How Much Lifting is Enough? How Much is Too Much?

0:00In 1989, researchers at the University of Florida took 117 sedentary adults in their 20s and had them lift weights for 10 or 18 weeks. Some trained two days a week, some trained three, and some didn't train at all. The entire workout was one set of leg extensions for 7 or 10 reps, taken to failure, and then went home. At the end of the study, they didn't test a squat or a deadlift. They tested how hard the subjects could push against the leg extension machine when the pad was locked into position and wouldn't move. After 18 weeks, the three day group had gotten 28% stronger. The two day group got 21% stronger. Would you believe me if I told you that this is the study the lift weights twice a week recommendation came from? Because it is. It showed up for the first time the following year in the American College of Sports Medicine's position stand, the first one that ever included resistance training. The authors gave their reasoning in two short sentences. The first, quote, programs lasting more than 60 minutes per session are associated with

1:00higher dropout rates. And the second, quote, although greater frequencies of training and additional sets or combinations of sets and repetitions elicit larger strength gains, the magnitude of difference is usually small. They knew more was better and they recommended less anyway because they felt people would quit when the workout takes too long. That doesn't make much sense to me because if you look at the same amount of training and split it up into more sessions, each workout would be shorter. After all, exercise frequency, which is how many days per week you exercise, is mostly just a tool to distribute the training in a way that fits your schedule. And in this particular study, where they only did one set per workout, which the study says lasted 40 to 60 seconds, well, I don't know about you, but doing an extra minute or so of work to get 30% more strength seems like a good trade off. So I went and looked at what that study cites for the recommendation it says it's supporting. Reference one is a personal communication from ML Pollock chairman of the ACSM revision committee dated November 1988.

2:01Well, ML Pollock is the third author of the very study we're talking about. Did you catch that? I'll slow it down. 1998, a committee has a draft recommendation of two days a week sitting in it. 1989, a paper comes out with that committee's chairman as an author and the thing it cites as support for two days a week is a letter from the chairman 1990, the finished position stand cites the paper. The recommendation is its own evidence and the study attached to it found that three days beat two days. Later in the 1990 guidelines, it says that health and fitness are two different questions and that this document is answering the fitness one. The health one came out five years later and it didn't discuss lifting at all. 18 years later in 2008, the federal government took the two days per week number out of a fitness prescription and printed it as the health recommendation, but nobody ever did the health version of the work for lifting weights. When it comes to exercises connection to health, there are really two questions here. One, how much training does it take to change you and your body?

3:02Two, how much do those changes improve your health? Those are two different questions that may produce two different answers so we need to keep them separate. Last week we went through 150 years of people telling you not to lift. All of it built on vibes and most of it was proven wrong when it was actually studied. This is the same problem in reverse, where the study identified the correct answer, but the recommendation ignored it and was based on vibes anyway. And it's led to an interesting belief about the risk of lifting weights. The warning used to be that lifting weights is dangerous period. Now the warning is that lifting is dangerous if you do too much of it. Today we'll find out where that one came from, whether there's anything behind it and then try to answer the actual question. How much lifting should you do? I'm Dr. Jordan Feigenbaum and this is the Barbell Medicine podcast. I'll give you my full answer at the end with the obligatory snark, but here's the short

4:05version so you can see where I'm going. I think that most people should be doing roughly double what the guidelines say because I think that many of the health benefits from exercise keep going and I don't think anybody has found the top for all of them. Before you can even ask how much lifting is enough, you have to decide what counts as lifting and this turns out to be a pretty complicated undertaking. In 2022, researchers went to the Active Life Survey, which is the Sport England Survey of what people actually do with their free time. They pulled answers from over 250,000 adults aged 1965 regarding how many of them were meeting the Strength Training Guideline. They counted the same people in three different ways based on different definitions of what counts as muscle strengthening activity. Using the broadest definition, the one that's been used in National Health surveys for years, which counts anything you said put your muscles under tension in a challenging manner, well 28% of men and 25% of women met the guideline. That's how football and tennis became Strength Training. Using a stricter definition where they only counted activities with some evidence of a

5:07health benefit, it dropped to 16% and men and 9% of women. This definition counts running as resistance training. Yeah, not good. And using the definition written into the actual UK guidelines, the one that describes what the guideline authors meant, which is different forms of lifting weights and, yeah, yoga, it came out to 5.6% of adults meeting the guideline. Just in case you missed it, it's the same 250,000 people taking the same survey with three different definitions of what counts as lifting. 28% of men meet the guideline, or 16%, or 5.5%, which includes yoga. A five-fold spread and the only thing it changed was a definition. Every number you're about to hear about lifting and health comes from a number like that one. The surveys themselves are in no better shape. A review went through 156 papers and found 58 different survey systems across 17 countries, all trying to measure the same behavior. How are people exercising? About 85% of them recorded how often you lift, about a quarter recorded how long you

6:09lift, and only 1.3% recorded how hard it was. Even one of the best studies on lifting and health has this problem. There's a 2026 paper, which followed about 147,000 people for up to 30 years to see how exercise influenced their health. It asked them how many hours a week they lifted. It didn't ask them how heavy they were lifting, or how many sets they did, or how many reps they did, or even what type of exercises they were actually doing. Two hours of yoga per week is a lot different than two hours of barbell training. It's going to be hard to conclude what lifting actually does from your health from that study. That's troubling, but I guess that most people aren't lying awake at night worrying about survey methodology. Instead, what they're actually interested in is how much they should be lifting, and whether or not lifting is going to hurt them. The organ that most people worry about hurting first is the heart. The heart, as you probably know, has four interconnected chambers. On top are the right and left atria, and on the bottom are the right and left ventricles.

