Transcription
Um, I have to tell you there's going to be something a little different with this next one. Um, Dr. Vincent Ben Biko—that's right! You have to learn that just like the rest of us, he has been a leading figure in health and fitness for decades, pioneering slow resistance training and emphasizing the link between diet and exercise.
But before I get on to the prompt to please welcome him, I actually want to share with you a personal story. I've asked him to give me a few minutes of his speech so that I can share this with you. Dr. Ben, as he's known—no joke—has changed my life.
See, my entire life, I’ve, as I would say, gotten by. I’ve done things like say marathon running; I make sure I walk a lot, and in many respects, among my engineer friends, I look like a fitness god. But I’m going to be honest: you don’t need any tickets for my gun show; you’re good, you’re fine.
But I understand—and you should know this as well—that maintaining strength is important, especially as you get older. So, while I’ve always managed to keep things going on the cardio sense somewhat, I’ve never really gotten into strength training, frankly because it’s boring to me and time-consuming.
As I’ve gotten older, I’ve been more worried also about injury. You know, I’ve had other middle-aged friends going, “Dang it! I need to get back to the gym.” They go back to the gym, they work out hard, then they actually get some pretty serious injury that they keep. So, I had these two problems that kept me away from strength training: time, because I wanted to be short, and fear of having injury.
I saw Dr. Ben’s talk through one of Doug’s conferences and I was very impressed. I was chatting with him about it and I said, “So, what does it really take if I'm trying to get the minimum viable?” He said, “I’ve got the program; it just takes like 15 minutes twice a week.”
Like, “God, it sounds like everything you ever see on TV!” Well, I’m telling you, for the last 10 months—which is the longest I’ve ever maintained any strength training—twice a week, I meet Dr. Ben on my iPad. That’s our appointed time, and for 15 to 20 minutes, I do this workout.
I have to say it has truly changed my life. Now, here’s the kicker: in no way am I being compensated, nor is there any affiliation. Part of why I feel so compelled to tell you this today is because not one time, in spite of every offer I’ve made, has Dr. Ben allowed me to compensate him. He said that this was something he wanted to be able to do as another pay it forward in my direction, and I’m just so appreciative of him being able to help me out on a personal level.
So, with that, please welcome for me, Dr. [Applause] Ben!
Alright, I’ve got a little froggy voice, so please forgive me—or not. Um, I’m thinking back; it’s been about 50 years since I did my first one of these conferences. Um, I was the young buck on the block then. Now, look at me. Anyway, I’m going to go into, excuse me again if I’m froggy, I’m going to go into the lipid energy model. Let me get my clicker here.
Um, I assumed this was going to be a very scientific meeting; usually my talks are kind of baseline for the average schmo, but hopefully some science. This one, I’ve gone a little bit scientific, so if I bore you, I don’t know—there’s some stuff you could do on your phone or something.
And like I say, it’s been such a long time since I started; the world has changed so much. You know, I was thinking about all the terminology—people, a he and a she and an IT and a they and whatever the hell it is. So, I came up with this one: I said, “What do you call a guy who’s attracted to both sexes but neither sex is attracted to [Applause] him? By himself!”
Alright, let’s see if I can work this thing. Okay, so we know about the lipid energy model—maybe we don’t know about the lipid energy model—but to me, metabolism is all about energy. Okay? Um, and I think if we’re testing or getting metrics about metabolism, it would behoove us to do it in a dynamic way instead of a snapshot of a lab. Maybe what’s the trajectory? What’s going on?
So there’s no better way to actually assess that, I don’t think, than exercise. The implication that exercise might provide—so how can we drive towards health and away from dysfunction? I think that’s what our business is really, and the lipid energy model to me is just a part of the entire energy model. You can’t separate the glycolytic energy model.
Okay, this muscle fiber chart—I put this in every talk I can because—and I’m going to try to spend some time on this, hopefully I won’t lose anybody—I actually teach this slide at medical school to orthopedists and all kinds of GU MDS to try to have them understand what’s going on with exercise.
