,
Dr Mike T Nelson: cool.
Dr Mike Roberts: Where did you find [00:30:00] on that? Yeah, it's great. So we saw the same rate of atrophy in those that had prior training experience and those that were untrained, we were floored because we thought, well, I guess in retrospect it's not surprising, but we thought one of two things since people with prior training experience had more muscle to lose, right?
They lost it at a faster rate. There could have been that option or prior training experience. Lends itself to protect you from muscle atrophy when you have to be in a leg brace. Right. But it's a bit nuanced because again, the rate of decline or the percent of muscle loss was by and large, similar between train v untrained for that two week period.
What gets interesting is that then you look at eight weeks of resistance training following [00:31:00] that two week period, the rate of hypertrophy was actually enhanced in the untrained individuals.
Which is to say that they saw hypertrophy above pre-intervention levels compared to the train group, which just recovered their muscle mass loss.
Dr Mike T Nelson: But that's, and I assume that's because they're. They're untrained. So it, they have more of a air quotes, the newbie type effect, because they're newbie games. Literally untrained.
Dr Mike Roberts: Yeah. And they're further from their ceiling. But what I wanna underscore here is we're talking about percent changes. It's all relative.
Ah, sure. Yep. Because when you look at absolute indices of musculature, right? Those that had prior training experience at all of these time points had way higher musculature. So that's another way to look at this, is we have a physiological reserve when we resistant strain, and if we lose muscle mass, right, we still on a, [00:32:00] on an absolute level have more muscle mass.
Yep. So, anyways, fascinating. Again, max drove that study and now what he is doing, so he looked at a few molecular outcomes with our biopsy data and he was interested in, this pathway in muscle and all other cell types called ER stress signaling. So we didn't see a lot change with er stress signaling between trained v untrained over time.
And as a matter of fact, just over time there wasn't a lot going on with er stress markers, so we thought they would be up. A few of them did show effects over time in terms of directional change, but there wasn't a clear picture there, so. Or his dissertation, he's leveraging the rest of that muscle tissue and he's doing large and small RNA sequencing as well as global proteomic analysis.
And the intent of his dissertation will [00:33:00] be to say at the molecular level, what is everything that is going on. Right. We looked at a targeted approach with er stress, we didn't see anything. So now we're gonna really widen the scope of this and look at transcript expression, look at global protein expression changes with the paradigm.
And we're gonna try to use bioinformatics and machine learning to more or less predict, okay, when we see this muscle atrophy, what are the genes or the proteins that best explain that? Right? And then when we see the recovery hypertrophy, what are the genes and the proteins that best explain that in terms of changes in these things?
So we're doing this in collaboration with Marcus Bauman. He's at IC Yeah, I in Pensacola. Yeah. He post a lot of really cool stuff. Oh yeah. Marcus is great. He's a good friend. He's [00:34:00] only three hours from us and he used to be at UAB, oh, that's right. Yeah, so he was only two hours from us at the time, but luckily he did not move far.
So still, we drove down there and we were doing some analysis with Marcus and I've given the same hypertrophy talk, well iteration of the hypertrophy talk I gave at ISN. But no, Marcus is fantastic. He's been an awesome professional mentor. He's always just been so kind. Max the, per the student that's doing this dis use atrophy project, he's gonna go postdoc with Marcus.
Oh, cool. So, yeah. Yeah. No, Marcus is fantastic. So yeah, we have that project. So I think this is a really long, I'm, giving you all the insight in terms of what we do here. So I think I'd mentioned the length and partial project by Danny. I mentioned the disuse and recovery resistance training project by max.
I have a few other students working on different things. So I have a student, Nick Contos, he's working on [00:35:00] whether or not certain nutraceuticals can affect cardiomyocytes when they undergo hypoxic stress.
And so he's, he has a really nice cell culture model. It's a ischemia reperfusion type of model which would induce cardiomyocyte damage.
Dr Mike T Nelson: Yep.
Dr Mike Roberts: And so reperfusion injury, the, yeah, the reperfusion part of it. Right. And so he's seeing with these nutraceuticals, can we pre-treat the cells? Implication being if we're always supplementing this as humans, right. And then we have an event can we mitigate that risk or damage? So he's doing just a purely cardiomyocyte a project.
Can you say what compounds he is
Dr Mike T Nelson: potentially looking at?
Dr Mike Roberts: Well, we don't want to, we don't want to tip our cap too much. Okay. I'm just checking. Yeah. No. So, I will say this one. That's okay. So it's a combination of things, and we're not developing IP, by the way, because these are sold over the counter.
Speaker 5: But
Dr Mike Roberts: the one that is what I would call the most active would be creatine. Creatine. Sure.
Speaker 5: [00:36:00] Yeah.
Dr Mike Roberts: Yeah. So, so we're there's a ton of good data indicating that creatine can enhance bioenergetics and obviously elevate phospho creatine levels in, in all types of cells. And so we're gonna see if, creatine is as, is has magic in that regard in terms of preventing or mitigating this ischemic stress or this stress following reperfusion.
So, and with that, he's gonna look at a lot of mitochondrial markers and things of that nature. So that's three projects. Fourth project we have going on. Would be a very applied study where we're looking at the effects of protein only supplementation versus protein plus carbohydrate supplementation on hypertrophic outcomes.