7:11The left ventricle is the chamber that pumps oxygenated blood out to the body. It fills during relaxation of the heart, which we call diastole, and it ejects during contraction, which we call systole. Now, plenty of things can go wrong with the heart. You can get inflammation of the muscle. You can get abnormal protein deposited where it doesn't belong. You can get a blocked artery that starves part of the heart itself. You can get an electrical problem, and so on. But none of that is what we're talking about today. What we're talking about is the load. Specifically, how much blood the left ventricle has to move and how hard it has to push to move it. And there are two ways that that load can go up. The first is called volume overload. More blood is coming into the left ventricle, so more blood has to leave it. The ventricle responds by getting bigger, with the chamber dilating to hold more blood and the wall thickening because the muscle it contains has to be bigger to pump the blood out. Because these adaptations were thought to be driven by processes occurring during the relaxation phase, where the muscle fibers of the heart lengthened to accommodate being filled with

8:13blood, this was dubbed eccentric hypertrophy. The second is pressure overload. The chamber isn't handling more blood per se, but it is pushing against higher resistance on the way out. We call that resistance after load. Here, the ventricle thickens the muscle in its wall without an increase in the size of the chamber for the same reason your quads get bigger when you squat heavy. Because this was thought to occur while the heart was actively contracting, shortening against a high pressure circuit, it was called concentric hypertrophy. To recap, eccentric hypertrophy, presumed to be from endurance training, leads to a bigger chamber and a thicker wall, from volume. Concentric hypertrophy, presumed to be from resistance training, produces a thicker wall and the same chamber size, from pressure. Now you might be wondering why we care so much about how the heart changes with exercise. Well, an aortic valve that leaks sends blood back into the chamber that was supposed to leave, so the chamber enlarges. High blood pressure means more force is required on every single heartbeat, so the wall thickens.

9:17Aortic stenosis, where the valve the blood exits through gets narrow and stiff, does the same thing for the same reason. And hypertrophic cardiomyopathy, which is mostly a genetic thing, also shows up as a thick wall of the heart. When the muscle mass of the left ventricle goes up, however it got there, we call that left ventricular hypertrophy, or LVH, which tends to travel with bad outcomes and is why doctors pay attention to it. So you've probably already put this together when I was talking about moving blood around the body, but just so we're on the same page, exercise can change the heart too. Now imagine you're a doctor looking at an ultrasound of the heart and you see a thick end left ventricle. Without knowing anything else about the patient, how can you tell if it's disease or if it's exercise related? And what happens if the picture from the ultrasound wasn't very good to begin with? That could be a big problem. The idea that lifting weights makes your heart wall thicker come from a study published in the 1970s. The swimmers took echocardiograms, which are ultrasounds, of 56 athletes split across

10:20four different sports. The swimmers and the runners representing the endurance side had big roomy ventricles with normal wall thickness. The other group representing the resistance training side had normal size chambers, but thicker walls, around 13 to 14 millimeters thick. And who was in that group you ask? Wrestlers and shot putters. The swimmers and runners, they wrote, showed changes similar to those in chronic volume overload. The wrestlers and shot putters showed changes, quote, similar to those in chronic pressure loads. Both groups got explained by comparing them to a disease. For the lifters, the diseases they got compared to were the hypertension and the oort extinosis bucket despite not a single weightlifter bodybuilder or powerlifter in the study or anyone's blood pressure being recorded. And from that, we've got what's been called the Morgan Roth hypothesis, which is still in textbooks telling soon to be doctors that endurance training makes your heart bigger and strength training makes your heart walls thicker. Now, what could they actually measure in 1975 with the available technology?

11:22Turns out not that much. Echo Cardiogram was fairly new. It started out in the early 1950s, but again, this is ultrasound. So it uses sound that bounces off tissues and when it comes back, it can give you a handful of distances. How wild the chamber is, how thick the septum is, how thick the back wall of the heart is. The paper reported left ventricular mass in grams, which is calculated from taking those few distance measurements and feeding them into a formula that assumes the ventricle is a particular shape. If you change the assumption or the distance measured by a millimeter or move the probe slightly, the mass can change a lot, which is important because the thing that they were measuring was 13 or 14 millimeters against 12, a one or two millimeter difference. In 1975, on an ultrasound, in 56 people. 16 years later, in 1991, a research group used ultrasound again to measure the hearts of almost 1000 elite athletes across a lot of different sports. What they wanted to do was establish the upper limit of how thick a heart wall can get from

12:23training alone. That matters because a thick wall can also mean hypertrophic cardiomyopathy, which is a real disease that does kill young athletes, unfortunately. The thickest wall in the entire group was 16 millimeters. Walls of 13 millimeters or more turned up in 16 athletes out of nearly 1000 and 15 of those 16 were rowers or canoeists, the 16th was a cyclist. Across the other 22 sports, not one athlete had a wall that thick. Two years after that, the same group went looking specifically at strength athletes. They took 100 weightlifters, powerlifters, wrestlers, bobsledders, and throwers, and these people had been training for an average of seven years, though some of them for over two decades. Nobody exceeded 12 millimeters. The range was 8 to 12 millimeters, and their walls were slightly thicker than match controls who didn't exercise by about half a millimeter on average, and their chamber size was identical. The conclusion of that paper is that if you're looking at a strength athlete with a wall thickness over 13 millimeters, you should start thinking about disease because training doesn't typically

13:26do that. Now so far, all of the studies have been cross-sectional in nature, where researchers looked at the hearts of athletes who had already been training. No one had really investigated what happened when people started exercising. In 2011, a group of researchers finally did that, and they used a better machine to measure the heart too. In this study, researchers took untrained young adults and assigned them to six months of supervised endurance training, or six months of supervised resistance training. Nobody got a cardiac MRI before, after, and again, after six weeks of doing nothing, of detraining, to see how the heart changed during that time period. Heart mass went up in the endurance group. Wall thickness went up in the endurance group, but neither measurement changed in the lifters. And to show you how important the machine is when it comes to measuring the heart's dimensions, let's look at a 2013 review where researchers grouped together imaging studies of the heart in athletes. They sorted the studies into endurance athletes and resistance trained athletes, and compared every measurement of the left ventricle between them.

14:28Both groups had bigger hearts than people who didn't exercise, but of all of those measurements, the only two that separated the groups were chamber diameter and chamber volume, and both were bigger in endurance athletes. But wall thickness didn't separate them at all, which is the measurement the Morgan Roth hypothesis claims should. Lifters were supposed to be the thick walled group, and across the literature, they weren't any thicker than the endurance athletes. OK, it's scoreboard time. What we have here is a 1975 study of 56 people on early ultrasound, where the entire finding was a one or two millimeter difference that produced a hypothesis that is still in textbooks today. A thousand elite athletes later, the thickest walls in a sport belong to endurance athletes. A hundred strength athletes, some of them training for more than 20 years, topped out at 12 millimeters, which is normal. Six months of supervised lifting with an MRI before and after didn't really change anything, and when somebody combined the imaging literature, the one measurement the hypothesis is named for didn't separate the groups at all.

