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- [00:00]
A
Foreign.
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B
What's up, everybody? Welcome back to Iron Culture, presented by Mass. It is me, Eric Drexler, here down under in Australia with the Dr. Eric Helms. Helms, how are we doing tonight? We agree on the time zone.
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A
Finally, we're in the same place. So I think that means we're in the same time zone and the same day.
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B
Yep.
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A
And I'm doing well because we just had our. Another episode that we just recorded and we're, we're feeling good, we're enjoying it, and we're going to do another one. So obviously it's good convo and we want to keep it rolling.
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B
Absolutely.
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A
I'm good.
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B
Yeah, there's. There's no room for any banter or chatter here.
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A
We're.
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B
We're all business. We are here for work. This is the SNA conference. You only get one a year. So it's time to dive in, I think.
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A
Yep. And we did get some comments. We, we got some, we got some DMs specifically asking us, hey, you guys kind of glossed over some pretty big things that you changed your mind on. And because our last episode that we recorded not in the same physical location, we brought up three things that we had changed our mind on each. And I think we got. I got some questions related to MRV Mav. Yeah. Because I think there was a lot of people who were like, hey, hold the phone. I thought you were on a fundamentally different pages, Mike Israel. But you guys are living in 20 something teen and I think you wanted to expand a little bit more. Maybe like leptin, nocebo, placebo. I can't remember exactly what. But yeah, good stuff to talk about.
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B
And I didn't know that living in 20 something teen was still an option. Can I do that?
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A
It was before COVID It was a good time.
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B
I had a really good time in the 20 teens. Like, I wouldn't mind going back a little bit. I don't want to go back to like the 1800s, but the 2000 teens I could definitely live with.
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A
Yeah, there, there. There's some issues of going back too far.
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B
Right.
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A
But I think seven years is totally, like, a solid option. Yeah.
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B
So you've really piqued my interest. I want to get on that train. But any case. Yeah. So for folks who are, you know, a little disoriented, I forget the episode number, but it was about humility and science.
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A
Yes.
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B
And we were talking all about things we've changed our mind on. You talked about, you know, changing your mind on kind, and we're glossing over it for the details for all the nuances, you know, check out the full episode. But the whole all foods fit mantra, you know, say ah, maybe there's some times where that's maybe not the way you want to go. Talking about going from, you know, very specific macro targets to setting carbon protein minimums with a calorie range.
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A
Well, honestly, even reasonably broad macro targets, but just going to the idea of having a minimum intake of. For the. That are goal specific and personal preference specific for carbs fat protein than a calorie range just being pretty much in every instance. I can think of better. So long as you also have a consistent meal rhythm and pattern.
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B
Exactly, yeah. And then I talked a little bit about, you know, the first prep I ever did for bodybuilding. I worked with, you know, an old school coach who had a lot of success at the pro level. He was a WNBF pro and he put me on a pretty standard bro diet. A lot of sweet potatoes, a lot of lean beef, a lot of chicken. You know, and at the time I was like, ah, this is the old way. You know, this. Now we know so much better. Everyone's eating pop tarts. Why, why hasn't he figured this out? But then you go back to, you see, you know what, as the research evolves and you start really interrogating it, looking at it from different perspectives, there's a lot of value there from, from
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A
having in my life hard.
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B
Yeah, yeah. So, but yeah, what we wanted to do was drill down on the things that we got more questions about. Right. So we covered, I think very concisely the kind of umbrella, the genre, the little interconnected cloud of topics being, you know, which foods fit bro diet versus the meticulous, you know, if it fits your macros, building all these convoluted meals, macros versus having more basic ranges and minimums. So those we all kind of covered in the last episode. But yeah, MRV and related topics. Messing with leptin dynamics via refeeds and diet breaks. Questions come up about that all the time and of course placebo and nocebo effects. So let's start with mrv. You mentioned that you have evolved on this. So if we go back to the 20 teens, metaphorically, we're still working on the technology that we just discussed to actually go back. But what was your stance and what has kind of caused this episode? Evolution.
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A
Yeah, I think I, and I'll do my best. Even though he's not here to, to properly represent where the concept came from, from Mike Israel. And.
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B
And we can talk a lot of. About Mike.
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A
I mean, it's very popular these days.
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B
Yeah.
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A
Yeah. So it'll be fine. Yeah. Screw that guy. Yeah. So. But I. Even though we could. Yeah. I'm actually going to try to accurately represent his positions in the 2000 teens.
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B
Yeah.
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A
Because there was a specific roundtable that myself, him, and like, three other people were on, where we essentially prompted the creation of mav. So the original model that Mike came up with, it had a minimum effective volume, and it had a maximum recoverable volume as kind of the two initial volume landmarks. And believe it or not, there was not the maximum adaptive volume concept. And that was something that I took a real big issue with, because it was the idea that volume would keep going up, going up, going up, going up, and going up. And then at the point where you can no longer recover from it after that, you would then get a. Some type of negative response or injury or whatever. And I didn't think at the time that there was sufficient data to just. Especially with how we define recoverable, which we'll get into next, to say, like, well, how do we know there's not a plateauing point where you're adapting maximally, but you are not making any more? And then at a certain point, you're doing more volume, but you're actually getting a negative response, like a slower rate of gain first and then actually a potential, like, negative effect. Right. Yeah. And because the model kind of just went like that. Right. Yeah. And it just didn't make sense conceptually to me. And I also took issue with saying, you know, this is not just a volume thing, it's a dose thing. Right. Yeah. Um. And that was something he'd always acknowledged. And early on, even tracking volume was weird. You know, like, we didn't have the same meta analyses that looked at things. We weren't counting sets. We were looking at, like, tonnage. Right. And early. Early on, I remember a specific Facebook post where the data was kind of indicating that at certain load thresholds, volume counted more. Yeah. And it was probably actually just a proxy for a decent proximity to failure and people not being able to not tell because they're doing really, really high reps. And Mike was like, I think you should just try to do as much volume as you can recover from just doing as many reps, over 70% of one arm as you can. And in fact, since you can keep the load lower and it's not as hard in the joints, just do 70% of one arm and just do a whole Lot of reps. It was one of his typical kind of I'm thinking out loud posts. And I was just like, nuance, you know, and I was freaking out. So, you know, we had this, the, this, this roundtable and it resulted in a, you know, the eventual creation of mav. And now you've got your three volume landmarks. Right. There's the most you can recover from and get back to baseline. There's where we think you're getting the best adaptation. But the, that first peak, then it might plateau and then there's what do you need to not lose gains? And I agreed that those are conceptually useful things to understand. But my perspective was that you should only be increasing volume. This is at the time where you need to, based upon fixing everything else first related to quality, to see measurable progress based upon what should be reasonable for you. And that was. I still think that's a very good way to go. But I also think that now the data has evolved to suggest that if you can recover from the volume you're doing, you actually will benefit it. Benefit from it for hypertrophy. With the one major caveat that recover from it means something different than what Mike proposed back in the day. And it is something that is very, very challenging to measure currently. And that may, maybe even arguably should not be the thing that we determine recovery on if we use a strict sports science definition. So taking a step back, the original concept of recovery and the model of training that, that this conceptual model of volume landmarks existed within was one where you're adding sets and adding sets and adding sets and adding sets. Right. So you would go from doing say eight sets to maybe 20 sets over a, you know, six week period, adding two sets per week or something like that. Yeah. And the point at which you would see your week to week performance degrade in the same workout would be determined as your maximum recoverable volume or going just past it. Yeah. And then you would, that would be your overreaching, then you deload. And that was proposed to be a way of growing even faster. Right. So recovery was based upon the true sports science definition of getting back to baseline for performance. Yeah. Now the thing that we've come to realize is that there is not necessarily a perfect syncing between the acute volume and total dose of training and the actual performance response. In the short term, it does show up. In the long term, it does show up if you back off enough. And in practice, this is anecdotal, what I see is that when someone is really pushing the limits of Their recovery with volume and an effective training stimulus, they have this very almost bipolar response. You will get these random PRs that are huge and you'll see them. And if you can focus on the good days and not the bad days where you just feel like trash and you can't, like just can't do it. Yeah, you're actually going to see a whole lot of PRs, but you're going to see this kind of lot of
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variance day to day.