Okay, exercise is really just the manipulation of muscle fiber recruitment. So, how long do we do it for? How intensely? How often? The recovery? Understanding the metabolites, the energy that goes in, in what ratios, and what happens metabolically—what are the aftereffects chronically and acutely?
Alright, so let me see if I can get this. Oh, look at me! Okay, alright. Now, this is an older designation; I like this a lot. I use it because we go from type 1 to 2A to 2 AB to 2B. What happens is they are either glycolytic or oxidative, and they’re almost always—meaning they burn sugar and they burn fat—but they are almost always in some combination.
So, let’s just go with a kind of walking-jogging scenario. If I’m hanging around and I’m walking, I’m going to use these type 1 fibers. They are steady state; they don’t produce much in the way of lactate or any other thing. You could do this for about 8 hours—a normal person. It’s the least—it produces the least effect on the system; it’s not taxing.
However, if we want to walk a little bit faster or up an incline, we need to produce a little more force, a little more power. We will recruit upwardly to these next fibers. Okay? So the first ones are pretty much purely anaerobic. These fibers start to get into a little anaerobiosis; they get a little anaerobic, but they’re mostly still aerobic.
Okay, if these can’t handle load—if I want to start to run faster—these muscle fibers have to come into play. Understanding that these fibers would not recruit upwardly, okay, if they could handle the load. So the proof of them not being able to handle it is that these muscle fibers come in.
They’re a little more anaerobic as opposed to aerobic. It’s a subtle difference, but it makes a difference. Now, we start to work a little harder with fuel that’s, let’s say, more higher octane. When we get to the point where we have to work as hard as we can, these type 2B fibers come into play. They’re the highest glycolytic percentage, the lowest fat percentage, even though they’re still burning fat—understanding in this concept, please.
Okay, whenever these fibers are working, the fibers beneath them have to be working as hard as they can. If they weren’t, they wouldn’t recruit upwardly. Okay? So, they’re on. You still—what makes high-intensity exercise really metabolically so demanding is that we are trying to overcome inhibitions of glycolytic metabolism aerobically.
Okay, so that’s why it becomes so tough; there’s a lot of inhibition going up and down these things. Alright, so again, endurance—high endurance, of course—if we’re just walking, we have higher endurance. As we go faster, a little less endurance, and if we’re working as hard as we possibly can, you have low endurance. If I ask you to sprint, you’re not going a mile.
Okay, strength—these don’t need much strength; just kind of superficial force promotion. As we need more and more strength or speed or power, we go down the line. Okay, but remember these fibers are trying as hard as they can before they recruit this way. It’s called orderly recruitment; that happens in all humans.
And these muscle fibers and the metabolism the aerobic metabolism that they fuel by is still trying to work as we get into this anaerobic—purely anaerobic phase. Excuse me.
Okay, so the lipid energy model is magnified and clarified through exercise. Lipid energy, I don’t think, can be separated from carbohydrate energy. I mean, there’s a whole energy deal going on, and you’ll see that in this U transition through exercise.
Um, so the transitions—I’ve set up this next slide; I’m going to spend some time on. Um, how is the lipid energy model affected in this next slide? And I’ll show you what happens with progressive exercise. Okay, now, oh, this came out better than I thought!
Okay, um, if you see up here, we have different—I’ve categorized this into three phases of exercise: phase one, phase two, phase three. And you see this vertical line. Okay? That’s how we designate, and then we can refer from this—all these responses to exercise, we can refer right back to that muscle fiber recruitment page. These are all connected.
So here’s what happens when we exercise progressively. Okay? We’re starting at rest and we’re gradually increasing, increasing up to high intensity to what we call—maybe V2 Max—which is something else I could do a whole another talk on. But alright, so oxygen—if I do this, does that come up on that screen? No? Okay.
Alright, so we’re constantly utilizing, exchanging more oxygen as we increase intensity. When we get to this level, right about here, you have about 2 mmls of lactate. We start to build a little lactate, but we can still utilize more oxygen until we get to this very point, our V2 Max.