15:28That is where the lifting makes your heart walls thick, and that is bad, currently stands debunked. OK, so resistance training doesn't make the left ventricle get any thicker compared to endurance training. But if you've spent any time around the gym, you're probably thinking about the hearts of a different group of people right now. People who use anabolic steroids, a Dutch study called the Harlem study recruited men who are about to start a steroid cycle, 31 men with an average age of 33 who are taken around 900 milligrams of testosterone a week for about four months. For reference, a man's body makes something like 50 milligrams of testosterone per week on its own. The researchers scanned each man's heart three times, once before they started the cycle, once in the last week of the cycle, and once about a year after the first scan. During the cycle, while they were taking high doses of testosterone and other agents, the heart mass went up by 28 grams. The septum and the back wall both thickened, ejection fraction, which is the percentage of blood the left ventricle pushes out with each beat dropped by about five points.

16:33Blood pressure also went up about six millimeters of mercury over five, and the higher the weekly dose the man took, the thicker his walls got. By that third scan, roughly eight months after the last dose, almost everything had gone back to baseline. Heart mass, wall thickness, ejection fraction, blood pressure, all back to normal. And these guys were in the gym about seven and a half hours a week the entire time. The researchers put training time into the model specifically to see whether lifting explained any of the heart changes, and it didn't. The heart changes reversed while they kept training just as hard. But that's just one steroid cycle. What about people who have been doing it for decades? The Norwegian group looked at that. They took 101 weightlifters who would use steroids for an average of 11 years and compare them to 71 weightlifters who hadn't. What they measured is the same thing that we've been talking about, the mass of the left ventricle, adjusted for body size so that being a bigger guy doesn't artificially inflate it. In the steroid users, it averaged 106. In the controls, it averaged 80.

17:33So there was about 30% more muscle in the wall of the left ventricle. In an athlete, that's where the story ends well. More muscle and the thing pumps fine. But that isn't what happened here. Adjection fraction, which is the percentage of blood that the left ventricle pushes out with each beat, averaged 49% in the users against 59% in the controls. In below 50, is where cardiologists often start using the word dysfunction. About 1 in 9 users had an ejection fraction of 40 or less, which is very concerning. The right ventricle was often impaired too. So they had more heart muscle, but it worked worse. And that is the entire difference between a heart that's adapted to exercise and a heart that's sick. The dose data makes the same point. The dysfunction is the problem driven by anabolic, not necessarily just an increase in the thickness of the heart. Among current users, the more steroids a man had taken over his lifetime, the worse his ejection fraction was, but the lifetime dose didn't track with how much the wall had thickened.

18:34Former users who had quit an average of 6 years earlier looked like current users. Even in 10 of them also had an ejection fraction of 40 or below, and it hadn't yet come back. Then the researchers ran a regression to ask what predicted the reduced ejection fraction. The answer was the history of steroid use. So that's the heart. Every time somebody went looking for a risk from lifting weights, they found a measurement problem or they found drugs. Lifting weights, even if you do it a lot, does not seem to hurt the heart at all. Okay, so that should satisfy the moms and the doctors listening. But I bet that when most people say that they're worried about lifting too much, they aren't talking about their heart. They mean they're back. So let's talk about getting hurt. On average, all forms of resistance training have an injury rate of somewhere between two and four injuries per thousand participation hours in training. For context, that's similar to other non-context ports, and is just a little higher than walking in cycling, which are both between one and two. It's also much lower than any context port, and it's lower than running, which is around

19:36eight to ten injuries per thousand hours for experienced runners and over 15 injuries per thousand hours for those who are new to it. So lifting weights is pretty safe, but I'm sure there will be someone in the comments of your next lifting video saying that you're going to blow your back out if you keep going. Except the overwhelming majority of resistance training injuries are chronic overuse problems, and not the acute structural failures that your disc will explode narrative describes. The strongest evidence for this is how quickly these things resolve. The average symptom duration for a lifting-related training injury is just under two weeks. If these were the catastrophic structural failures that people are really afraid of, like blown discs and torn ligaments, people would be out for six to twelve months and potentially headed for surgery. Instead, they're usually back in the gym within ten days without ever seeing a doctor, which is what happens when people do too much, too soon, and are forced to back off. It's not what we see with a traumatic injury. Good programming and progressive loading, along with a little luck, would help avoid that

20:36happening in the first place. Now, let's say you were to come across a viral meme circulating the internet, say, of the second most handsome doctor in North America who was dead lifting, where his eyes appear to be bulging out of his skull. You might buy into the most dramatic version of worrying about lifting, which is dropping dead in the gym. There's a study out of Seattle and King County that looked at every sudden cardiac arrest in a public indoor location over twelve years. Out of 849, 52 happened at a gym. When they worked out the rate per site, indoor tennis facilities, ice arenas, and bowling alleys all came out higher than gyms. You may be interested to know that the authors didn't comment on how many bowlers had proptosis while trying to pick up a spare. In any case, if you're going to have a heart attack indoors, the gym is one of the best places to be. In this study, survival to hospital discharge was 56% at gyms against 34% everywhere else indoors, because people at the gym usually notice, and there are generally more people there who know CPR.

21:36There's also usually a AED on the wall. Interestingly, in the 2023 American Heart Association position stand on resistance training, they cited a review of 23 trials of people with coronary heart disease. There were 63 non-fatal cardiovascular complications during the recorded exercise sessions, and all 63 happened during aerobic training. Resistance training? Only one. By now, it should be clear that lifting weights is safe, but a somewhat new objection has turned up, with some recent scientific papers suggesting that doing some lifting, yeah, that's beneficial for health, but if you go beyond that, it stops being healthy. In 2022, a group of researchers in Japan set out to answer a question that their own government was arguing about. Japan was revising its physical activity guidelines, and there was an active debate over whether lifting should be in them at all. So they went to the literature to find out what lifting does to your risk of dying and your risk of getting sick. They searched two databases from the beginning of when they recorded all the way through June of 2021, and they kept only prospective cohort studies, meaning studies that measured

22:40what people did first, and then followed them afterwards for years to see who died. 16 studies made the cut. The main finding is good news. Across seven of those studies, which included 263,000 people and 42,000 deaths, people who did any lifting at all had about 15% lower all cause mortality than people who did none, and that even held when adjusting for their cardiovascular fitness. They found the same relationship for heart disease, cancer, type 2 diabetes, and so on. Things were even better when people did both cardio and lifting, as we see time and time again. Then they asked a second question, how much lifting do you need, and is there a point where more of it stops helping? So they built a graph, which is sitting in figure 4 of their paper. Across the bottom is minutes of lifting per week, and on the vertical y-axis, the risk of dying. Each of the six studies hands you a handful of points. The surveys in those studies gave people ranges to pick from rather than asking for a number, something like none, under an hour week, one to two hours per week, or two hours or more.