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Yeah. At least that's been my experience. When you're not, not just from doing high volume, to be clear, when you're pushing a level of volume that you are barely able to manage and recover. But when we look at the data, like we think about Pellen's data, we see that acute strength responses max out quite low, especially with specific training in terms of volume. But you can continue to get more and more hypertrophy and it's just very difficult to track that in the long term. So that model where you're looking specifically at performance in short time, in short term time periods and well trained lifters, I think is probably not the one you should look at. But if we had kind of this more holistic understanding of. Okay, well getting, you know, back to baseline, that's not really a thing for hypertrophy. Right, right. So that doesn't quite make sense. But if you are able to recover by. If we, if we say adapt to now, all of a sudden MRV and MAV mean the same thing. Yeah. And that actually seems to comport with the data. Yeah. Right. So the final thing I will, I will say is that I do still think though that if you are not seeing any type of progress over a reasonable time scale across multiple metrics, you probably aren't recovering. But the likelihood of that happening before some other issue crops up, based upon our understanding of which metrics of performance start to actually go down, is really important to understand. There's never actually. There's maybe even one instance of overtraining syndrome in the literature that from resistance training alone.
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B
Right.
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So what this means is that, you know, high intensity performance, the ability to contract your muscles, jump, sprint, lift, heavy things, that's something that your body preserves almost at all costs. Yeah. And it makes sense, you know, evolutionary biology, you know, just you being in the room, I get to, to be about that. Yeah. You'll co sign that.
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B
Of course, that's what I do at work. I don't know anything about that stuff, but I'm like, hey, I'm here and I'm Allowed to talk. There's skeletons in our building.
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A
There you go. Yeah. And if you start digging into the, the fatigue literature specifically related to resistance training, you find that things like voluntary activation and well trained lifters are incredibly robust. Like they'll acutely go down, but then they'll come back within minutes sometimes. Yeah. And the, when you look at well trained lifters and you do a maximal contraction and then you actually do an evoked electrical response on the nerve on top of it, it's like that much more so like unlike.
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And since this is an audio medium, a very small amount.
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A
A very small amount. Right. We're talking maybe a 2% difference. Yeah. If, if measurable. Right. So I think that this, all of that is to say that you will probably get injured, sick, burnout, or just have crippling degrees of doms or tendonitis that prevent you from the whole system, not just your muscle, from doing the amount of volume that would actually result in you seeing these measurable, consistent, lasting for months. Because that's the definition of overtraining syndrome. Degradations and force production, which would then prevent you from actually producing a sufficient overload to grow further. And that's probably why we haven't seen it even when people are doing 30, 40, 50 sets. And the things that, you know, Andrew Fry somehow got away with in the 90s with making people do overtraining, where they're only counting reps that you fail on a 1 RM on a back squat until you get 10 and doing it every day for two months, that's. Yeah, that's 10 by 1 RM, not counting the ones that you get. And then when you fail, you go to the next set, you reduce the load, you do it again for eight weeks straight. And seeing one person maybe overtrain it in the study, it's like, oh, shit, maybe we shouldn't be benchmarking. When do I need to deload based upon performance. Yeah, something else. Right, right. So I think if you take that pure sports science definition of recovery and you apply it to volume, you will get to a place that you should not be doing in terms of volume very quickly if you can force yourself to do it. But if you slowly build up to it and you are still seeing gains and you apparently seem to be adapting, you're benefiting from it, even if it becomes a relatively ridiculous amount. But at a certain point, the investment that you're putting in for the return just makes so little sense. Yeah. So it is a, it's a funny thing where I've, I've kind of come around to essentially thinking that MRV is the target. So long as you redefine recovery. Yeah.
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And so when you say, you know, as long as you're still adapting and making gains, how are you assessing that? Like, what's your metric?
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Great question. So are you able to sustain it in a more holistic sense? So one way to do it is how often do you need to modify your training, take a deload, take a day off, like if you're scheduled to do rdls and good mornings, you know, in the same week, how often do those become back extensions? How often do you go, nine happen? You skip it. Yeah. I think many times people attempt higher volume and then they end up reducing something else that contributes to the training dose in a meaningful way. So I think someone is not ready for a sufficient amount of volume or for a certain amount of volume when they're trying to increase it, if the increase results in some other measurable decrease that they can't sustain. So each time you make an increase in volume, it should be incremental. You should be feeling capable of handling what you're currently doing. And it shouldn't result in an increased frequency of deloads. It shouldn't result in a drop in an average rir. It shouldn't result in an amount of doms or physical discomfort or mental fatigue that you can't work through. Because I think that is a bottleneck that should be considered holistically, not just I'm, I need to push through it. If you start to get tendinitis, pain or other issues that seem to be more volume dependent, that those tissues just aren't ready for it yet. Right. At least at that intensity. And then again, if you have to drop intensity, then you shouldn't be doing that much volume. Right. You're, you're, you're paying Peter, you're robbing Paul to pay Peter. So I think especially when you're operating in higher volume ranges, because it's a diminishing return effect, you can argue that any degradation in any other element of the dose or the stimulus is probably not worth the increase in volume. Yeah. I think one way to demonstrate this is the other meta regression done by the Data Driven Strength crew, the FAU crew. If you look at the very, very, very shallow slope of going from like a 10rar to failure, it's a linear relationship, so it's additive. And if you have 20 sets that you're doing, you think, I want to go to 24, which you're sliding, starting to slide down, you're like, ah, but, but yeah, one RIR is almost the same as two, but it's like, no, you're doing that 20 times.
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So if.
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If you go to 22 sets, but your average RAR drops from two to three, that might actually be worse, you know, like. So if you're gonna go up in volume, I see it as quite literally as an analogy of turning up the volume on the song. Yeah. And if it sounds qualitatively different, if you start to blow out your speakers, don't turn the volume up that high. Yeah. You need to get better speakers. You can get a better system if you want to blow up the block when you thump it. Right. Yeah. And that's kind of the way I do it as a coach and with myself is that I'm only increasing volume when I'm able to holistically be able to adapt to it and see that it's not having any negative effect on anything else that I think could contribute to the stimulus. Yeah. And that's why it's taken me tracks like two and a half years to build up from what would be considered high volume to what would be considered. What's wrong with you? Volume. Yeah. And where are you at now, by the way? So. Good question. I am basically doing the volume. I'm like playing the stocks. Right.
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Yeah.
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So right now the constraint is not what I can recover from. It's my time. Yeah. As like the coder and dawling all the shit that we talked about in that episode where I just complained about people asking more of me. Yeah. So right now, because of my. The current demands that I have at sprins, I'm training about an hour per day, Monday through Friday. And then I get into one hour long sessions on Saturday, Sunday. Yeah. So it ends up being about 11 hours. And I am doing exclusively like antagonist paired sets, peripheral sets, and some my reps, drop sets and super sets. So it comes out to being about 20 to 25 sets per muscle group on average.
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B
Okay.
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Which isn't crazy, but it's probably an average RIR of one, I would say. So I'm pretty damn close to failure. Yeah. And then when I have the time, I'm doing two a days and I'm getting that up to like 25 to 35. It's not tremendously higher because when I do two days, it's not just to do more, it's also to preserve the quality.