It has been done before. This is not necessarily a novel thing but surprisingly hasn't been that done that much. So Yuha, who me, would be one. This is published in isis NI think around 2013 showing some mixed effects. But ag our [00:37:00] approach, what we're aiming to do is do it in people that have prior resistance training experience because based on the Rob Morton and colleague analysis, meta-analysis, it would seem as if supplementation really has more benefits when you become resistance trained, closer to that ceiling effect of hypertrophy.
And so we're looking at the effect or not, that is a project where we're looking at the effects of protein only versus protein plus carb supplementation in trained individuals.
Dr Mike T Nelson: Is that more of a, like a timing study? Like the old Paul crib study where they had the two groups and they gave one group the AM version of protein, carbs and region, I think, and then the pre and post training group, and they just saw pretty big differences.
And then that wasn't really replicated. And there's, there still seems to be a lot of questions around something that, like you said, appears to be rather basic, but there's a lot of conflicting data.
Dr Mike Roberts: There are a lot of conflicting data, [00:38:00] especially as it relates to protein supplementation. Right. When you look at force plots on meta-analyses, the pooled effect seems to favor we a, we need more protein.
Yep. When we're resistance training, I think the main driver of adaptation. Would be training. Yep. Yeah. The stimulus. The stimulus when we optimize, I think it certainly makes a difference consistently consuming more protein. I'm not gonna be naive to say that. Yeah. But I think at times, especially, when you look at some of the tracer work that Stew's done, which has been great. And Stu will even say what I'm going to say, but, those bar graphs are really, they show like pro protein synthesis with resistance exercise versus protein synthesis with protein post-exercise leads to this robust increase in NPS when you just compare it to resistance exercise, but no [00:39:00] supplementation.
And so there was a lot of research really honed in on that. And think a lot of people back in the. Early two thousands focused on those acute studies where you can see these bar graphs that are relatively exaggerated. But then when you carry this out and just look at the effects on the body's musculature, after eight or 12 weeks of resistance training, yes, there's an added effect, but it's not as enhanced as that acute effect on muscle protein synthesis.
Right.
Dr Mike T Nelson: Definitely diminished. Would you say that it's probably not even, I'd have to remember the studies, but probably on a chronic study, not even, maybe one or two pound difference, I remember it beings statistically significant, but not like, oh my God, you gained five more pounds of lean muscle.
Like you're not anywhere close in that area. It's still a very small effect. Yes, exactly.
Dr Mike Roberts: And your numbers are spot on. I'm teaching nutrient timing in the summer here. And we just talked about that Morton Meta. Oh, nice. Yeah. Yeah. And [00:40:00] it's a one kilogram. Conferred benefit when you're supplementing with protein as a trained individual.
But do keep in mind, right. I think the limitation, even though that, that certainly diminishes the excitement. You're like, one kilogram, who cares? A I care like one. Yeah. 2.2 pounds, man. I'll take it. 2.2 pounds B right? These are shorter term studies. So these are eight to 12 weeks. What if I'm supplementing for two years, right?
Yeah. Could that be five pounds? Could that be eight pounds?
Dr Mike T Nelson: So I, and in the context of muscle growth, if you've been training for a while, it's just a slow process to begin with. A hundred percent. A hundred percent.
Dr Mike Roberts: Yeah. Yeah. And that brings up an interesting question, and it's one that's very hard to tackle.
Is there a genetic potential?
Dr Mike T Nelson: Right?
Dr Mike Roberts: There, there probably is. I'm not naive to say there's not. We have one paper actually in collaboration with Stu. We did a GWAS approach. So we did a DNA microarray on [00:41:00] 120 some odd college age men limitation. We didn't have the skeletal muscle or the DNA from females, but what we showed was looking across the genome and different polymorphisms.
I think there were over 300,000 polymorphisms that we were able to interrogate with our microarray. None of those strongly associated with the gains in muscle mass.
Following 10 to 12 weeks of resistance training. Now, does that mean genetics are not involved with skeletal muscle hypertrophy? The answer is no.
It doesn't disprove that. In addition to that, DNA microarray is different than. Then full genome sequencing. I think truly what needs to happen is we need a large cohort, like, we'll call it 1000, [00:42:00] 2000 participants, men and women younger and older. Right. And we need to see using whole genome sequencing.
And by the way, this would be just a tremendous amount of data. So there would be certain challenges to this. You need large computing to look at 3 billion base pairs per individual and whether or not any of those bases, or a combination of polymorphisms or other sources of gene variation like sequence repeats, microsatellite repeats, et cetera.
Whether any of that is explanatory, and I think the answer is probably, and in addition to that. People will hand wave and say, oh, it's not just the genetic code, it's the epigenetics. Right. That could be explanatory. And yes, I will tip my cap and say indeed. But we again, we don't know.
Yeah. Which dmr are, we'd
Dr Mike T Nelson: even look for that.
Dr Mike Roberts: Yeah. You can do a same thing. You can do, we've done [00:43:00] epigenetic scans with muscle. We worked with Adam Sharples. He's at the forefront of this technology. And you can do, I think it's called pyro sequencing. So instead of doing like an epigenetic sort of, or microarray approach, which is what we've done with Adam you can do sequencing and you can look at, a more than 850,000 sites that would be differentially methylated.