So you see there’s pretty much a linear progression of utilizing oxygen as the intensity gets higher. Okay? Uh, by the way, if we’re looking at here, we’re probably looking at type A, type 2, type 2A in here, type 2A, maybe type 2B, but up here, type 2B muscle fibers—high intensity. Okay? That’s where we’re going; this directly correlates to that graph that I showed you before.
Um, expired oxygen—okay, so when we’re hanging around, we’re breathing in more oxygen than we need. But as we start to demand a little more, then we’re expiring less oxygen because we’re using more of it, and at some point, we’re expiring more as we get into this beginning of anobiolosys.
Okay? We’re expiring a little more because we can’t use it; it’s just too much for us to handle. We can’t translate it into muscle action. With regard to CO2, there’s a constant increase in CO2—a little bit of what we call breakaway here—and it keeps going straight up. So we’re retaining more and more CO2, which means we’re in an acidosis state.
As far as expiring CO2, we expire a lot, a lot more—more and more—because we’re breathing more, and when we get to this second anaerobic threshold, I think that’s Waserman and 78 that described that.
Um, when we get to that threshold, we can’t even expire it anymore, and now it builds up. This lactic acid gets to be insurmountable. This is respiratory rate, okay? Point 7 to 1.0 means pure sugar, pure fat.
Okay? Um, and as we get more and more intense and use more and more of the anaerobic fibers, this respiratory quotient goes way up. Okay? Almost exclusively burning glucose—glycogen.
Heart rate, okay? So the heart is trying to stay up with the demand that the muscles are making. Understand exercise has local and global effects and responses. So globally, your lungs and your cardiovascular system are trying to deliver more and more and more energy—oxygen.
Okay, and they keep going up even though at some point we can’t extract any more oxygen at the sight of the working muscles. So this keeps going up, up, up until this is where we reach failure; we just can’t extract anymore. For any more oxygen.
Okay, this is ventilation. This is the breathing rate of breathing. Okay? You’ll see at the start of this phase two, when we get a little bit of the anaerobic aerobic fibers starting to contract to work, there’s a little bit of what we call a breakaway.
This is described by McDougall as the anaerobic threshold—meaning it’s the beginning of anaerobiosis—which gets confusing because Waserman says that the anaerobic threshold is this breakaway.
But in any case, this is where it starts. You’re about four mmls here and about eight here, and then it goes through depending on your conditioning—how much lactate you can use—and this is lactate. Okay? So in the beginning, there’s a little bit of lactate built up, but it’s buffered by bicarbonate.
It’s not; you can do it. Mitochondria have no problem with that stuff. Then we get a little bit of a breakaway here on lactate when—again—the anaerobic fibers, the type 2 AB, the type 2B fibers come into play. Then, when we get into real anaerobic, then this lactate just goes through the roof, and at some point, we can’t convert it to pyruvate—we’re screwed.
Okay, it’s over! Now, I know that’s a lot, but my point basically for this whole thing is: look at all the things that are going on with energy-gas exchange, metabolites, enzymatically—it’s a lot of stuff going on that we can measure progressively through the application of exercise.
Okay, so lipid energy models can be magnified, clarified if we adopt some exercise input.
Um, did I go backwards here? Yeah, I think I did. Alright, hang on; I’m not that right apparently.
Okay, there’s that muscle fiber chart again, in case you forgot it.
Okay, so the three phases of—what I call—the Holy Trinity of metabolism and exercise metabolism. I’ve showed you the chart of what happens.
So in phase one, again, there’s a lower fraction of oxygen expired, more CO2 produced and expired, V2 is up, lactate increases a little bit. Right now, we are producing a little bit of lactate, but very little, and the respiratory quotient is low—like around in the sevens for a normal healthy person.
Mitochondria, type one fibers, maybe type 2A can handle this kind of work all day. Alright, this is not a problem—that’s that phase one.