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B
Right. Yeah. Because I was going to ask. So when. When you try to jam those two sessions into One, you just find the quality degrading, you know, as you get into that second hour of training that you say I'm better off resting, get a meal and me coming back later.
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A
Yeah. And I actually do think, I do experience some reductions in voluntary. I mean, I think I can't push harder. Maybe it's actually something that is subconscious but not occurring at like the nervous system level where I think it is. Yeah. But I will notice that when I'm pushing hard and trying to get a lot done in a session, there is a point for certain movements, muscle groups and a point of just mental fatigue in the session where I'll start to see loads drop off or reps drop off at a much steeper decline. Yeah. Than is my normal fatigue patterns. Yeah. You know, so like for example, if I'm doing a typical chest pressing exercise and I'm failing in the 8 to 12 rep range, I'm typically losing a rep to 2 reps or I'm going up 1 to 2 RPE, right. Or down to RIR. When I get later into a session sometimes and I'm like, now I'm doing the triceps after I've done two chest presses and one other tricep and quads and calves and ab doctors and forearms or something like that. Like I'm getting it all in because I, I have the time and I'm going to do it. Sometimes I'll be on that last tricep exercise and it will be like I'll drop, I'll have to drop the weight, stack two plates so to stay in the same rep range. And I'm like, this, this isn't right. Yeah, this never happens. And then I will typically just stop. I'll just cut it off and be like, okay, that, that's going to go tomorrow. You know, we'll fit it in somewhere else. This is, this is not going to be effective. Yeah, yeah.
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B
Because Zordos, obviously he's written a few times about two A days in Mass and he's talked about when it makes sense, when it doesn't. Of course, obviously, as any, you know, kid who played football in Ohio knows it's just badass to do 2A days. Right. That was always August comes around and it's a rite of passage, you got
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to do your 2A days.
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But yeah, I could, practically speaking, I so much prefer to just get in there, lock in and just knock it out. But yeah, I, I've done some of those. Like really, you know, you start doing like a 9,000 minute full body session. Yeah, man. By the end of it, some of the quality is just crap, you know,
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So I, I organize it so that I do full body push, full body pull. Yeah. And then I will just kind of split it up so that there's, I, I, I think about the overlap within the same day. And the huge caveat here is that I have an office in a sport research institute.
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Yeah.
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There's, there's a gym there. Yeah. I also have access for free to the city and the North Shore gym. The city gym is a 15 minute walk from my house at Aut, and the north Shore gym is the next building over from where if I'm at that campus, I'm working. I have a home gym and I also have a membership to the ymca, which is literally a hundred feet. It's, here's my complex, here's the street, there's the ymca.
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B
Okay. Now did you get the home gym like during COVID or something, was it. Yes, because I was going to say that it's preposterous that you would do that if you live 100ft from an actual commercial gym, but that makes sense.
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A
Well, here's the thing as well. My home gym is I have adjustable dumbbells up to 40 kilos. I have a dual cable stack. Yeah. And I have a leg press, hack squat. And I have a, like a combo rack. Right. Yeah. So I can do anything in there with that setup, but it takes far longer and I can't superset things. So the same workout in the home gym takes me maybe 30% longer than if I went to the Y across the street. And because no one, it's, it's a ymca, but like people don't use it the way I use it at the times I go. Yeah. So it's very, very convenient for bodybuilding. But I, you know, I built my best powerlifting tools in that gym. And also people take holidays seriously down under, you know, like, so, you know, Queen's birthday or I guess King's birthday now, you know, like the Waitangi day, which is kind of like our independence, if you will, New Year's. Like there's, there's very few gyms that are open around certain holidays and some of them have very restricted hours. So I probably train once or twice a month at my home gym. Yeah. Which is still a lot, you know, like 12 to 24 times. It's definitely still something I do in bar trains there quite frequently. Yeah. But, and if, and also like sometimes I'll go to the gym on the weekends and It'll be adjusted hours and not necessarily closed. So they close at 1. I've got a podcast at 10 or something like that, and I'm like, okay, I need to go home and finish up my, my arm work, my calf raises. So I, I don't count those sessions, but I still do that maybe once every two weeks. Yeah.
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B
That's nice, though. You got like a whole network of, of training opportunities.
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A
And one now that I've taken on the co director role, my back seat is my belt, my sleeves, and my Versa grips and my gym pin and my, my handles that I got from, from Porter Phys. Ed. Excellent. They're. They're, they're awesome. They're like spin handles. They're, they're, they're sick. They're. They, they're great for all kinds of, like, delt work back work.
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B
Nice.
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A
Yeah. So anyway, I'm a traveling. I'm ready to train.
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B
Yes.
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A
Did this, did the meeting get canceled? Getting more sets in. Yeah.
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B
Nice. Well, cool. All right. So a lot of good background there. Yeah, I hated that in our, our previous episode, just because we were short on time, we had to rush through that, and it just deserved a little more discussion and elaboration. So that's good stuff.
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A
Yeah. I mean, I fought tooth and nail against, against Mike and then just basically kind of adopted a similar version of what he had. So I have to flagellate myself a little bit. Right.
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B
Yeah. But I feel like you're not doing a very good job as an academic because a true academic would say I was right all along, all along. And my version of it is 1% different. And therefore I'm going to totally steal those ideas while also dissing them, make a 1% change, and then put my name on it.
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A
The carbohydrate insulin model has morphed to become almost indistinguishable from the energy balance model now. But they really just hate the term seco, which I love.
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B
Yeah, the. Even though the model has changed a lot, the vitriol of the arguments is still completely the same.
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A
And I think we have to give a little bit of credit because, like, models are meant to be debated and chipped away at until they become something that is not falsifiable. And since the energy balance model and the carbohydrates and model are almost identical now in 2026, that's, that's actually a good thing. And it's kind of consensus.
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B
Yeah, absolutely. I mean, listen, I won't get too into it, but, like, you know, I think you know, Herman Ponter and I, we, we just, we published a paper a few, few months ago in current biology. It was kind of like a 10 year update on his first like big here's the constrained energy model paper. And it's different now, you know, it, it has changed it. It's not quite the same in the sense that carbohydrate insulin model is just slowly becoming the model it aims to antagonize. This was more filling in the gaps, saying, well, the last time, you know, 10 years ago when we talked about it, we didn't really talk about the energy intake side.
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A
Yeah.
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B
And that seems to be an important thing. And it also helps make sense of. What do you mean my energy expenditure adaptively drops when I do more exercise? Why did these athletes eat 4800 calories a day? And it's like. Well, because they are fueling at an obscene level in order to make that sustainable. So yeah, it's changing. We talk about resistance training in that paper, you know, which was clearly not part of the paper 10 years ago. So it's adding in elements, walking back certain amount. I don't think you're going to see much of that figure anymore of greater physical activity level leads to greater adaptive change. Because it's really in that context you got to remember that's coming from studies mostly in hunter gatherer groups.
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A
Yeah. Or you know, chronic low energy availability.
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B
Yeah. Or coming from you know, like, you know, fixed energy intake, weight loss trials where more, more exercise necessarily means larger deficit. Right. And so yeah, I don't think you're going to see a lot more framing it in that specific way.
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A
You need to have the background of energy, energy surplus, deficit or maintenance there to then start to see that.