Dr Mike T Nelson: So, so you capturing into what, if it's in a methylated state or not, then when you're using that type of method, like to see what's Yeah. Increased or turned on, or not exactly.
Dr Mike Roberts: Increased or reduced methylation. Okay. You're more or less cap capturing. So how, golly what do I even wanna say?
It's a lot of words, but yes. I think genetics and epigenetics are involved in the adaptive response to resistance training, no question. But we don't have, you would be surprised how little we know when asked. Okay. Which genes, [00:44:00] which gene promoters are methylated in Somebody that doesn't respond, hypermethylated or hypermethylated, which polymorphisms are explanatory for the exaggerated hypertrophic response, i'm gonna, I'm gonna shrug and say, frankly according to our data, at least we don't know. So there's a lot to be done there. A lot of opportunity. It's just gonna take a lot of money, frankly, like, I don't think it, like, certainly we cannot afford it, and I could not convince a sponsor outside of like a federal sponsor to give us enough money to even begin to interrogate that issue.
There is a consortium called Motor Pack. Where they were funded to look at the effects of 12 some odd weeks of exercise training and it resistance training. The problem, I think is it also involves endurance training. So you're,
It's a little messier.
It's a little messier. I'm not gonna say that these folks [00:45:00] won't gain muscle, because I think with a common combined training, sure, especially with newbie gains you're gonna see even with combined training this increase in musculature, but you're not necessarily optimizing the hypertrophy.
So, how do I, how do I wrap this conversation up and move on to another topic? I think there is genetic potential for gaining skeletal muscle mass with resistance training. And aside from our data, there was the famous study by Eric Hoffman's group showing just individual polymorphisms did provide some explanation in terms of resistance training adaptations, be it strength or hypertrophy.
But I don't think we know, again, we don't have a solid, like we know that mTOR signaling is very important. For resistance training induced hypertrophy. We know that's something that we can wrap our arms around. All we can say is genetics, epigenetics, but we can't provide like that [00:46:00] simple, oh, it's mTOR, right?
We just say, oh, hand wave genetics, epigenetics, there's genetic potential. So that, that's gonna be something I think that innovative researchers in this field can help tackle, if that makes sense.
Dr Mike T Nelson: Yeah. Would you agree that there are extreme responders? My bias is you see some data.
I remember Stu presenting this data years ago, I think on one of the very first chronic studies he did in the early was May, 2005, 2006. And he put up the actual scatterplot of the data and most of the people are in the middle. I think it was like an eight or 12 week study. One poor bastard was below who technically got worse.
And then it was like these two guys way at the top, like one or two standard deviations above everything else. But if I remember correctly, that's what had him and his grad students look at, maybe it was testosterone was being more excreted during exercise, which was later disproven. And so it does seem like there is data for some extreme responders, but in terms of [00:47:00] what's, why are they extreme responders still seems to be this mystery.
Dr Mike Roberts: Yes. The answer is yes to all of what you just said, except, well, I, we have added clarity to the field. So, shameless plug here. Oh, plug away. And if you could help spread the word, this would be great. And I, by the way, I get no financial gain from this, so just full disclosure. But I am a co-chair Yuha, TN at Sula in Finland is he and I have organized this conference at Sula in November.
It's gonna be a week before Thanksgiving discussing response heterogeneity. To resistance training. Oh, awesome. So the extreme responders and all that. And so I'm talking you. Hi Tina's talking. Marcus will be in attendance and giving a lecture. Stu Phillips will be giving a lecture. Brad Schoenfeld will be giving a lecture.
Abigail Mackey will be giving a lecture as well. And she has [00:48:00] fascinating data looking at the morphology of muscle cells. She's gotta be talking actually about my nuclear permanence. And so I'm really interested in what Abby's gotta say. She's a, we've collaborated with her and I think she is driving the field on the human side of research with regard to aging resistance training and the like.
Dr Mike T Nelson: Is that similar to the my nuclear domain theory of hypertrophy or is it a little bit different?
Dr Mike Roberts: Yeah it's involved with that. Okay. But really what my nuclear permanence sort of centers around is this notion of when you resistance train, or if you take anabolic steroids and resistance train, you're gonna have hypertrophy and you're gonna have muscle stem cells donating nuclei to the growing muscle fibers.
Right. When you stop training and or you sees taking steroids, you have this contraction and return to baseline with the fibers, but you don't lose the nuclei.
Dr Mike T Nelson: Yeah. It seems to stay there.
Dr Mike Roberts: Yeah. Yeah. So this would implicate that there's mononuclear memory, hence [00:49:00] like this could be a form of muscle memory.
So I don't wanna spoil too much except to say that. Yeah. Yeah. It's gonna get a very good talk there. We'll have Gustavo Nader, we'll have Troy Hornberger also giving talks. So the intent of this Congress that we're putting on in November, is just to have, everybody who's looked at response heritage give a talk to this group that attends the conference.
And then we're hopefully going to leverage that meeting into some sort of meaningful collaborative study. Like we're, we're gonna talk study design stuff. We're gonna, yha is collecting a lot of muscle with the current response heterogeneity study he's doing. So we'll discuss ideas in terms of what to look at with his study and so yeah, it's going to be a very exciting time if you're a listener or you, Mike if you really get geeked out about response heterogeneity.
