 So 12 weeks of high-intensity strength training increases VO2 max by an average of 1.9 milliliters per kilogram per minute. You see why it's a bit of monopoly money. You can move your weight up and down. In my case, this would be about a 5% increase. My VO2 max is 47 without doing any cardio. In order to be at the elite level according to the list that they put out there, you have to be at 50. So that's not bad training 13 minutes once a week. And they did it in 72-year-old men. And again, I talked about the compromise with aging in the heart earlier. Biopsies showed a 15% increase in capillary density and 38% increase in centrate synthase activity. Capillary density is typically only seen increases in this. It's the amount of arterials feeding the muscle tissue directly, supplying the blood into them. Normally what happens when you strength train is that your muscles get bigger and you see a reduction in that capillary density because the volume of those capillaries has stayed the same. You still get just as much blood into the muscle tissue. Of course, this doesn't matter, as I told you earlier, because you're more efficient. So you don't need more capillaries if you can move more blood through them. The other thing here is that centrate synthase, I want you all to go back to high school biology, chemistry, physiology, it shows up in all of these, is the rate limiting step in the Krebs cycle, citric acid cycle. So acetyl-CoA is a substrate that glucose, glycogen, fat, and protein can all move into and become in the body that passes into the cell and the first thing it has to be acted upon is citrate synthase before it becomes citrate and starts moving around and throwing off ATP like mad. If you can increase this rate limiting step by 38%, you can deal with more substrate coming down. You are a more aerobic animal without doing any aerobics because we're just a bag of chemical reactions. So if you can get these rate limiting steps bumped up, you can run with your friends, sprint past them, and keep going without ever doing any cardio. I think you would have something better to do than go jogging with your friends, of course. So in expansive review of depth and breadth of adaptations has been published by 21 Conventionalumni James Steele, Deuce, there's actually a James Steele a third if you accidentally type in three I's. And Doug McGuff, magical deity, I mean medical doctor. Sold out from, actually Doug's got a great story. He's been writing articles and things for years and years and years and he had this one talking about sort of bringing doctors back down to earth and he said two things. He said, MD does not mean magical deity and you might think being a doctor is a great job and it's hugely rewarding in a number of ways. But how many of you have to stick your finger in a sphincter on a daily basis? That's why they pay him the big bucks. I'm sure you could privatize that too. I'm sure there's gotta be a way to privatize a sphincter poke. Gene expression defined, hey, here we are. It's the conversion of information into messenger RNA from the gene and then it becomes the phenotypic manifestation of the gene. Genes are knobs and switches that are influenced by the way you live. They are not genetic destiny except for talk sounding exactly like your father years later. If I simplify that, it's the building blocks that make you, you in via environmental influences and again, this is called your phenotype. Your genes are gonna determine how tall you are, the max amount of muscle tissue you can have, the max amount of VO2 max, but that's a giant range in which you can operate under and make improvements in. So yeah, I mean, you know, Gattica, lots of G's, A's, T's and C's and that's your gene being expressed through messenger RNA in result to input from the outside world. So you've got all of these genes associated with aging corresponding with mitochondria dysfunctions, the powerhouse of the cell. If you run out of power, if you can't metabolically continue to support that cell, it's gonna die. There are some immoral cells, but this in a general sense is what we're talking about with mitochondria dysfunction. Muscle atrophy and dysfunction they associate together and they might be causally related. That's science you speak. They are causally related, but in studies you have to say might be causally related. Gene expression is blunted or eliminated with inactivity, the youthful gene expression, even in the early stages of a resistance training intervention. When you walk in, if you've never trained before, whether you're 20 or you're 70, you cannot access your biggest strongest motor units. Your central nervous system does not know how to make these muscles contract to its maximum voluntarily. And that actually might be what makes Olympians better than the laypersons is that they can do that better than anyone else. They can use the breadth of their muscle tissue from day one, but if you use this as an intervention late in life, initially you can't get to those fast-switch fibers and even then as I explained earlier, some of them have turned irreversibly to connective tissue. So in this particular study, they showed that strength training in the elderly reversed oxidative stress and returned gene expression in 179 genes to a youthful level. Moved them back about 10 years. Let me repeat that. The genes got 10 years younger. That's impressive. Here's how it looks. These black lines where all the genes express either down-regulated or up-regulated in these elderly populations, and after training they move closer to that line. That's flat. If I make that three-dimensional, give you an X and a Y axis, or not three-dimensional, an X and a Y axis, you see this black line here is a youthful gene expression and these twin peaks are the genes moving back to center. So at the start of the study, these peaks would have been out here. They would have been way off on the ends and they shifted in. That's pretty staggering stuff. You just anti-aged. You just reversed aging by 10 years. And it wasn't a clarylchronite cream for the crow's eyes either, promising that stuff. Telomeres, telomeres, telomeres, telomeres. They are regions at the end of your chromosomes that protect the gene. Because through replication, the gene is exposed to damage and they help to reduce that. And if they divided without the telomeres, they would lose the ends of the chromosomes and the information they contain. So these caps, these little tiny helmets are there. And that's what they protect the gene to continue to either not recreate out of control cancer or become so short that you're eroding genetic information. But aging does that. Telomeres are your protection, they're your shield, you want that strong. So regular physical activity, we were sought to reduce telomere length, which is actually true in endurance athletes. So endurance activities are gonna kill ya. If you still wanna do them, good luck to you, but don't sell them as a healthcare intervention. Things are different with regards to strength training. Not entirely, but I'll get to that. In this particular study, power lifters had a longer mean and minimum telomere compared to sedentary men, except for the strongest in the squat and the deadlift. The guys who were the strongest had the smallest telomeres even though they were better than the sedentary population. And so talking about this, when you train you're recruiting satellite cells for regenerative events. That shows improvements in the telomeres. But if you can't, don't give those satellite cells enough time to fully recover the tissues that you've acted upon, you are short-circuiting this process. And based on this data, what I think is happening is that these guys who are really, really, really, really strong are the hyper responders. And so they, on a muscle plasticity level, get stronger, stronger, stronger living in the gym. But at a genetic level, they're actually short-circuiting the way in which their cells grow and change. Can't prove it, but these two seem to suggest that. And so in this case, stress is also involved. The active individuals with the lowest amount of stress have the longest telomeres. Strength training is a stressor. Too much of it is going to shorten the telomeres. And these guys like training. They really like training. That's going to reduce the length of their telomere because they're living in the gym. So here's some hormones and some protein. I'm sorry, some proteins are involved in this. M-tor is typically antagonistic of AMPK. You see increases AMPK in endurance cardiorespiratory training. M-tor goes up with strength training. And they regulate cellular aging genes. And so in order to restore the length of the telomere, you need telomerase that keeps that going. So if you alter AMPK levels, you improve the telomerase output which increases the repair of the telomere. You don't get that being sedentary. That actually drops off fairly substantially. So there's no doubt, there's a link. Now we're on to the biological immortality. This is Michael Rose. This is not Ira Glass of... He's an evolutionary biologist. The university, UCAL Irvine. Strangely enough, he and Art Devaney, both. If you're familiar with who Art Devaney is, they're both there, they never interacted. That's problematic, humanities. We'll never see the social sciences. We'll never see the natural sciences, liberal arts. They all stay away from one another, unfortunately. First, what biological immortality is not, it's not Greek-like immortality, or to put it another way, one does not simply stop aging. If we define biological, or sort of biological mortality, it's a change in the structure and functions of humans with the passage of time that does not result from disease or gross accidents. Read that, everyone good? So if right...