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B
Exactly. Yeah. So there needs to be kind of a caveat of explaining. Well, if we expect this relationship between level of energy compensation and level of physical activity, there is some assumption about how much energy intake is coming in or what is total energy balance. Right. So all that is to say, yes, models are made to be changed. So I. You never want to get into that spot where people are shy about updating their beliefs because they think someone's going
- [27:58]
A
to dunk on them. Yeah, 100%. And on that note, have. I haven't looked for a while, but have you saw it? Have you, have you looked to see what Speakman has, where he's at with the dual intervention model, if he's modified that in a bit? I haven't, no, I'm neither of I, I need to do that. Because I'm like, it. That was a 2011 paper that I feel like is last week, but that was actually 15 years ago.
- [28:19]
B
Yeah, no, I'll look into that. Yeah. And, you know, speak me. He's a straight shooter. You know, he's. I think he's got a lot of intellectual humility. I'd be curious to see if he's updated that at all. But I really do. I'm very partial.
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A
That model.
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B
I like that model a lot.
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A
Comports with reality that we experience.
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B
It's a nice thing about models when they. When they seem to comport with reality.
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A
You know, some people in the industry don't really seem to value that.
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B
Yeah, well, what are you gonna do?
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A
Can I make an infographic out of it? Does it sound controversial? And do I like the six studies out of a hundred that do support it model? Yeah, definitely.
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B
All right, Helms. So here's what I want to do. I'm gonna say, would you rather talk about placebo, nocebo effects, or would you rather talk about evolved perspectives on trying to tinker with leptin via, like, refeeds and diet breaks? I think we'll have to do one or the other.
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A
Which one do you think has more meat on the bone?
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B
Oh, boy. Maybe the leptin dynamics.
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A
Let's do it.
- [29:19]
B
I think so. This was one of the ones I changed my opinion about, or at least I'd say I've evolved my thinking about it. Right.
- [29:27]
A
And actually, another reason why I think we should do leptin is that it quite nicely dovetails off of Speakman.
- [29:32]
B
Sure.
- [29:33]
A
Yeah. So the whole dual intervention model evolved from the set point model. Yeah. Which is actually centrally based upon the discovery of leptin.
- [29:42]
B
Yeah.
- [29:43]
A
And in fact, the model existed before they discovered leptin. And when they found leptin, they went, that's it. That's your set point. Yeah. It's the amount of leptin. And they were, at best, half right? I would say. Yeah.
- [29:55]
B
Yeah. So leptin, obviously, it's this hormone, you know, produced by adipocytes. And it's produced at a rate that is linked to essentially how full the adipocyte is. Right. Adipocytes, you start gaining weight, storing more fat, filling up those adipocytes with more actual, you know, lipid, more energy content. They start increasing their leptin production. Right. On the flip side, you know, those adipocytes, you're, you know, in a famine from an evolutionary perspective, or dieting really hard, getting really low body fat, those adipocytes shrink and Shrink and shrink and shrink. They are producing less leptin. And the reason that matters is, you know, your leptin is going to find its way up to your hypothalamus, interact with the receptors up there, and basically provide a little update. How are we doing in terms of energy? Right. So fat cells are reasonably full. Plenty of leptin tells the hypothalamus we're good, you know, and so the hypothalamus is great. If we want to do some physical activity, if we want to do some fidgeting, we're all good, you know, no need to, you know, sound any alarms related to ravenous hunger. We're pretty fine here. And as that leptin level starts going down and down and down, then the hypothalamus is getting the signal like, hey, things aren't so good in terms of our resources available energetically. And that's where, you know, insert every anecdote about lean bodybuilders. Right. This ravenous hunger, significant lethargy, not fidgeting as much, not walking around as much, you know, mindlessly, even maintaining a different posture, you know, not quite sitting up as straight, things like that.
- [31:38]
A
And leptin is very, very upstream of a lot of those things. It's not the one that is directly causing many of those. Yeah, but it is the initial signal to the hypothalamus that we think creates the cascade of all of those things that we collectively put under the umbrella of adaptive thermogenesis. Low energy available, Know, we should say reds or red s rather. Sure, yeah. And even things related to the constrained energy model. Right, yeah, yeah.
- [32:04]
B
Because, you know, when you think about the hypothalamus, I mean, it is just this master regulator coordinator of so many different things, you know, you know, insert your favorite hormone cascade, you go back far enough, you're probably going to end up in the hypothalamus.
- [32:19]
A
Right. Well, how many axes do we have that start with H?
- [32:21]
B
Exactly, yeah. You know, your sex hormones, your thyroid hormones. Yeah, hypothalamus. And then of course, the appetite regulation, you know, just involved in so many. Even temperature regulation. Right. So the hypothalamus is. Is quite a multitasker. And so leptin provides this really critical signal to it. And so back in the day, Helms not that long ago, but it feels like about 70 years, you know, 2013, 2014, there was a lot of research going on. It's really interesting when you look at, like, the bodybuilding research. There's a little bit going on in the 80s and 90s, and then a bit of a slowdown, a bit of a dead period. And then there was this big push in, you know, 2013 to 2018ish, where a lot of people are like, hey, let's dig into this more, you know, and you start seeing some of these case studies kind of trickling out. You start seeing some kind of small cohort studies trickling out. And one of the most vexing problems or intriguing problems with natural bodybuilding is things get really weird when you start getting really lean. And that sets you up for this really chaotic rebound stage, unless you plan for it really well. And so 2013, 2014, leptin was on the mind for me because it, it was very clearly something that plays a big role in this whole series of adaptations that we associate with being very
- [33:51]
A
lean and energy depleted.
- [33:53]
B
And the thought was, and also seemed like it was kind of setting us up for that rebound. Right. You're in this, this low energy state and you're kind of primed with this ravenous hunger for a big, a big rebound and, you know, rapidly filling back up those adipocytes until, you know, you get that signal restored from leptin. And what we know about leptin, of course, it's responsive to the fullness of adipocytes as like a long term energy sensor, but it's also responsive to short term fluctuations. Right. So short term fasting, and specifically short term fasting or short term, short term carbohydrate avoidance.
- [34:34]
A
Yeah.
- [34:34]
B
So, yeah, if you really want to get a quick spike in leptin, carbohydrate overfeeding is the best way to do it if you really want to drop it. Obviously fasting is a way to do that. But even just dropping carbohydrate really low can acutely kind of, you know, move the needle. And so among me and a whole lot of other people, we're really fascinated and like, well, what can we do in terms of leveraging the short term dynamics to try to game the long term dynamics? Right. We know that a surefire way to get leptin back to a higher level and alleviate some of this ravenous hunger, of course, is to refill the adipocytes, gain a bunch of fat. Well, I prefer not to do that as a bodybuilder. Right.
- [35:19]
A
Slightly counterproductive to my goal of actually doing the exact opposite.
- [35:22]
B
Exactly. And so the idea was, well, what if we're either on the way down or even after shows, what if we try to game the system a little bit? So on the way down. What if we do these back to back days of high carbohydrate refeeds, let's get the calories up specifically from carbohydrate, get a spike in leptin and try to coast on that for the next five days until we get to the next one. Right. Same thing with diet breaks, the Matador study, you know, some of these studies here and there indicating, well, wait a minute, if people are dieting, if we give them this one week or two week break where calories and carbs come up, back to baseline, leptin goes up, theoretically, and then we're ready for another little dip in terms of, you know, recreating that deficit. And the idea was, you know, it's very clear by the way that when we look at metabolic adaptation and dieting, this reduction in total energy expenditure that is adaptive in nature, we can reverse that in a heartbeat if we just inject you with leptin. Right?
- [36:26]
A
Yes.
- [36:27]
B
And so that was the whole. Even like frankly, amenorrhea and oligomenorrhea also respond to exogenous leptin. It's not quite as simple because those are very complicated. Trying to restore a regular menstrual cycle.
- [36:39]
A
But, but you know, it doesn't respond to leptin injections. What, obesity?
- [36:43]
B
Yes.