I think this is the thing to attend.
Dr Mike T Nelson: And that's in Finland in November, is that correct? Finland, in November. And I can send you, yeah, send us [00:50:00] the info. We'll definitely put it in the notes and everything. That sounds fascinating. Yeah. Yeah. And
Dr Mike Roberts: again this is going to be extraordinarily high quality.
Dr Mike T Nelson: Oh yeah. Those are all like the researchers doing it.
Dr Mike Roberts: Exactly. But your question is, do we have a good idea as to what drives response heterogeneity? I think we're getting a better idea. So one thing, and I talked about this at ISSN, is it seems like ribosomes and ribosome biogenesis is super duper important.
So, for those that aren't aware, your muscle cells contain a lot of proteins, obviously. And macromolecules, you would say ribosomes are these macromolecules and they're the only thing in the cell that can catalyze protein synthesis. And for form peptide bonds between amino acids, which, then that those molecules themselves become the enzymes in your cells and the.
Transmembrane proteins and the nuclear proteins and the mitochondrial proteins and the contractile proteins. Most importantly when you talk about muscle. And so when you lift weights, if you're somebody that can [00:51:00] upregulate and increase the number of ribosomes, multiple independent studies in laboratories, including our own Marcus's lab, Marcus Bauman some laboratories in Europe have shown that ribosome biogenesis is, seems to be a driver of skeletal muscle hypertrophy.
And in fact, the extreme responders seem to show that the highest upregulation in this.
The other would be muscle stem cells. So, Marcus Bauman most famously showed this with J Kim, who was a postdoc with him in the mid two thousands, but extreme hypertrophic responders. Start before they even start lifting weights, they have more muscle stem cells in, in, in the muscle tissue.
And then after 16 weeks of lower body resistance training there is a doubling more than doubling of muscle stem cells. In addition [00:52:00] to that, there was evidence that some of those stem cells had fused to preexisting muscle fibers, and so those muscle fibers had more mono nuclei. So, so my viewpoint is if you're an extreme responder, you're going to upregulate the production of ribosomes and your muscle will trigger this proliferation of stem cells, and some of those stem cells will probably fuse to the muscle fibers so that they can continue to grow.
Now we've looked at a lot of things that don't seem to be predictive. And that's gonna be my talk in Finland, which is to say all the stuff that didn't
Dr Mike T Nelson: work.
Dr Mike Roberts: Yeah. So we were looking Josh Godwin in my laboratory looked at certain connective tissue attributes. One thought was, well, heck, that deep fascia is thick.
Right? And what if fascial thickness prevented hypertrophy? Right. That was
Dr Mike T Nelson: John [00:53:00] Paulo's theory years ago, I think. Wasn't it like the fascia, the pillow sheet analogy he gave, I think.
Dr Mike Roberts: Yeah. And I'd seen this in particular there was a pretty compelling study. The first author's name was Hammond. This was in the journal Applied Physiology in 1992.
I'm not familiar 'cause I'm not a cardiac guy really. But they showed that removal of the pericardial sheath in pigs and then sewing up the chests and then taking the heart out, like we'll call it two weeks later, led to a robust ventricular hypertrophy.
Dr Mike T Nelson: Oh, interesting. And so it's like,
Dr Mike Roberts: well, why don't we just apply that to muscle?
Yeah. Remove fascia, do fasciotomies or whatever. Yeah. Or find out, at least, by the way, we would never do a any sort of fascial like manipulation, at least invasively, that sort of thing. But we did not see that the thickness of the deep fascia constrained hypertrophy, which is to say that in [00:54:00] Josh's publication he reported that the lower and the high higher hypertrophic responders.
To 10 weeks of resistance training had the same fascial thickness at the DL site. Right. Okay. Interesting. In addition to that, we obtained skeletal muscle biopsies, and we looked at different cells in the extracellular matrix that were not satellite cells. So we looked at fibroblasts, we looked at, I believe macrophages, we looked at FAPs, which are, what are fabs, fibro, I not familiar.
Epigenic progenitor cells. Okay. And they have an interesting sort of story because they can they can become fibroblasts. They can become adipocytes. But long story short, none of that stuff seemed to predict response heterogeneity.
And so initially we thought there was some sort of involvement be it the extracellular matrix [00:55:00] where these, these muscle cells reside.
Or be it connective tissue itself. We thought there would be differences between higher and lower responders. We haven't seen much, but we did see one marker and it was called m and p 14. So this is a matrix metallic protease. And it was down regulated robustly in the high responders. Come to find out, the Kentucky group in Charlotte Peterson's laboratory also in an older population implied that m and p 14 is indeed a potential marker that delineates the hypertrophic response.
And so, what you have is the beginnings, I think, of a working model to interrogate this target and further examine, right? If MMP 14 is involved with, skeletal muscle hypertrophy. But aside from that, again, we didn't see anything ECM related. That seemed to be [00:56:00] driving it.
Now, Josh Godwin, he was in my lab. He's currently with Gustavo Nader and if I didn't mention it, Gustavo is also given a talk in Finland. He's, Gustavo does a lot of ribosome stuff. He actually is the first to discover that ribosome, biogenesis and muscle cells is in part driven by mTOR signaling, which is a very cool finding.
And Gustavo did that while training as a PhD student in Karen ER's laboratory.