Uh, Jesus, yeah, oh I see—so up means up and down means down. Alright, alright. Phase two, this transition phase, I think is pretty important. Um, as lactate seems to increase above 2 mmls, it can be buffered by bicarbonate.
I told you a lot of this stuff. The reason I’m stretching this out a little is because I thought I had 15 minutes to talk and Dave was going to take four to introduce me. By the way, Dave, thank you for that; the check is in the mail. Forget this compensation crap!
Alright, um, so this phase two is that described by Waserman as the anaerobic threshold, when the anaerobic stuff starts to happen.
Um, as the crossovers, mitochondria need some help now to start to continue to produce ATP from the cytosol. Phase three—anaerobic—intensifying; the type 2A, type 2B fibers are recruited 70 to 100% Max V2, and heart rate continue to rise until performance failure.
Lactate begins at four mmls and increases throughout until V2 Max. Ventilation—VCO2—so breathing rate—carbon dioxide—in the blood still rises up to try to compensate for the rise in lactate. Expired CO2 decreases and expired oxygen rises—which means we can no longer get rid of the CO2.
Okay? Which is now going to be blocking our further use of fuel, and we’re expiring more oxygen because we can’t use it. We can’t use it anymore; we have to get rid of it.
Okay, this is purely high intensity. I would call this 200% more than V2 Max. Okay, what’s interesting, when we start to get these measurements at this demand, this is the kind of work that Dave does and that I do: 15 minutes, twice a week.
Okay? When you get to this level of demand and muscle fiber recruitment, the respiratory quotient approaches 1.0, so it’s almost purely glycolytic—even though those lower fibers are trying to deliver energy oxidatively.
Okay, but what’s interesting and most non-exercise physiologists—and most of them don’t know—is that at this level, about 30% of the oxygen extracted is used by the ventilatory muscle.
So, we’re breathing so hard that we can’t deliver oxygen anymore to the working muscles because the ventilatory muscles are working so hard and they need oxygen.
So that’s why some of these measurements get screwed up. The mitochondria and cytosol can no longer deliver energy at the required rate; they can’t make it.
Okay? Therefore, mechanical failure, and that’s McDougall’s anaerobic threshold in ’79. By the way, these guys that I refer to, McDougall and Waserman—I know these guys; I did work with them—that’s when this stuff happened.
So, the role of the lipid energy model, um, I think it affects demand obviously, but I also think it affects supply based on the conditioning that exercise could provide—importantly in lipid, especially in lipid metabolism.
Exercise communicates and drives ATP sites; okay? So myocytes through vesicles deliver messages about utilization of fat—breakdown into fatty acids, things like that.
This I think is really important; I’ve had this discussion with Dave a few times. Exercise drives LPL—lipoprotein lipase—and hormone-sensitive lipases responses and levels.
So, what does that mean? These are just enzymatic influences that either tell muscle cells really to store fat or to utilize and burn fat, and that’s very important as we try to condition our people to be better fat burners.
These numbers should change; we should become—and high-intensity exercise does this in spades! Okay? It induces hormone-sensitive lipase upregulation—which means a higher rate of fat burning.
So if someone says to you, “You know, you can’t outrun a bad diet,” okay? That’s beautiful; the sky is blue. What else, you know? You’re telling me.
But if I can increase this—which I can—okay? If I can communicate from muscle cells to adipocytes to release fatty acids—which I can through exercise—okay? Then I think we got something.
Exercise bypasses and reduces the insulin elevation for glucose translocation. So, what happens? We have glucose in the blood; we want to store it healthfully in the muscles and the liver.
Why can’t we? Maybe we’re a little bit insulin-resistant. Exercise can bypass some of those translocation—I would call them toll booths—before we can get and produce a store—glucose into glycogen through AMPK.
Again, I don’t hope I’m not too much deep in the weeds, but that’s what happens. And we know that exercise can bypass, even in type ones, can bypass the need for exogenous insulin.
Um, exercise reduces—oh, what was that? Welcome!