- [36:44]
A
And that was the first type of leptin injections that people tried to do. Yeah. Discovered the hormone, they went, oh, this is, this is the thing that drives people. Uh, so therefore people with obesity must have low leptin, will do injections. Oh, hold on. They actually, there's one specific type of obesity that it does that I actually have low leptin, but it's incredibly rare. Yeah, but, yeah. Oh, hold on. Is it leptin resistance? And I, I don't think we have truly studied leptin resistance and understood that fully. That's more of a conceptual idea of why leptin doesn't operate the way it's supposed to. Yeah. In people with obesity. But it's also fully comports with the model of leptin as a one way street. Right. As a, as a signaling. Yeah.
- [37:25]
B
You know, low leptin is your signal, shit's wrong.
- [37:29]
A
And so what you're proposing anything of that is fine.
- [37:32]
B
Yeah. So yeah, it could be that, you know, that we're having just like with insulin resistance, maybe we're having issues with ligand binding to receptor creating this intracellular cascade of events. That's one possibility. Another possibility is. Yeah, there's just a kind of a ceiling effect. Once you have basically enough leptin. More leptin doesn't seem to do anything right in any case. Yeah, the, the hope was, oh, leptin, when it gets low, that's the signal. You're starving. So therefore, if we make it really high, that should be the signal. Stop eating. That's not how it works, certainly not in the vast majority of cases of obesity. So everyone got really stoked when leptin was discovered, poked around a little bit and said, oh, that's kind of disappointing. It didn't do exactly what we thought. But what is clear is low leptin puts you in a state of, you know, you're very hungry. And it, it does play a huge role in all that stuff downstream in metabolic adaptation. So that was the goal was, let's try to get some little spikes. We don't have exogenous leptin for recreational bodybuilding use, especially in the natural game. And so the thought was, let's just try to get these little spikes and coast between them. Right. And so, you know, we've done some studies on it, and it's interesting because my, my view has changed, but I'm not ready to slam the door on certain applications. And what I mean by that is we tried to do some studies where we. I mean, listen, you know, when you're a researcher, a lot of folks get to enjoy the privilege of kind of talking about fitness stuff and then saying, someone really ought to look into that, but they're not researchers, so they don't have to. But when you actually have a foot in the lab, it's like, well, you either gotta, like, shut up about it or like, actually, yeah, you gotta do it. Right. And so we, we tried to do some studies where we strategically use, you know, diet. You've done them? I've done them. Refeeds, diet breaks. You know, you were involved with the Ice Cap trial and, and exactly.
- [39:40]
A
You're involved with the, the, the refeed data by. Led by Campbell, right?
- [39:44]
B
Yeah.
- [39:44]
A
Seibler.
- [39:45]
B
Yeah. And so generally speaking, I think it's fair to say, in those projects we took people who are, you know, what was it? How would you describe the demographic for the Ice cap truck trial?
- [39:58]
A
I would say resistance trained. Athletically lean. Going from athletically lean to leaner. Yeah, yeah. And associate with Seidler's data as well.
- [40:07]
B
Yeah, yeah. Pretty similar. So this isn't your typical. We're doing weight loss. So therefore untrained, obese individuals. Right. These are people who lift weights, you know, reasonably. You know, like you said, athletically lean, not shredded. And let's have them lose some weight and let's do either refeeds, your diet breaks. Play the leptin game and see if we can create more fat loss, more weight loss and or greater preservation of metabolic rate. You know, trying to attenuate some of these metabolic adaptations on the way down. I think it's fair to say that neither of those studies really panned out. I think in terms of like massive advantages on the metabolism or fat loss side. I think that's fair.
- [40:46]
A
Yeah, I'll, I think if it's worth just actually going through the data real quick. So we've got Campbell did two day refeeds and, but not diet breaks.
- [40:55]
B
Right.
- [40:55]
A
Seidler, same lab group, but Madeline, she looked at I think one week diet breaks in women as well. And then POS data was 3 on one off I think as well, eating at maintenance carbohydrate predominantly. And in the two diet break studies there was no body composition advantage. There were other data you're about to talk about. And then in the Campbell study there were some indications that could have been at least partially confounded by the methods, you know, when you're, when you're, they're trying to correct for potentially not having an, an impact on fat free mass of the glycogen and water associated from the refeed itself. But there did seem to be a positive effect on body composition with the methods available for the two day refeed. And I think pios wrote a, a reasonable critique of that saying hey, this was probably glycogen. And also it doesn't make sense that two days, does it? But when you go to seven days that effect goes away. Yeah. Which I think is probably the more, the stronger part of that argument. But even, and then they tried to do a novel method of fat free water, corrected mass, trying to pull the water out differently. But you know, that hasn't necessarily been validated against like say, you know, some of the more modern methods we have of assessing muscle glycogen. Yeah. So yeah, it, the, the, the refeed data is the only one that looks at that model and is positive for body comp. And all of the rest of them are body comp. No like no clear meaningful or, or statistical difference between groups. Right. Although there is a meta analysis that I want to talk about after you kind of get into.
- [42:42]
B
Yeah, sure, yeah. So, so all basically, you know, we line them, line it up, you know, take a crack at it. Nothing really jumping off the page, I would say in terms of massive Metabolic advantages, massive advantages with, you know, changes in body composition. And so a lot of people said, oh, well, you know, case closed, these things don't work. Whatever. Like you said, there, there's, you know, meta analysis on the topic that says, I don't know, maybe things are leaning, you know, in that direction. But I think what I have kind of taken away from it the way. Well, before I get into that, it's worth acknowledging in the studies we're talking about, the total magnitude of weight loss wasn't very substantial. People and certainly people were not getting shredded, right?
- [43:33]
A
No.
- [43:34]
B
And so when we go back to why people thought this would be useful, we're talking about the people who are, you know, couldn't get a drop of leptin to save their life. Right. They're getting very lean, they're losing 35 pounds in their bodybuilding prep and they're getting down to essential body fat levels. Right. Or as close to it as they can. And so it's frankly in these studies a different metabolic state. No one would look at these individuals and say that is the same thing as the original idea that got you interested in this. Right. And so that, that's one, one scenario where I say I kind of have to wear like two different hats here. If I'm talking like, you know, I, I teach a course on public health now.
- [44:15]
A
Yeah.
- [44:16]
B
If I'm talking public health, refeeds and diet breaks, physiologically, whatever effect we could be getting there, I can't really pretend it's going to move the needle. That's where I'm at on it.
- [44:28]
A
I think that's an interesting way to put it because I had a bit of a, I argued with myself about this a fair bit when the. I think it was the poon that it announced. Yeah. 2024. I think he's actually someone you've collaborated with. He's.
- [44:39]
B
Yeah, we actually, we have a paper that's in review right now that is actually doing the kind of five day and two day, like refeed type thing.
- [44:49]
A
Is he based in Hong Kong or.
- [44:51]
B
Yes.
- [44:51]
A
Yeah. I actually meant to catch up with him when I was in Hong Kong. I. We didn't. But I need, I need to actually meet him because he emailed me. Yeah. But anyway, so really interesting thing with that meta analysis. I want to say the. So first off, significant finding that indeed intermittent diet restriction, including diet breaks and refeeds and other stuff like five and two diets. Yeah. Did have a significant effect positively on preserving energy expenditure. Yeah. The unfortunate thing is I think it was about 80 calories.
- [45:20]
B
Right?
- [45:20]
A
Like 79. Yeah. Really interesting sub analysis though. And this broke my brain at first. Was that the effect in the lean people, like I was like, oh, can't wait to see this. Sub analysis was like 30.
- [45:32]
B
Yeah.