Speaker 6: Oh, okay. Got it. Speaking to Karen,
Dr Mike Roberts: er and her influence on the field. But Josh his dissertation involved looking at what's called an intermediate filament it's called.
And you would expect to find ton inside of muscle cells.
Well, the beginning of what Josh saw was with resistance training. The change in muscle fiber size was explained via correlation in part by this change in [00:57:00] Mtin. And he had found that it's localized actually in the extracellular matrix, not in the inner part of muscle cells where you would expect to find it.
We then worked with a really bright and emerging researcher at Nebraska Yvonne Chetty. And by the way, Brooks Mobley, I think I had mentioned him and Myis in talk. Brooks is currently at Auburn. Brooks was a postdoc at Kentucky, but Brooks heavily helped us through this process with Josh's data in terms of immunohistochemistry and putting us in connection with Yvonne Chetty.
Brooks let us use some of his rodent muscle he had collected during his postdoc and he had brought to Auburn. But long story short, Josh's second sort of ECM paper. Centered around this mtin protein. And the story goes that with resistance training or mechanical overloading rodents, we observe this upregulation in mtin.
Instead of being [00:58:00] this intermediate sort of scaffolding protein that we find inside of muscle cells, we see it localized to the extracellular matrix and it's highly enriched with mechanical overload. If we genetically interrupt that, and we did this in mice, we actually reduce satellite cells in their involvement in the hypertrophic process.
So we find that interesting. And as a matter of fact it could be the other way. I'm thinking of this backwards. When we reduce satellite cell number we reduce ance. So there seems to be some sort of involvement of satellite cells via mitten localization to the ECM. And then yes, when we genetically disrupt.
T upregulation with mechanical overload. We get this highly disorganized regenerative phenotype where there appears to be almost excessive MyFi splitting. So a lot to wrap your head around there. If I were to take one step back, I would [00:59:00] say I do think that the extracellular matrixes is important for delineating the hypertrophic response to resistance training.
I think we're gonna become more keen with that idea as we continue to research some of this extracellular matrix environment and proteins that reside there, et cetera, et cetera. And we think that there's more meat on the bone there in terms of investigation. So we seem to think that, m and p, MP 14, biome mitten, these are two examples where you can have ECM involvement.
It could be many more examples. There's also growth factors that reside in the ECM that really haven't been investigated too much. One that comes to mind is Decorn. I talked to Darren Willoughby about Decorn, and he had some excitement as to the potential of decorn being a signaling ligand when you mechanically perter muscle tissue.
But yeah there's a lot there. So
Dr Mike T Nelson: there's some work on like titan also, I think as a filament related to structural integrity and potentially [01:00:00] muscle hypertrophy, or maybe not. Yeah, there is.
Dr Mike Roberts: Yeah. So road models have suggested that Titan and its ability to auto phosphorylate may initiate like a downstream signaling cascade, A phosphorylation cascade that feeds into M Toric activation and muscle protein synthesis.
We're not bullish on that idea. Oh,
Dr Mike T Nelson: okay. Interesting. The reason
Dr Mike Roberts: being because we actually tried to look at tighten phosphorylation acutely following an exercise bout. What we found was a lot of that tight is fragmented.
And so it can act as a signaling protein because you're disrupting the structure of the protein altogether.
Oh, interesting. And that led us to we have a paper in experimental physiology. Danny Plotkin was the lead author on this. We also see a lot of myosin heavy chain fragmentation acutely post exercise. So now we're working on that story a little bit. We think this is a very good marker of the disruptive response to muscle, looking at the fragments of [01:01:00] mycin hours to potentially days following exercise.
And we now in working with Marcus Bauman's muscle are showing that people who are high post-exercise myosin heavy chain fragments seem to have more of an inflammatory response versus those that don't have. Much fragmentation at all.
Dr Mike T Nelson: Yeah. And that would make sense, right? So you assume that's part of the process to clean up the mess you made.
Dr Mike Roberts: Yeah, exactly. Now, so, so the, this works into response heterogeneity. What we need to really determine right, is does fragmentation of myosin, if it's excessive enough following exercise, is this working against people putting on muscle mass? So all of this is to say that yes, we think genetics are involved.
We don't have a good idea though, which polymorphisms or epigenetic modifications are driving that. [01:02:00] It's gotta be a combination of both. And you're looking at probably hundreds of candidates in terms of this combined, profile. But I do think that ribosome biogenesis is important.
I do think that the muscle stem cell response is important. I do think there is enough evidence to suggest that there's some extracellular matrix adaptations, examples from our lab being MMP 14 and m mitten that drive the hypertrophic response. And then there are other things that probably do, but people just haven't thought to look at it.
People have talked about the blood flow, the perfusion of tissue. Tim Snyder's he has a lot of I'd say a lot. There's evidence from his lab like Rasmus in his lab to suggest that more capillaries before training in muscle tissue promotes. Yeah, I see a better response. Yeah. But my caveat there is I think that is true, but I only think that's true for the older deconditioned individual.
I think the unhealthy or the other, it's not a rate limiter over healthy. It's not a rate limiter. Exactly. Ah, [01:03:00] so, yeah, there's a lot there, man.