Okay, let’s try this again; I almost made [Laughter] it! Okay, so here are some thoughts and questions that I have. I’ll leave you with: how is this LPL HSL regulation affected? Supply, demand, or both? I think it’s both.
Okay? And exercise, again, can magnify the significance of that differentiation in the enzyme mure.
How can mitochondria be trained to compensate and respond to increased demand and metabolic health? I firmly believe that we can train mitochondria just like we train muscle fibers. In fact, if we look at the responses to those different levels of exercise that I showed you on the muscle fiber chart, we can see that the mitochondrial morphology—the way mitochondria line up in the cell—is different for type 2B muscle fibers, and between the type one and 2A, there’s a different geography.
They actually stack up more deeply in one—they’re separated in another. So, I think we can actually train mitochondria to do what we want.
I think we can train mitochondria to be more aerobically efficient; the best way to do that is to have them recover from anabolic failure.
So, we can train—the best way to train aerobically is to produce anaerobic failure. During that recovery, we will get—we will approach 70% purely fat burning during the recovery from anaerobic.
So, if anybody says again, “Exercise has nothing to do with losing fat,” they’re silly. That’s the nicest word I can think of.
Okay? That’s how fat oxidation can be influenced by exercise. I already went over that—vesicles from myocytes to adipocytes.
How does this translate into resting and active RQ? RQ, respiratory quotient.
I think that most—since most of us are in the business of reducing fat, losing weight, fat—um, becoming more ketogenic fat—I think that RQ, God! Why do I do this? What is going? Okay, I’m sorry.
I think that RQ, respiratory quotient, is the ratio of oxygen—I’m sorry—the ratio of fat to carbohydrate that we burn.
If we’re low—let’s say you have a patient that’s insulin-resistant, and their resting RQ might be 0.95, let’s use the number. If we can get that resting RQ down to 0.85, we have drastically increased the probability of them utilizing fat—oxidizing fat—and not being resistant.
And that’s important; I think all of us are trying to do that. I don’t know why we don’t use—I don’t know why we don’t use RQ.
And when we promote this RQ change—respiratory quotient change—through exercise chronically, then what happens is the adaptation happens in a homeostatic way. We’ve made an improvement in that person’s fat metabolism.
So lastly, one thought I have here is: um, how can we not appreciate the role of the muscle system in affecting the related health status involving the lipid energy model?
I think we have to take it into account. I hope I’ve provided some evidence—hopefully not too much in the weeds—but there’s a lot of good stuff that happens when you do exercise.
The most good stuff happens when you do high-intensity exercise—not to be feared! Everybody can do high-intensity exercise; it’s just something that you’re not used to.
So, my rehab patient, my 400 lb first-time moving off the couch person, and my world-class athlete all have the relative challenge of doing something a little more intense than they’re used to, and they would upwardly adapt.
And that’s what we’re all about. Thank you!
Oh, one other thing: since we’re in Sin City, I have to tell you a quick joke. Um, this guy goes into a bar; he has this big suitcase on top of the bar. The bartender says, “What’s that?”
He said, “That’s, uh, something I want.” He said, “What do you mean ‘you won’?” He takes out this piano and a little one-foot-tall guy in a tuxedo plays the piano beautifully. The guy goes, “Wow, where the hell did you get that?”
He says, “Well, look in the suitcase; there’s a genie in a bottle.” “Yeah, yeah.”
He says, “Yeah, give anything you want—one wish; she’ll grant it.” So the bartender says, “Alright, give me—” he says, “I wish for 100 bucks!” Next thing you know, ducks—little tiny ducks—all over the freaking place; ceiling, the parking lot, the roof.
So the guy says, “See, the genie is pretty good.” He says, “Yeah,” he says, “but I didn’t ask him for a million ducks; I asked him for a million bucks!”
The guy says, “Yeah, that’s the only problem; that genie doesn’t hear that well.” He says, “You think I asked him for a twelve-inch pianist?”
[Applause]