- [45:33]
A
But the effect on people with obesity was closer. It was a little over a hundred, I think. And that's. Now we're actually talking about something that might matter. A hundred calorie discrepancy, you know, that's the realm of I care. But not nearly the kind of like, you know, wave the, wave the flag. This is amazing. Yeah. And then I was like, oh, hold on, like, what, what are we talking about here? Leptin dynamics are directly proportionate to the amount of fat mass you have. And leptin changes are proportion to the amount of fat mass you lose. And all of the lean people trials, they're losing 2 to 3 kilograms of fat mass. Right. And we're talking 11 to 15 ish. Yeah. And then people with obesity. So on one hand, I agree with you. Going from 10% body fat to 4% body fat. Like if I was to start a prep, oh, maybe 12% body fat to 5% body fat, whatever, that is different than losing 2 kilograms when you're 15, going to 12. Like these studies. Yeah. But that is also different from going from 40% body fat to 30% body fat. You know, like we're. And you would see a larger leptin change there and then you would see us getting that bottoming out. Really, really negative signal in the bodybuilders. And then the middle range is actually when you might see the least someone going from, you know, not low enough leptin to really cause an issue, but not high enough in body fat to lose enough body fat in the type of length trials we're talking about. Yeah. Because the meta analysis would actually predict that, oh, refeeds are actually physiologically better for people, people it looks like, who have obesity. But in actuality, what it's saying is who lose more body fat. Yeah. So that is something that I think is worth pointing out because it does kind of hold a little bit of mechanistic rationale that does comport when you think about it, because it has to do with how much do you lose rather than where you're at now.
- [47:26]
B
How do you reconcile that, though, with the concept that, that, you know, we were talking earlier about the asymmetry of leptin.
- [47:32]
A
Yeah.
- [47:32]
B
And the idea that maybe once you have plenty having more, it just kind of doesn't matter. So if we are talking about these people who at baseline have well, more than plenty. And then in their weight loss trial where they are losing those 11, 14 kg and it's not like they're getting to perilously low leptin levels. Right. So that would kind of you, I think baked into what you're saying would be the assumption that those folks must be getting to leptin levels that are below whatever that maximal level is. But it's hard to know where that's supposed to be.
- [48:06]
A
Yeah, it would, it would rely on leptin resistance rather than just it being a one way street. Yeah, that would be one potential way to get there. Or it could be completely unrelated to leptin. And there are a lot of things that just happen when you lose a lot of body fat. Yeah. Or at least in short term time periods. Right. Yeah, um, I think so. It's a tough one. But I think it's, it's interesting that more like, like the way I would look at it is, oh, more body fat loss means that there is potential benefit of intermittent restriction. But it, it, it could just be like if you look at what there's. I can't remember who did the modeling. It might have been Kevin hall on the proportionate amount of hunger you experience based upon weight loss. And one thing that I found really interesting about the very first, not the very first, the first intentional diet break study, the burn study. Yeah, it looked really good was it was an outpatient, gave them food scenario and it had good data for like lean mass corrected RMR and it looked like. And then on the six month follow up they retained more of that loss which made me think this might have been them getting to practice maintenance a lot. And they actually learned how to do this over time. And then I think an important thing we haven't actually mentioned yet is that what both Seedler and PIOS found with two different ways of measuring it and one actually found a physiological difference. So physiologically satiety hormones were better in the group that did intermittent dieting as well as disinhibition. I think it was in seedlers. Yeah. And then it was just better hunger management overall in poses along with that physiological change. Yeah. So a very consistent finding that they reportedly was easier to do that which kind of supports that indirect finding of better weight loss maintenance and burn. Yeah. Which could also explain some of what we're seeing. It's, it's more of. In people who are. Maybe it doesn't comport because like, okay, if they're, if they're getting better adherence and they're losing more weight. That should show up not just on metabolic adaptation, but it should also show up on weight loss. Right. Yeah. And it wasn't super clear that they were losing more weight. Yeah. So, yeah, I don't necessarily know what's going on, but I find it fascinating.
- [50:24]
B
And that is the root of, I think, what I'm trying to convey. And when I say that I've adjusted my perspective on this, it's to be totally honest. Like, like, for example, when you were just laying that out, you were physically reaching. Yeah, yeah. Right. But if we look at this part of that study, that part of that study and that part of that study, it makes sense. Right, but. And there's. And that's the right way to do it when we're talking about sparse data.
- [50:55]
A
But it should just be sampling.
- [50:56]
B
So I'm not. Yeah, I'm not like criticizing that.
- [50:59]
A
Yeah.
- [50:59]
B
But when I first got into this in 2013, I said, it's so simple.
- [51:05]
A
Yeah. You know, we had a mechanism.
- [51:06]
B
Yeah, we had a mechanism. The mechanism is supposed to do this. We should see it in these contexts. And where I'm at now is wrestling with a lot of discrepancies and trying to build them, reconstruct the model based on. But every time we say something promising about it and say, but how do you, how do you reconcile that with this? And you're like, well, there's. There's a way we could reconcile it, but there's. There's so much theory that it has to got. You have to like, work your way through the data and piece it together. And it's just a lot, It's a lot more messy and convoluted than I ever expected. And so that's where I'm at with it is it's. And again, I have a paper in review on the topic. It's not like I said that stuff's useless. It's a dead end. Cut bait. But where I'm at now with it is, oh, wow. We need to figure out, does this work only in obesity? Does it work only in people that are more. In people that are truly shredded? What's going on in the middle? Is it purely just a matter of total weight loss? Whether you're on the higher or lower body fat side of the spectrum? Maybe it is just who loses 30 pounds? People who prep and people with obesity, not athletic people who are like, fine, I'll do your dumb little study, but lose eight. But yeah, I'm gonna lose six pounds. You know over 12 weeks. Because I'm not going to kill myself for this study and try to get absolutely shredded. Right. It's just you're not going to be able to get a lot of average college kids and say, hey, by the way, we're going to do our own little Minnesota starvation experiment with you. Right. So all that is to say we have to figure out is this a magnitude of weight loss thing, Is it certain parts of the body fat spectrum, what element of it is behavioral versus physiological? Are we interested in differences in body compensity? Because.
- [52:54]
A
Can we talk about the behavioral aspect a little more? Sure, yeah. Because I think that's the one thing where I don't feel like I'm reaching or I do feel like it's pretty consistent.
- [53:02]
B
Oh yeah, I'm on board with you there. Yeah. What I'm talking and it's worth going into. But what I'm saying is there's I think a debate right now which is valid and it'll be interesting to see how it shakes out. It's not is there a behavioral, know, potential for advantage. It's. Is that the whole advantage? You know what I mean? Where, where it's, this is. At first, I think a lot of people were looking at this. When I say a lot of people, I mean me as a pure physiology intervention. We are doing this to spike leptin which has, you know, this effect. Now I think there's a lot more appreciation for. Oh, it looks like there is kind of psychological and behavioral advantages which may be partially or some people might say fully driving the benefit.
- [53:49]
A
And you know, going back to last week slash last hours episode that we did. Yeah. Where so much of our interest has been kind of in the evidence based community when we're a little more physiology and less psychology focused was, hey, we think it's, you know, it's hypothyroidism, it's, I have some type of issue PCOS or I am an outlier just in terms of my, my, my metabolic rate. And then we go, wow. Like the things that have really moved the needle has been behavioral things, appetite regulation and you could lump them under physiology. But things that we kind of perceive with our original western model of mind and body being separate as the mind stuff.
- [54:26]
B
Yeah.
- [54:27]
A
Even though they're not, you know, and we don't have as nearly as much agency that we think we have.
- [54:31]
B
Right.
- [54:31]
A
You know, we give us a hunger regulation drug that really works and obesity fixed. Right.
- [54:37]
B
Yeah.