Dr Mike T Nelson: Do you. What are your thoughts about doing like an eccentric type emphasis to maybe, who knows, disrupt more of the extracellular membranes or maybe cause more damage on purpose, and that might be beneficial for hypertrophy?
Dr Mike Roberts: Yes. I think that's good. And I think the, I have no direct evidence except to say that I know Brad Schoenfeld Good buddy.
Speaker 6: Yeah, Brad's awesome.
Dr Mike Roberts: Right, so he's done the stretch studies where there's Yep, he's done that with stretch. Yes. Stretch. And there seems to be an effect. So while there wasn't the biopsy approach, the interrogation of ECM remodeling approach, et cetera, et cetera, what we would expect to see there is probably that perturbation of stretch is passive and it's gonna lead to some of the remodeling.
But what we can do with the project that's upcoming with Danny Plotkin. Length and partials, right? In theory, you're in stretch position [01:04:00] under load and so, we're gonna see at the fiber specific level what's going on. We also have biopsies where we're just gonna analyze proteins of interest.
And so we can see in relation to like m and p 14, MTIN, some of these things I've been preaching, are those proteins up regulated in the length and partial leg? Chronically when you compare it to the conventionally trained leg, the full range of motion legs. So, so yeah we're gonna try to get at that here with Daniel's project.
Dr Mike T Nelson: Yeah, no, that's interesting. And it also parallels one of my thoughts. Like I, I do some work with Beyond Power. So they have a Vulture one device where it looks like a little cable box, but you can program eccentric and concentric for just adding onto your weight rack separately. Yep. We bought two of 'em recently.
Oh yeah, they're great. So I can do a row with a hundred pounds concentric and then have it hit an extra 50 pounds or whatever on the [01:05:00] east Eccentric. Yep. And it's crazy how different that feels. It feels, yeah. Yeah. And I destroyed my back for, in a good way. Like, no, no pain or anything like that. But yeah, that's why we
Dr Mike Roberts: bought, that's why we bought the Ultras.
So yeah, we're definitely an advertise. This is like an informal advertisement, so Yeah. I know I put them, I've tried 'em, I, again, I don't get paid to do this. But the classical eccentric studies. You don't see these methods in the paper, but I've seen one done.
You can either use a Isokinetic dynamometer
And you can, overload ally and so that's a lot cleaner. Yep. If you're doing compound movements on a leg press, right. It's like, okay, we're all gonna, lab assistance are gonna help on the push and then we're Right,
Dr Mike T Nelson: right.
Dr Mike Roberts: We're
Dr Mike T Nelson: trying to throw more plates
Dr Mike Roberts: on the eccentric portion and yeah.
No, but with the vulture, right. And you can do compound, you can, you have floorboard deadlift capabilities, you can do IMTP, so we're excited about doing isometric mid thigh pulls without [01:06:00] Yeah. Using for plates, but instead using the data we get from the Vol Ultra. So yeah, just what a cool device.
But I funny you bring that up because we had talked about a Dakota td, he's a student laboratory right now and he's interested in sort of a concentric, eccentric overload type of paradigm and whether or not that adds any sort of molecular benefit. Just comparing it to conventional, straight load concentric, eccentric.
So we were thinking, all right, well now that we have these vultures, we can potentially do that, if that makes sense. So, yeah,
Dr Mike T Nelson: and it's a cool way to do it in the lab too, like you said, with an actual calibrated machine that's relatively easy to use compared to, try and configure bio decks or do other stuff like that too.
It makes it actually usable for people and if it does show to be in effect, yeah, it's something that more and more people can get access to now too to replicate on their own, in their own gym.
Dr Mike Roberts: And I'm gonna, I'm gonna, so I may bother you. This is, I'm just, we're like going on this vulture tangent, but Yeah.
Yeah. But I'm looking for [01:07:00] a strap mount. I don't know if you have an extra one laying around.
Dr Mike T Nelson: I don't, but I can put you in touch with Elliot if you want.
Dr Mike Roberts: That'd be awesome. And I could tell him how much money we've spent on two Yeah,
Dr Mike T Nelson: yeah, for sure. Floorboard and say, can you
Dr Mike Roberts: just strap Mount man?
Dr Mike T Nelson: Yeah, for sure. I'll do that. Cool man. Cool. Once as we wrap up, like what would be like your top four things? So obviously you spent your life studying muscle, you lift yourself. Yes. From a practical aspect, if you're like, okay, here's my top four things of, I want to gain as much muscle hypertrophy as possible, what would be on that
Dr Mike Roberts: list?
Great. So consistently working out in the gym, that's very open-ended, but I think I, I mentioned this in is at ISSN. That means that you're working out in the gym two days per week on average. Right. And we're talking full body workouts. Okay. I've talked to Brad Schoenfeld a lot about this 'cause [01:08:00] he is the foremost thinker in this area for sure.
He seems to settle on between 10 to 20 sets per week per muscle group. So, practically speaking, right? If I think compound lower body 10 to 20 sets per week, what does that mean? Well, that means two days a week, either five sets or up to 10 sets per exercise session of compound lower body, right? Which is to say that I may go to the gym in my, my, if I'm doing full body two days per week, then I'm doing two exercises, three sets of like chest press, two exercises, three sets of something that's an upper body pool, and then two sets excuse me, two exercises, three to four sets of like lower body compound.