23:41Now that you have your points, you've got to fit a line through them, and they use what's known as a spline curve, which is a line that's allowed to bend. The first bend in the graph is the change in mortality from baseline, which got to its lowest point, where there's a 17% reduction in mortality at 40 minutes per week. Then the line starts curving up, crossing zero, which is where lifting with theoretically not provide any mortality benefit at 140 minutes of lifting per week. Above that, lifting would appear to actually hurt you. And if you go into those six studies one by one, the people who reported doing the most lifting did come out with a higher risk of dying than the people who didn't lift at all. But every one of those estimates has a huge range around it, which includes no effect. For example, in the study where people who lifted the most, the risk was somewhere between 41% less likely to die and 80% more likely to die. The biggest study in the set, with about 18,000 deaths in it, put the lifters at 1% more likely to die, with a range running from 7% less to 9% more.

24:44The authors wrote in their own conclusion that the benefit of a higher volume of lifting is unclear. So to me, a reasonable read of this paper is that lifting is associated with living longer and with less heart disease, less cancer, less diabetes, and so on. And most of that shows up in the first half hour to one hour a week, passed about two hours a week, and all these researchers couldn't find any more benefit. So what happened next? Well no one ran a headline that lifting was going to kill you, but the journal's own press release said that there was no conclusive evidence that more than one hour a week of lifting reduces health risks any further. Except that same press release called it a J-shaped curve, where the curved part of the J refers to the risk being lower, and the straight part where the J goes upwards signifies increased risk. The following year, a group of cardiologists published a review in Missouri Medicine, and one of its sections' headings is, quote, J-shaped risk reduction from strength training. In it, they say, and I quote, in this recent comprehensive metanalysis by MoMA and colleagues,

25:44the survival curves were J-shaped. Benefits were completely lost at strength training durations of about 130 to 140 minutes a week, with possible harm at progressively higher doses. Possible harm. The paper, their sightings said the benefit up there was unclear, but now, one year later, it's possible harm. And then they turned it into a prescription. Their summary recommendations say, aim for two sessions a week of strength training for a cumulative time of about 40 to 60 minutes per week, ideally not exceeding 150 minutes a week. That's an overreach, especially when you consider what and who these studies are actually measuring. Almost nobody in these studies are actually doing a lot of lifting. Most adults don't lift at all, and in the English and Scottish health surveys, half of the people who lift at all are doing under an hour a week. So the group reporting two and a half hours is a very small minority. And the thing being measured is minutes somebody wrote on a questionnaire, usually once, at the beginning of the study. Depending how many minutes someone lifted per week, 10 years before they died, makes a lot of assumptions.

26:46Think about what has to happen for lifting to keep you alive longer. You lift, that changes something about you and your body, and that change is what hopefully shows up as better health. These studies measure how many minutes people lifted and whether they died. They didn't measure the part in the middle. Did the exercise change the person? Did they get stronger? Did they gain muscle? Did they improve their cardiometabolic health? Did they reduce their blood pressure? We know lifting can do all of those things, but if you don't know how somebody responded to the lifting they did, or what kind of lifting they did, you can't tell apart two guys who both lift two hours a week, but one of them put 50 pounds on their squat, and the other one is doing the same six machines he's been on for 10 years. We know that people respond differently to a given exercise program, and that doing more training produces more strength, more muscle, more bone mineral density, better blood pressure reduction, with the increments getting smaller as you go up and lifting volume. But nobody knows where that actually stops. Show me people who trained more, who got stronger, who improved their health markers, and still died sooner, and I changed my mind.

27:47But I don't think asking how many minutes people lift per week tells me enough about the relationship between training and health. Which leaves the question nobody seems to want to answer. How much lifting is enough? Remember that leg extension study from the beginning of the show? Let's come back to it because something interesting happened this year. The American College of Sports Medicine published a new position stand on resistance training. It's an enormous document, and they went through 137 systematic reviews. And in the discussion, they comment on their own 2009 position stand, which told beginners to do two to three full body sessions a week from muscle growth. At the time it was written, it was graded as the highest possible quality of evidence. Later, it was informed by only three studies, with 59 total participants, and two of the studies did not investigate frequency at all. They later write that training frequency does affect strength. Quote, resistance training frequency was found to impact strength. However, there was insufficient evidence to conclude a dose response relationship, and the impact is diminished when volume is equated.

28:49If the effect of training frequency shrinks when you hold volume constant, then the variable you're really looking at is volume. A meta analysis of 12 studies and 74 training groups on this very topic concluded, quote, In resistance training is volume equated for combined multi-joint and isolation exercises, there is no significant effect of resistance training frequency on muscular strength gain. After admitting their previous guidelines stretched the evidence, I wish they would have been more careful here. Which brings me back to the resistance training guidelines, which recommends lifting two days per week. But days per week doesn't do anything once you account for how much work you did, which makes sense if you think about it for 10 seconds. Three sets on Monday, and three sets on Thursday is six sets. Six sets on Monday is still six sets. And then the new position stands says one more thing, weekly volume load, meaning load times reps, times sets across the week, which is the thing that would actually represent your dose of training was rarely considered in the included reviews. Nobody's measuring the dose in the dose response literature.

29:50Okay, so if the guidelines can't tell us how much lifting you really need to do, then let's build the answer ourselves. When you ask how much lifting is too much, you're really asking about four different constraints. Constraint number one is time. At some point, your life outside the gym does not allow for additional training. The second constraint is recovery, which is based on your current fitness. Doing more than that drives up injury risk from overuse, so there's a physiological constraint too. So those two limits are about how much training you can do. The other two about how much lifting is worth doing. Right number three is where the adaptation runs out. Every increment of training generally gets you some amount of fitness adaptation, where eventually the next increment gets you very little, perhaps a negligible amount. The fourth constraint is where more training adaptation stops improving health. For example, taking your squat from 500-600 pounds, while likely to impress dudes, probably doesn't improve your health even though the adaptation is still occurring. So when I think about how much lifting someone should do, I'm trying to figure out where

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36:03There's also a zip pocket on the side, so when I go running, I can put my keys in there. And there's a liner for where the phone goes, so that I don't sweat through the shorts and onto my phone. They're also four-way stretched. There's no pinch in the waistband, and they're gusseted so they don't write up. I've got a pair I've been wearing for over three years now, and they show no signs of slowing down. Now the price is real, but you can see where it goes. If you want to check them out, head over to 10,000.cc. And use code podcast 15 for 15% off your first order. That's 10,000.cc code podcast 15, 10,000 built for however you train. What we're about to find out is that the answer is different from every outcome. Strength, size, bone mineral density, and cardiometabolic health don't all saturate at the same point. So let's go through them one by one, starting with strength. There are two relationships here that keep getting mixed up, so I'll try to keep them straight. The first is how much training to do and how much adaptation you get from it. The adaptation we're talking about here is strength. The second relationship here is connecting adaptation and health.