- [54:38]
A
So.
- [54:38]
B
And then take the drug away and
- [54:39]
A
we go right back to the Game. Exactly. So I think there is absolutely an acknowledgment that even if it was just behavioral, just like we would blame everything on physiology when it was just behavioral, something that we think is positively modifying physiology may just be positive. Positively modifying behavior. And we, we experience it as a, as a physiological effect. Yeah. And I think that comports with bodybuilding because the barrier for most people with getting shredded, at least earlier in their career is that it's too hard. Yeah. And it's, it's, it's. And that's not something bodybuilders like to admit. But they, sometimes they have to like I binged, you know, or yeah, I couldn't get it done in 12 weeks. I couldn't sustain the deficit. So something that makes it feel easier to get to the same point allows you to push further. So, you know, our experience of diet breaks and refeeds being, I would say even almost game changing at a certain point for getting certain people over the line and having a push pull approach. And you know, we get, it's like we don't get there at all or we do get there. Yeah. And I have to, if I don't take that approach, this client is going to be around 8% body fat. And then the wheels start to fall off mentally, behaviorally. But they may not want to report that, may not want to admit that, and that may not even be what they experience. So I think that could be enough to define it. And there's even other data besides kind of the secondary markers that Seedler and POS took. There's ones that have more directly. Look at this. There's a really cool study where they had two parts to it. So the initial phase was they asked people just with two ways of getting to the same energy intake, how would you feel about having, I think it was 1500 calories seven days a week or 1300 calories on five days. And then you get to have two days that are that additional two, like whatever that is, like another thousand calories added to it. So two days at like 25 or 2300. I can't remember the math. Yeah. And most people chose that. I would like to have that light at the end of the tunnel because those equally suck whether I'm on 1300 or 1500. But I get to look forward to two days at 2500. So sign me up. And that was like a huge majority of the participants. Yeah. And then the follow up was a four week dieting study where they actually had them do that or not do it. And what they found was that self regulation, which we're seeing is a huge component of successful behavior change broadly. Yeah. And this actually goes into my talk that I'm doing. But successful weight loss interventions, weight loss maintenance that was improved when this was intentionally done, framed this way and said oh, basically at the end of. And it was only four weeks but still they lost more weight. And weight loss correlated to self regulation. And self regulation was higher in the group that had that end of kind of like every week. I've got a light at the end of the tunnel.
- [57:32]
B
Yeah.
- [57:33]
A
And it seemed to improve their ability to self regulate on low calorie days knowing that they had that. Yeah. And I would say from probably both of our coaching experience, that's not true for everyone. For many people, the refeeds prompt going off the rails.
- [57:48]
B
Yeah.
- [57:49]
A
They turn into unrestricted eating. But then the final link is that there's an actual study on the first four weeks of contest prep in competitive bodybuilders. And those who had higher trust in their satiety and hunger ability to perceive it rated themselves or they scored higher on intuitive eating score and had better emotional self regulation were the ones who had more control over their energy intake on unrestricted refeeds. In the same model they had the weekends unrestricted eating. And it was the people who had that, those better self abilities. So I think when you use intermittent dieting strategies in such a way to purposely develop self regulation and use them and frame them in the manner to give people a quote unquote break from a deficit that they can look forward to and they know is coming and they also have. You've built that skill up in them. They had that self efficacy and self regulation then I think it does make things demonstrably easier. And there's actually a relatively robust amount of data that's five studies, you know, that, that show from different ways very similar outcomes from similar patterns of intermittent energy restriction. Yeah. And if that was all it was, I would happy to say, yeah, I was wrong about the physiology. You know, you, you, you'd be happy to say that as well, but I'm not wrong about the outcome. Yeah.
- [59:11]
B
Yeah. And I think that's where I've, where I've kind of gravitated, you know, back when I was still coaching people one on one. What's interesting is I got into this place where I was like, you know what I'm less certain about, you know, when, when I first got into it, I'm like, this is you know, essentially a pure physiology intervention. It's going to have these large magnitudes of effect. This is going to be a game changer. And what I really got myself to, the point I got to working with individuals was even after I lost some degree of confidence in this kind of simplistic perspective, I would still use them sometimes. And like you said, it kind of depends on the person. But it's a weird place to be where for some people I'm just like, could there be a physiological benefit? Maybe. But do I think this is right for you psychologically and behaviorally? Yes. And so we would use it and it would go well. And at the same time, with my own dieting, we've talked about this before, I was doing a prep where my approach to it was I just don't want to think about. I want to set it and forget
- [60:22]
A
it, live in a deficit.
- [60:23]
B
I'm going to watch my body weight go down and my body weight stops going down. I'm going to make a cross qualitative change, which of course leads to a quantitative change. I don't even want to deal with the quantity. I just want to live my life aside from the numbers, because the numbers are depressing as hell. And so when I was with my own, you know, working with my own diet, I just knew because of my perspective, temperament, preferences, whatever, I, I don't feel good after I have the two days up there and then I go, oh my God, day one of five, feeling without, you know, having the absence of the. It's because there's going to be two different kinds of people. There's going to be the people who settle in on the low calorie days. The big deal, I got the two high calories coming down the way. But for me, I'm just kind of wired in that way where for me the low calorie days are the days where there's an absence of the good thing. Not viewing the refeed days as the bonus at the end of the and
- [61:25]
A
also thing back in the 20 scenes, we got there differently. Refeeds were it fit your macros driven. Let's see what we can fit in. Yeah. And I look back and sometimes I was eating lower total food weight on my refeed days and I would get hungry, hungrier on them. Yeah, like my, my energy density went up so much and the refeeds that I do now, which are very intuitive and autoregulated, it is, oh, let me get like additional pieces of wheat toast at breakfast and I'm gonna have two pieces of fruit at lunch and then for dinner I'm gonna have salad and. Oh my God, also potato. Yeah. So it's like there wasn't any reduction. I didn't. I wasn't maximizing the reduction in fruit and vegetables to increase like Cocoa Pebbles. Right. Like, like was. Was the norm back then.
- [62:07]
B
Oh, yeah, yeah.
- [62:08]
A
How do I fit in the Pop Tart so that that can qualitatively change the experience because the diet is the same but you're adding a bit extra or you're having more of the same that you don't. That it's not super hyper palatable. That doesn't feel like a treat. Yeah. It's just kind of like a breath of fresh air. Like I got to have like a little more of the same. Yeah. That can be one way to alleviate that. It can be a little bit easier. Yeah, but. But not for everybody.
- [62:35]
B
Yeah. So for me, yeah. Again, my whole thing was I want to have an approach where I don't feel compelled to really do any. I just really enjoyed that stability psychologically of every day is the same. And therefore I could convince myself, when you feel like it's a really hard day, bro, it's the same as yesterday. Like, just move on with your life, get busy with something, forget about it. So. So where I got with it was I didn't rule out the possibility that there are physiological advantages on the table, but for my own case, I decided the psychological benefits of the stability, the predictability and not having to go up and down and up and down outweighed whatever physiological benefits may have been on the table from my situation. So that's where I got with it. And I'm still out with it. Is it's a tool in the toolbox. There's a time and a place to use it. I certainly don't look at people who are using it and say, what an idiot. That's 2013 logic. Definitely not there. But my view on it has evolved in the sense that it went from pure physiology. Obviously this is going to work and have a huge effect on energy expenditure and fat loss rates. And now it's maybe there's some physiology. There's definitely some behavioral and psychological elements to it. Those probably vary. Well, they certainly vary from person to person. So it's just a much more complicated utilization of the tool. But it's not like we took the tool and said, we'll just throw this in the junkyard because it's crap. It's just a really complicated thing.