Does that make sense? Yeah. Butcher that. But full body, two days per week, make sure you hit all the major musculature. Do that for years, if not decades. You're gonna, you're gonna see this enhancement in muscle mass. It's tough to say how much, [01:09:00] I was asked that recently by somebody, how much muscle have you gained, do you think that you otherwise wouldn't have gained since training in the 10th grade. I'm like, oh god, how do you know that? My, I weigh two 20. I'm not necessarily lean by any stretch, but I would almost estimate that I otherwise wouldn't have like 40 pounds of muscle on my body had I not consistently resistance trained over the years. Yeah. So there's that consistently doing that.
I do think nutrition is important. Is it, you don't need to take 20 supplements to, to reap the benefits of working out. But at the same time, there are meta-analyses out there where we know if you're in a caloric deficit, you're not going to optimize. Your gains in muscle mass.
So there's that. In addition to that the Morton meta-analysis would indicate, and this has been the most highly cited, protein meta out there. Even though they're metas that have been published since, you need to consume what would be around 1.6 grams per [01:10:00] kg per day of protein.
So for me, I'm a hundred kgs, that means 160 grams of protein. Spread that out over four meals, that's 40 grams of protein per meal. Yeah. So, working that into your own arithmetic based on your own body mass, do the math. I think that's important. So consistency in the weight room and nutrition in particular, not being in a deficit as well as making sure you're getting high quality protein.
The third would be making sure that, it's really like the type of protein. The only reason I bring this up is because there's enough evidence. I've seen Mark Talsky from McMaster show strict vegans. If you're a strict vegan, I think there is a little bit of cause for concern because long-term strict vegans tend to have a robust reduction in musculature.
Which is to say that I think according to his data, [01:11:00] looking at mixed meal eaters, strict vegans had 20 pounds less of skelet muscle. Yes. So if you are a strict vegan working with AI or a good sports nutrition dietician to make sure that you're getting enough essential amino acids is important.
Right. That's three things, but it's only still two things. 'cause it works. The protein calories. I think perhaps the most important thing, and I don't know if I'll ever get to research this and I'll stop it at three things, is to make sure that you're exercising when you're a kid.
Dr Mike T Nelson: Yes. If I were to go back again, I, if I wanted to gain as much muscle as humanly possible, I would've started exercise way sooner.
When you're
Dr Mike Roberts: five or six, you can start informal training. Now we're not, I'm not promoting that we're putting a squat bar [01:12:00] no. On five year-old's back with wheels on it. Right. But what I am promoting is that we go to the playground and engage in plyometric type of exercises that we've all engaged in when we had recess time and now, recess is reduced and my kids have 20 minutes at recess.
Hell, we were out there for 45 minutes. Jumping down from tall things. Oh, yeah. Having bars and doing pull-ups. Yep. Right. Carrying our friends on our back, picking back rides. This is what I'm talking about. And doing it consistently. We can't be kids anymore, Mike, but like my kids, we all go in the backyard and do backyard Olympics and they're, that's awesome.
Five to nine years old. We do sprints, we hop over boxes. I have pull up bars. I have a little bar where they can learn how to do pushups. Sort of an incline pushup. And yeah, they're fast and they're strong, duh. Like, so my feeling is and this [01:13:00] was instilled to me by Frank Booth, my postdoc mentor, is if you're a kid and you consistently engage in that, by the time you hit 30, you have worked your lifetime peak musculature and strength and function up to the point where then you train to maintain.
Right. If I'm somebody that has never trained before, and I don't have a lot of good data on this, except I used to be a personal trainer and I've trained hundreds of people at Gold's Gym when I was in Waco what I saw was the people that were in their middle aged years had never lifted weights, had never exercised, and then really wanted to have this transformation.
They just couldn't have a robust transformation. Yes, they can lose weight, right? They can always reduce calories. Anybody can lose weight by reducing calories. But as that, as it related to strength and toning, it was harder to get those folks that had never engaged. So to your point and to what I'm [01:14:00] saying is I think if we have kids or your listeners have kids, start now and not only will functionally, they'd be, they'll be better for it.
They'll be faster, stronger. That sort of thing, but it instills that habit of exercise and the importance of exercise so that they'll carry it on as they're adults. So those would be my three things.
Dr Mike T Nelson: Yeah. And the last part is there's some even arguments with bone health that you might be able to even reach a high enough peak by your early twenties, that even if you screw it up the rest of your life, you might still be okay.
Yeah, that's crazy.
Dr Mike Roberts: I've heard Wendy Court, she's yeah, in Boulder. She's great. Preeminent researcher on bone health. Buddy of mine kaylyn young he researched this stuff too. I'm not a bone, I'm not either physiologist, but to your point, like the goal with muscle and bone strength is to peek it out in your thirties.
Well, how can you do that? You work backwards. You're like, okay, I start when I'm six. So [01:15:00] if you can't do it as a listener and you have kids or grandkids, then I heavily implore you to have them do it. And it doesn't have to be enrolling in all these sports. It can be backyard Olympics, it can be just basic stuff
Dr Mike T Nelson: kids wanna do.
Yeah,
Dr Mike Roberts: exactly. Exactly. So I'll get off my soapbox, man. I had a great time. Thank you so, so much for this.
Dr Mike T Nelson: Yeah, thank you. And working this opportunity, people find out more about you and are you taking any graduate students? Are you full or tell us more about that. Yeah.