37:07In this case, how strong you get and how healthy that makes you. For the strength adaptation itself, it appears to be a dose-dependent relationship, and nobody has really found the top of it. The new ACSM position stands says it in their own language. Strength goes up with heavier loads, and they write dose response right next to it. In general, more weekly training volume keeps producing more strength gains with diminishing returns, but no true ceiling. It just gets less efficient the further you go up. That assumes that you're doing it right, obviously, meaning the right exercise is the right intensity, the right proximity to failure, and managed in a way that you can actually recover from. Inside those constraints, more training gets you more strength. So does more training make you stronger? Yes, and we haven't really found where that stops. But does being stronger keep making you healthier. The biggest study on how strength affects health is out of Sweden. Over 1.1 million men tested when they began their compulsory military service around age 18. They were followed for about 24 years. They measured strength on knee extension, elbow flexion, and grip.

38:09They split everybody into 10 strength groups. Risk drops as you move up through the first few and then in the others' own words from the fourth tenth on a plateau was achieved, meaning from the fourth group through the tenth, the risk reduction sits flat at about 20%. The authors went and looked at the other big study of this in the field which came out of the Cooper Institute in Texas. They took just under 9,000 men, age 20 to 80, and they followed them for an average of 19 years. They tested strength with a 1-wret max on a machine bench press and a 1-wret max on the leg press. They added the two together and they split the men into thirds within each age group. Then they counted deaths. In the middle third, about 2.6 men out of every thousand died each year. In the weakest third, it was 3.9, about 50% higher. Those surprised there getting stronger improves your health. But in the strongest third, it was 2.7, basically the same as the middle. When they adjusted for everything they could, so age, smoking, drinking, body mass index, activity, medical history, family history, while the middle third came out with a 28% lower

39:14risk of dying than the weakest third. About the strongest third, they were 23% lower, no better than the middle. The Swedish authors read that table and concluded that more strength, quote, does not provide additional protection against death compared with middle levels. And this keeps happening. In about 2,800 American adults over the age of 50, leg strength only mattered if you were in the weakest quartile of the group. As strength levels rose above that threshold, health benefits looked basically the same. In another Swedish study, over 38,000 men who were followed for 42 years, they said flat out, we observed no trend across muscle strength groups for any of the outcomes. So separate groups found a saturation point for where getting stronger stops improving health. Case closed, right? Not so fast. Go look at how strong these people actually were. In the Cooper study, the bench press and leg press were done on a universal machine. The top third, the strongest group, the people that this plateau was measured in averaged a 185 pound machine bench press and a 331 pound leg press.

40:17It's about 1.1 times body weight on the bench and about 1.9 times body weight on the leg press. In the study of American adults over 50, they sat people in a machine that moves your leg at a fixed speed and measures how hard you can push against it. Being strong in that study meant pushing with about 96 pounds of force out of one leg. Everybody really lifted anything. And the two Swedish studies, between them covering 1.2 million men, we don't even know what the test was. The paper says that the Swedish Defense Recruitment Agency considered the exact measurement protocol confidential and it wouldn't tell the researchers. I think there probably is a real saturation point for strength where getting stronger does not improve health. But I suspect it's higher than anything in this literature because this literature does not contain people who are actually strong. What those studies found is where the benefit ran out inside the range they measured, which is not very strong. If you want evidence that these studies aren't measuring strength the way you and I mean it, look at what the field uses as its favorite strength test. Grip.

41:18You've probably heard that grip strength predicts everything. All cause mortality, cardiovascular death, cancer death, respiratory disease death. In the pure study, 140,000 people across 17 countries, well for every 5 kilogram drop in grip strength, there was a 17% higher risk of dying from heart disease and grip strength beats systolic blood pressure as a predictor, which is mostly the case because heart disease is a long-term risk and lack of strength is more of a short-term risk. In any case, the equipment to test grip strength is relatively cheap. The test is quick and it doesn't really need any skill at all by the person doing it, so you can run it in pretty much any clinic. But that doesn't mean that grip strength is useful for predicting health. Here's how I think about it. Pure grip strength is basically BMI for your muscle. BMI is a screening test for obesity, a disease of excess body fat. Its job is to decide who needs a closer look and it works best when it's high. A normal BMI doesn't really tell me much because BMI misses a ton of people who are carrying too much fat but who don't have a high BMI.

42:20It's also noisy when using it to predict the risk of death. When a normal or low BMI shows up with an increased risk of death, it usually is because a disease drove the weight down, a hidden cancer, muscle wasting, or something else. A high BMI can if you're protective in those studies as a result, even though that's not really the case. Grip strength works the same way. It tests the whole chain. From your brain, down through the nerve, the muscle, the tendon, and the bone, plus all the coordination it takes to put those together. A lot of diseases break one of those links, so a low grip strength tells you something in that system isn't working right, and that's exactly why it predicts death. Which means that it's useful when it's low, and that's about it. If your grip is normal, all it tells me is that nothing is currently wrecking your neuromuscular or musculoskeletal systems, but it can't tell me whether getting stronger would make you healthier, and the reason is that it barely moves when you actually get stronger. A group took frail adults over the age of 65 and put them through 24 weeks of whole body resistance training. Leg extension strength went from 57 kilos to 78 kilos.