- [64:08]
A
Well said. And I think it also has freed me up now that because I See it exactly the same way as you is that I have a much bigger lever I can pull on the behavioral side and the physiology if it's there. We haven't been able to measure it yet, but we also haven't measured the thing I'm doing right. But I'm pretty confident saying the behavior matters more.
- [64:28]
B
Oh yeah.
- [64:29]
A
So that's freed me up to do things like I don't need to make it a high carb refeed. I don't, Yeah, I don't need to have it to be a refeed that even actually takes you to maintenance.
- [64:39]
B
Yeah.
- [64:39]
A
You know, so like if the coaching angle, if I was working with someone like you to where you know, the kind of the way you self regulate is. Yeah, I feel terrible today, but it's the same thing. Yesterday I would go, well tracks it is. But hey, I want to give you the option of having an apple in a glass case. You know, like break in case of fire. It's not a refeed. It's 100 calories, man. Like if you feel like trash today. And that's the thing like in prep, small things can like you're, you're, you're, you're, you're skirting around like a low ass glycogen levels. Your brain's trying to find some, some glucose. It's run out, it's get some ketones. The, I don't think people understand like when you're on 1600 calories, you have an apple and you get the 1700 calories and you feel about twice as good. Yeah. It doesn't make sense. It's a disproportionate benefit. Yeah. And that's the type of thing where if I had an athlete like you, I would be like, hey, you know one of those days where you could grind through it. We're doing really good. We're ahead of the game. I would actually prefer you to have that apple be a little bit better. Have more productivity at work and maybe get like just through the workout with less pain. Yeah, do that. Make that choice. It's totally fine. Let me know. Well, corporate don't think about it much. It's just an apple. Right. So that, that is kind of one of those things that, that I, I, I, I've incorporated with certain people. It doesn't need to be a refeed. It's a break in case of I feel like trash. And we don't need to feel that trashy at this point. And I don't want you to. Yeah. Because it's all kind of coming out of that same stress bucket. And that's an application of this, that isn't bound by this speculative physiology of, well, we need to get you out of a deficit and we also need it to be large with carbohydrate because of insert leptin physiology glycogen nonsense that hasn't really panned out and we're trying to go, okay, well, if the outcome I want to get to is making the diet feel easier, sustainability to be higher so we can push and you can get to a place where you're shredded and go, that wasn't as hard as last time. That's how you win. Shows. Yeah.
- [66:35]
B
Beautiful. All right, well, cool. So I'm glad that we took some time to revisit those topics because I think the 30 seconds each we gave them in that previous episode was a little light.
- [66:47]
A
Yeah, I felt like there was a,
- [66:48]
B
you know, some more stones that we could turn over there. So really enjoy the engaging discussion. It's easier in person if you could finally get the good sense to move to the beautiful state of North Carolina. Think of, think of this. Beautiful mountains teeming with vegetation. You can't get that anywhere else in the world. You have to get it in North Carolina. Carolina, the beautiful Appalachian Mountains. They don't have anything like that in New Zealand.
- [67:15]
A
You heard it here, Kiwis. We need to go to North Carolina to see beautiful mountains teeming with vegetation.
- [67:21]
B
Yeah, they shoot movies in North Carolina sometimes. Did you know that they.
- [67:26]
A
I think they might have shot a few in, in parts of New Zealand as well.
- [67:31]
B
Probably ones I didn't see.
- [67:33]
A
Hey, yeah.
- [67:34]
B
So in any case, the doors open if you'd like to, you know, make your way back to the beautiful states, Leave all New Zealand behind. I know you're, you know, running a big research institute there and things are going well and you have a happy family and you love your area and everything, but just for the podcast, it'd be a lot better.
- [67:55]
A
Well, two way transcontinental flight.
- [67:58]
B
Yeah, absolutely. Yeah. It's a quick 30 hour travel. All right, well, I'll tell you what we need to get out of here. A lot of things to do here at the SNA annual conference in Gold Coast, Australia. But before we do that, of course, we gotta plug all of our many things and we also gotta, you know, shout out our friends. So first, friends first, right? Listen, folks, you lift weights, you wear shirts, you do all this kind of stuff. If you are in the market for new gym gear, new gym apparel, and you think you know what? I want quality. I want substance. You go to elitefts.com the only way they did me wrong was back in like 2010. I bought two pairs of straps because I figured, I'm an idiot, I'm going to lose them or they'll wear down or whatever. I have barely touched the second pair. The first pair is still completely usable. I didn't lose them because when you see value, you grip onto it tight and you never let it go. Those lifting straps are incredible. And of course, they have much more than that. So Elite fts, great apparel, great lifting gear. You got to go there. You got to use our discount code. M sorry.
- [69:06]
A
MRR 10.
- [69:08]
B
MRR 10. 10% discount. MRR stands for Mass Research Review, the presenting sponsor of Iron Culture, mostly because we're co owners and co authors. So that was an easy deal to make. We just did it. Yeah, so, but Mass Research Review, if these kind of conversations where we think through things and we don't necessarily just say, let's go with the simplest answer because it makes sense to us and makes us feel better. If you actually enjoy dealing with those nuances and thinking not just what is the simple answer, but what is the most accurate way to think of this and what does that mean for how we apply this? That's what's happening in the pages of the Mass Research Review. Some things are a lot more straightforward than what do we make of refeeds and diet breaks and how do we apply them. But that is kind of the. The overarching goal with Mass is let's drill into the nuance and let's make sure that we are really looking at these key topics in exercise, nutrition, the psychology of training and nutrition, making sure
- [70:11]
A
we super easy to promote on social media as well.
- [70:14]
B
Oh, yeah, yeah.
- [70:15]
A
The TikTok, the Instagram account with that type of content, it is blowing up. So, yeah, I don't know that we can get followers growing any faster. And you should definitely follow us the Mass Research Review Instagram, because I don't know if they'll keep allowing it to grow at that rate. They're probably going to throttle us. They may stop follows from being allowed on the platform.
- [70:36]
B
I think they already have.
- [70:37]
A
Yeah, actually there was actually a purge recently. I lost 700 followers in two days.
- [70:42]
B
How can you tell that you lost 700, though?
- [70:44]
A
Because I dropped from 200k to 199.
- [70:46]
B
Oh, that's a painful job.
- [70:48]
A
I was like, oh, I've worked so hard for this. I'm gonna have to wait three weeks.
- [70:52]
B
So what do they purge? Like dormant accounts or bots?
- [70:55]
A
I think fake accounts, bots. And then things that didn't exist anymore. Okay. Because there was a. I googled it and everyone was like, what happened to my followers? You know?
- [71:04]
B
Well, hey, I actually, I don't think I lost. If I lost any. I couldn't tell.
- [71:07]
A
So yours are all real?
- [71:08]
B
Yeah, mine are all real. It's easier when you have a smaller number.
- [71:11]
A
Well, when you buy 198,000 of your followers, it's. It's tough in those streets.
- [71:17]
B
Yeah, some of those are going to be from bot farms, unfortunately.
- [71:20]
A
I don't care where they're from. Yeah, the numbers.
- [71:22]
B
But anyway, yeah. Mass Research Review. Not great for clickbait. Very good for learning how to actually apply cutting edge science of training and nutrition. So check it out, mass research review.com, folks, that's all we got for this episode. Live from. Well, not live, because we do live stream. So I shouldn't say that we're live. We're here in real time. Alive. Yeah, we are alive in person. From Australia for another very successful SNA conference. Folks, we do every year, so next year I'll probably be in the States, so keep an eye out Sports Nutrition association, see where we're. Where we're doing it next year and maybe join us if you're available. But that'll do it for tonight, everyone. Take care and we'll see you in a week with another episode.