Dr Mike Roberts: Right now I'm at capacity, but then I'm losing as in graduating three students this upcoming year.
So there's gonna be opportunity for one or two. If, if you read the research and you've read our papers and you wanna pursue. Four years of somewhat of an intensive but fun research environment then I would certainly suggest you reach out. That'd be great. Awesome.
Dr Mike T Nelson: And [01:16:00] then do you do any social media or you just stay hidden in the lab and just crank out papers?
Dr Mike Roberts: I'm, I do a little bit on Instagram, so, at Dr. Mike Roberts, all one word. And that's my same for Twitter or X or, whatever it's called nowadays. I'll just typically post. About the publications that we have coming out. I don't get involved in the debates or minutiae too much.
So you're not going the stew direction yet. Yeah, man, Steve's great. He's a great friend. But yeah, he loves Stew. He's always, hitting it, man, so, yeah. But yeah, no, yeah, if you wanna follow us, I'm a little bit more boring and, I should post more.
I don't, but yeah that's where I'm at too, so.
Dr Mike T Nelson: Cool. Awesome. Well, thank you so much. I really appreciate it. That
Dr Mike Roberts: was great. That was wonderful. Awesome. Thank you, Mike. And yeah, let me know when this comes out, and I always share this with my wife and my family, so, I'd love to listen to it again.
Dr Mike T Nelson: Yeah, we will. And thank you so much for all your time. I really appreciate it. This was great. I will let you know once it's out. All right. Sounds good, buddy. Awesome. We'll chat soon. We'll see you.
Dr Mike T Nelson: Thank you so much for [01:17:00] listening to the podcast. Huge thanks to Dr. Mike Roberts for sharing all of his wonderful knowledge. As always wonderful to chat with him and to have him on here and share about the underpinnings of hypertrophy and a lot of the stuff he talked about, as he mentioned, some of it's not even in publication yet, and even then, once it hits publication and makes it through.
Peer review into printed journals takes a while for it to disseminate from there. So I really appreciate him taking time out to come on here and chat with all the in-depth hypertrophy mechanisms and give us some practical takeaways on the things that we can do related to that. Make sure to check out our sponsors.
We've got element for electrolytes. We've got Teton ketone esters for ketones if you're looking for them. They will have some new really cool stuff out this fall. It's supposed to be out this spring, but got pushed out a little bit. So look for that coming out [01:18:00] this fall. Use the code, Dr. Mike, a full disclosure.
I do some work with them and am an ambassador for them, and then also check out a new sponsor. This is one that I personally wanted to add. They did not ask me to do this, but I really like the beyond power of the VUL Ultra one device. It's been super fun. I think I've literally used it like almost every day I've been training at home.
In the garage gym, you can do everything from isometric testing, isokinetic testing. You can change the strength curves on it, so you can even have a setup with heavy chains. So at the end range of motion, you have additional weight that is progressively added to it, like you would have chains on a bar.
You can even do an inverse chain, which is literally taking the strength curve on the opposite end of the spectrum. Heavy eccentrics. Concentric. And the other part I really like is you can just program the device directly. I do the old school method where I just record everything in a notebook and I don't have to fu with my phone or [01:19:00] anything while I'm training.
I just type in exactly the weight. And what I want on the device and it'll do it automatically. And you don't necessarily need a subscription to run neither. That's one of my pet peeves of, spending a lot of money on the device 'cause it is definitely not a cheap device. And then having to pay a subscription on top of that and then the subscription price getting more expensive over time.
They do have an app which is great, but you don't necessarily need it to run the device, so, check them out below. If you have any questions about it, make sure to hit me up. But it's been super fun. Thank you so much for listening. We really appreciate it. If you're interested in the Flexible Meathead Cardio course, hit me up on the newsletter.
You can hop onto the free newsletter to get all the information and just hit reply. I will get back to you there. Thank you so much for listening. If you can hit us up with the old subscribe button, especially on YouTube would be great. Trying to get our subscribers up on [01:20:00] YouTube. And as always, thank you so much for listening.
We'll have much more information coming up very soon. See you.
Speaker 4: Did you see that? Yes. The frog is certainly taking a beating on this show. Yeah. It's hard to feel sorry for him. We take a beating every show.
Speaker 8: This podcast is for informational purposes only. The podcast is not intended as a substitute for professional medical advice, diagnosis, or treatment. You should not use the information on the podcast for diagnosing or treating a health problem or disease, or prescribing any medication or other treatment.
Always seek the advice of your physician or other qualified health provider before taking any medication. Or nutritional supplement, and with any questions you may have regarding a medical condition, never disregard professional medical advice or delay in seeking it. Because of something you have heard on this or any other podcast, reliance on the podcast is solely at your own risk.
Information provided on the podcast does not create a doctor patient relationship between you and [01:21:00] any of the health professionals affiliated with our podcast. Information and statements regarding dietary supplements are not intended to diagnose, treat, cure, or prevent any disease. Opinions of guests are their own, and this podcast does not endorse or accept responsibility for statements made by guests.
This podcast does not make any representations or warranties about guest qualifications or credibility. Individuals on this podcast may have a direct or indirect financial interest in products or services referred to therein. If you think you have a medical problem, consult a licensed physician.