43:23That's a 37% improvement in six months, in frail people in their 70s and 80s. Their grip strength, though, barely changed at all, which was no different than the group that didn't train either. A review of 22 studies in very elderly adults found that resistance training produced a large effect on the strength and the exercises they actually trained, but only a small, non-significant effect in grip strength. And here's one that probably describes a lot of you listening right now. Researchers went to the World Master's Weightlifting Championships and measured grip strength in about 170 competitors. These are people training about eight hours a week, many of them, for decades. Training hours showed no association with their grip strength, neither did their competitive results. Their grip was actually lower than athletes from racket and ball sports. So, if the field's favorite measure of strength doesn't change when you get strong, how can it answer the question of where strength stops improving health? And the grip literature has the same problem that the lifting literature does. When somebody combined 48 studies covering 3.1 million people, the association between

44:25grip and mortality was clear between about 26 and 50 kilograms, and the line was still heading down, which means reduced risk of premature death when they hit 50 kilograms. Above that, it stops being statistically detectable, and in a population of adults between 35 and 85, half of them women, there aren't many people with grip strength greater than 50. So, how do we know where that limit runs out? The authors also say that the relationship looks different depending on what people died of, which is exactly what I'd expect. Strength probably doesn't influence diabetes mortality risk in the same way it influences cancers. So, where's the saturation point for strength? I suspect it's higher than anybody has tested. If you have a group of people who aren't very strong, and you have to break them into groups, say, thirds, based on how strong they are, there aren't going to be big differences in strength between them. And because the differences in strength aren't very big, you'll only be able to see where strength starts helping, but not necessarily when it stops helping. Again, since most people in the studies aren't very strong.

45:28Take that Cooper Institute study again. The strongest third, the group that the plateau sits in, averaged about a 330 pound lake press, the middle third averaged 300, and the lowest third averaged 276 pounds. The fact that a nearly 30% reduction in mortality was seen by going from 276 to 300 is pretty incredible to me. But just because there wasn't another improvement in going from 300 to 330 doesn't mean the identified a true limit for where greater strength improves health. One reason I suspect it's higher is that the underlying machinery by which we adapt to exercise to get stronger seems to be the same as that which produces health adaptations. For example, a large meta-analysis found that those who got the strongest in response to lifting weights lowered their blood pressure the most, and a similar relationship has been shown with blood sugar control. So where is the upper end? I'm not sure exactly, but I suspect it's not going to be picked up by grip strength, and it's probably higher than what's been measured in the few studies that report their subject strength and health trajectories.

46:28In our vital 5 action plan, I put forth the following targets for the top end of strength, where more strength probably doesn't drive more health. A leg press, one rep max of about 2.5 times body weight from men, and two times body weight for women. While I can't prove that this is where strength tops out, I think it's reasonable based on the available research. The takeaway here though is that when it comes to recommending the amount of lifting someone needs, we need to consider how much training is needed to make somebody get the adaptation, which in this case is get stronger, and it should also include the known variation in training response, and reasonable targets for how strong people need to get in order to see an improvement in their health, and where it might run out. Two days a week of muscle strengthening activities, which is the current recommendation, doesn't do that. Now, let's talk about muscle mass. As far as training increasing muscle mass, it's a similar relationship that we saw with strength. More training keeps adding muscle, with diminishing returns, but has no real ceiling provided you can recover from it. It's the second step, that's the problem here, which is how well muscle mass predicts health.

47:30It mostly doesn't. A large analysis of 18,800 community dwelling older adults across nine different cohorts asked which body composition measure predicts falls, fractures, mobility limitations, and death. Grip strength predicted all four. Gates be predicted all four as well, but lean mass on a dexascan showed essentially no relationship to any of them, knowing how much lean mass somebody was carrying told you nothing about whether they'd fall, break something, lose their mobility, or die. So the SDOC's position statement is one sentence. Lean mass measured by dexsa should not be included in the definition of sarcopenia, which is a real problem for the word sarcopenia since it means muscle loss or really poverty of flesh. Dynapenia, which means the loss of strength or poverty of strength, would be better, but I don't see a rebrand happening anytime soon. The problem with being so focused on muscle mass when it comes to health is that it's a lagging indicator. If the client's about three times faster than muscle size does, you lose function well

48:31before you lose the tissue. And the reason is that the first thing to go is the nerve supply feeding the muscle, specifically the large high threshold motor units. Those are the ones you would use when you catch yourself when you're about to fall. So you can get a dexascan that says your muscle mass is fine while your function is already sliding. And by the time somebody has noticed the muscle mass, they're already a long way down that road. The mass is one of the last dominoes to fall. To the extent muscle mass does predict how it comes, it shows up at the very bottom. And when it does, it's usually a disease that's driving it. We can see this in lab work. Creatinine in the blood is a breakdown product of muscle fibers. So how much shows up depends partly on how much muscle a person is carrying. When we see a creatinine of 0.2 or 0.3 in an older adult, where normal levels are around one, we start to wonder about either a lab error or does the person have so little muscle there that their creatinine level is basically 0. In general, the very low muscle mass is the footprint that the illness left.

49:33So going from almost no muscle up to a normal amount of muscle would be a big deal for those people. Though the biggest benefit is the improvement in function, like strength, that happens alongside of the muscle growth, which occurs in response to training and fixing the underlying disease. Of course, this doesn't say anything about going from a normal amount of muscle tissue to more muscle and its impact on health, which is the question we're actually asking. So, I don't think muscle mass saturates with respect to health so much as it was never really predictive. What predicts outcomes is what the muscle can do. Their function, not how much of it is sitting there. That's why there's no muscle mass number in our vital 5 action plan at all. Still, the two days a week of muscle strengthening activities recommendation does not take into consideration the dose response relationship for muscle function, like strength and power, let alone muscle mass. And more training would almost certainly be better for most people. Now, let's do bone because this time somebody actually nailed down the dose and they did it over 40 years ago. Two researchers took a turkey, yep, a turkey, and specifically they took a bone in the

50:34wing and surgically isolated it so that it wasn't carrying any load from the turkey's normal activity, whatever that is. Then they attached a device that could apply precise loads to it while the bird was alive and walking around, and then they varied how many loading cycles a day that bone got. With no loading at all, the bone lost mass, which is what you predict. With four loading cycles a day, the bone lost stopped almost completely. And with 36 cycles a day, the bone grew. Bone mineral content ended up at about 133 to 143% of where it started, so a third to 40% more bone in six weeks. And then they went to 1800 cycles a day, but nothing happened. In their own words, neither the size nor the character of the bone changes were affected by any of the additional increase in the number of load cycles from 36 to 1800. Now the year after that, the same group ran a slightly different version of this experiment. They held the number of cycles steady and varied how hard they pulled, and this time they found a graded relationship.

51:36Below about a thousand microstrain, which is how much the bone deforms, the bone lost mass. Above it, the bone grew. For reference, in human bone, the strain generated during normal activities of daily life is somewhere between a 100 and 1000 microstrain. In order to drive the creation of new bone, the strain must be higher, somewhere between 1000 and 3000 microstrain. Human bone typically reaches its limit around 7000 to 10000 microstrain, where a fracture may occur shortly thereafter. The osteogenic index, which we've talked about on this podcast before, is a mathematical formula used by scientists to quantify the actual bone building effectiveness of an exercise session, and this formula uses both the strain and the number of cycles. Now watch what that explains. There's a meta-analysis of 24 trials of lifting weights for bone density in post-menopausal women. The combined protocols, which were resistance training plus some impact training, improved hip and spine bone mineral density. Resistance training on its own, though, produced a positive effect that didn't reach significance.

52:37A skeptical reading of that is that lifting weights on its own doesn't work for bone, and you gotta do some jumping stuff, too. But I think the right reading is that those programs never cleared the threshold needed to drive new bone formation. Machines that relatively light loads for sets of 10, or Pilates, or yoga, don't produce the strain, magnitude that bone responds to, and the turkey wing data already told us that doing more of them won't help anyway. So what happens when you do clear the threshold? Well, the bone grows, just as predicted. There's a trial of post-menopausal women with low bone density, where the protocol was 5 sets of 5, around 85% of their 1 rep max, done twice a week for 8 months, and they used the deadlift, the squat, the overhead press, plus some impact loading. Spine bone mineral density went up 2.9% in the training group, while the control group lost 1.2%. And this is a group that everyone is terrified to put under a barbell, because more than a quarter of those women had already broken a bone from osteoporosis in the previous 10 years. There was one adverse event in the entire trial, though, just one minor back spasm.

53:39Unfortunately, no resistance training trial to date has ever been powered to detect a change in fractures. Not one. For an idea what that would take, the drug trial that established Zalindranate, brand name reclast, for fracture prevention, needed 2,000 women, followed for 6 years, and there was 312 fractures in that study, and they had to do all that just to get an answer. Nobody has run anything close to that with resistance training. So when somebody tells you that lifting hasn't been shown to prevent fractures, the accurate response is that nobody has studied the question. Still, the point at which lifting weights saturates in humans for increasing bone density is unknown. We do know that lifting heavy weights, like the 85% 1 rep max we talked about earlier, is heavy enough, though lighter weights can work too. It's thought that 65% or so of a 1 rep max generates 1,000 microstrain and gets you past that threshold, so anything there or above should work. But what we don't know is if bone grows more when a person does more training. The lift more study we talked about had postmenopausal women doing 150 reps a week plus some impact

54:42training, and after 8 months their bone mineral density in their spine went up 2.9%. Would it have gone even higher if they did 200 reps in a week? Would they have less fractures? We don't know. No one has studied it. My feeling here is similar to what I said regarding strength. It's probably higher than what's been measured. If the 150 reps per week used in the lift more study represents a level of training that produces a good result in a vulnerable population, I suspect adding incrementally more would generate additional improvements, where the ability to do additional training is kept by how much time a person has and what they can recover from. Then again, the recommendation that people should lift 2 days a week doesn't take into account any of this. Okay, last one. Every lifting related training adaptation we've talked about so far is kind of like a savings account, muscle, strength, bone. They all take a long time to build and a relatively long time to lose unless you're immobilized or very sick. Otherwise, they just sit there kind of waiting to be used, but there's another thing we get from lifting that's more like cash flow, which in this analogy is the day-to-day handling

55:45of fuel. How your muscle takes up glucose, what it does with the meal you just date. These run on a time scale of hours to days and are impacted mainly by how active you've been recently. Lifting changes how you handle fuel. Every contraction runs on ATP and a muscle fiber only holds a few seconds of it at any moment. The fiber is rebuilding ATP continuously rather than drawing down a store of it and it has three ways to do that. Fospo creatine sits right there in the cell and hands a phosphate over immediately, which covers you for the first few seconds. Glacolosis breaks down glucose or sugar and stored glycogen without needing oxygen and that comes online a little slower and lasts for tens of seconds and in lactate. Oxidate a phosphorylation burns carbohydrate and fat with oxygen inside the mitochondria. It takes the longest to get going but can run all day. A set of eight reps is about 30 seconds of work so it primarily uses the first two pathways. The rest period is where the third one earns its keep. Rebuilding the phosphocreatine you spent and clearing what glycolicis is left behind,

56:47which is the only reason you can do the next set at all. An hour of conditioning is a different arrangement. Oxidate of metabolism runs the whole time and at a moderate pace a big part of it comes from fat. So a lifting session is 10 or 15 minutes of actual work spread across an hour and it pays for that work mostly out of the carbohydrate stored inside the working muscle. You can watch this happen. A study took eight untrained guys and had them do about 45 minutes of resistance training fasted and they did muscle biopsies before and after. Glacogen came down in every muscle fiber type but it came down the most in the fast twitch muscle fibers by 40 to 44% against 23% in the slow twitch muscle fibers. Two hours later the glycogen still hadn't come back fully. The same study measured the fat stored inside the muscle fibers and that went down to about 27% but only in the slow twitch muscle fibers. Unlike the glycogen it was fully replaced within two hours filled and drained over the course of one session which brings up a counterintuitive finding.

57:50But inside the muscle cells tracks with insulin resistance and risk for type 2 diabetes pretty well. Unless you're an athlete comparing muscle biopsies in the quadriceps in endurance athletes with people who have type 2 diabetes the athletes had nearly as much fat sitting inside their muscle as the people with diabetes. But the athletes were the most insulin sensitive group in the study by a wide margin moving about 10 times as much sugar per kilogram of lean mass. What separated them was how fast the fat was moving or the flux. In the athlete fat in the muscle works as a fuel depot and is filled between sessions and drawn down during them sitting next to a lot of mitochondria. Those same biopsies showed that the train group had far more oxidative capacity than any other group in the study. In insulin resistance the fat piles up for a different reason which is that more fat is arriving than the muscle can use and what you measure in the biopsy is the residue of that energy mismatch. So lifting alters the flux of energy not only while you're lifting but afterwards too.

58:52After a hard session your muscle pulls glucose out of your blood more readily, your more insulin sensitive meaning that your own insulin does more work per unit and you clear the fat from a meal faster. That's all measurable and is probably doing a good chunk of the work behind every beneficial mortality study from resistance training we've talked about so far. The catch is these effects are on a clock. Researchers measure this by infusing insulin into somebody at a fixed rate and then feeding in however much sugar it takes to keep that person's blood sugar steady. The amount of glucose that they have to put in is the answer. Somebody who takes up a lot of glucose at that fixed insulin level is insulin sensitive and somebody who takes up very little at the same insulin level is insulin resistant. I'll call this method of assessing insulin sensitivity the clamp for the rest of this podcast. In 1989 a group in Copenhagen had six healthy young men do one hour of one leg in the extensions. Four hours later the researchers ran the clamp test with catharsis in the artery and both femoral veins so that they could ask each leg separately how much glucose it was

59:55taking up. The leg that I recently done the exercise took up more glucose than the leg that had been sitting there. 15 years later another research group from Denmark did the same experiment but three days a week for six weeks in 10 men with type 2 diabetes. The train leg cleared more glucose than the untrained leg once again. The leg that did the lifting didn't get any bigger so the increase in insulin sensitivity was for more glucose transporters which are the doors that let sugar into a muscle cell along with more insulin receptors and more of the signaling proteins in between. This improvement in insulin sensitivity after a lifting session lasts somewhere between about one to three days depending on what you did and how trained you already are and then it's gone. You don't bank it even if you carry a lot of muscle mass. How do we know? Well the same Copenhagen research group ran the reverse experiment in the same year. They took seven endurance training men and they got the clamp test twice. Once in their normal state 15 hours after a training session and again after five days of doing nothing at all.

1:00:55In their train state it took a blood insulin level of about 44 microunits per milliliter to get them half of their maximum glucose uptake. After five days off it took 54 about a quarter more insulin for the same amount of sugar. Now these were fit guys with VO2 maxes up in the 60s but the authors described that when those men took the five days off they had the same insulin sensitivity as untrained subjects. So what's doing that? Well glucose gets into a muscle cell through a transporter called glute 4 and glute 4 doesn't sit in the cell's membrane just waiting there. It sits inside the cell in vesicles and something has to haul it out of storage and put it in the cell membrane surface before any sugar can move at all. Insulin is one of the things that does that. Insulin binds its receptor and the signal runs through a few different steps until it gets to a kinase called AKT and AKT phosphorylates a protein called TBC1D4. TBC1D4 is a break.

1:01:56If you phosphorylate it the break comes off, the vesicles move, glute 4 is installed in the cell membrane and sugar comes in. Muscle contraction does the same job but by a different route. When a muscle fiber contracts it requires energy or ATP as we talked about before. As ATP is used for contraction the ratio of AMP to ATP goes up because you're getting rid of some ATP and that all activates AMP kinase which is the cell's energy sensor. A kinase, like kinases do, phosphorylates TBC1D1, the sister protein to TBC1D4 and it releases a different break on the same vesicles storing glute 4 which again end up on the surface of the cell and sugar can come in. But this one needs no insulin at all. The persistence of the effect is related to TBC1D4 which carries phosphorylation sites for both AKT and AMP kinase and it responds on a delay. After you train that break comes off more easily for a given amount of insulin so the

1:02:58muscle that worked puts more glute 4 on the surface per unit of insulin that it did yesterday which is the mechanism by which exercise increases insulin sensitivity. But again it's on a clock. Some people will tell you the whole thing comes from glycogen depletion that using up the sugar in the muscle is what does it. Well the group that measured glycogen coming out of those fibers stopped the same thing so they tested it directly across 13 of their own studies. Insulin sensitivity afterwards had no relationship to how much glycogen the session used or to how much was sitting there to begin with. Yep, fuel does come out of the muscle but that's not what's driving the insulin sensitivity improvement. So what does drive the size of the response here? Contractile work by the muscles. The floor for the benefit can be as little as one workout or even one set as some research on quote exercise snacks which are short bursts of exercise have shown improvements and how the body handles fuel. The more of it you do the more energy you move through working muscle but again it only

1:03:59lasts a few days. And so we don't really know where the benefits from increased flux from more exercise stop improving health. I suspect any real plateau is going to be related to someone's current metabolic health status where those who have insulin resistance will have a higher ceiling relative to someone who doesn't. Okay, let's put it all together. Almost every number in this literature marks where a benefit starts but very little of it goes far enough to show where the benefit stops. For strength this is basically not been studied at all. Most of it looks at grip strength which doesn't really change as you get stronger and the only study looking at dynamic strength found the floor. There's about a 30% reduction in mortality when going from the bottom third to the middle third in strength. But it couldn't identify a point where strength really stopped helping because the study didn't have a lot of people who were actually strong. For muscle mass the thing that predicts health is what the muscles can do and while more exercise drives more muscle mass and probably strength as a result muscle mass itself matters for health only when it's very low and usually fixing the thing that's driving muscle mass

1:05:03down is more beneficial than chasing mass for its own sake. For bone this is pretty well studied but there are still outstanding questions. We know that the weights need to be heavy enough to force the bone to remodel with the lift more study showing good results from 150 reps per week at about 85% of the subjects one rep max. But we don't know if there's more bone density or a reduced fracture risk that we can gain from more training just yet. But if we agree that more training improves muscle coordination and more function we might predict that the ceiling for lifting effects on bone to be very high. And for flux we know that a little bit of exercise improves fuel handling where even a few minutes can increase how efficiently the body uses sugar and fat. It seems like the more exercise people do the more benefits they get related to flux such as insulin sensitivity, reductions in harmful fats stored in places it shouldn't be and so on. But again we don't know where this tops out because the exposures are measured in time. Not sets and reps and nobody has looked above about 5 hours a week.

1:06:04The guidelines are written as minimums which is probably fine for a public health document but a minimum is not the same claim as telling you where exercise stops working. The guidelines explicitly say these are minimum targets so we need to take special care not to confuse the prescription as where exercise stops working. For lifting the 2018 physical activity guidelines for Americans recommend muscle strengthening activities of moderate or greater intensity involving all major muscle groups on two or more days a week. And how much they say quote no specific amount of time is recommended for muscle strengthening on load they say one set of eight to 12 repetitions of each exercise is effective although two or three sets may be more effective. The document does admit that lifting progresses the words are increases in the amount of weight or the days a week of exercising will result in stronger muscles but these are both wrong as written increasing the amount of weight lifted does not make you stronger rather it is the result of getting stronger and simply increasing the amount of days someone lifts weights

1:07:06without increasing the total amount of training they are actually doing is the same dose just split up differently it's the frequency error all over again and the document never takes the next step and says that getting stronger makes you healthier. Now compare that to what the same document says about conditioning 150 to 300 minutes a week and then they say the benefits continue to increase when a person does more than the equivalent of 300 minutes a week. They also say that research has not identified an upper limit of total activity above which additional health benefits cease to occur. They mentioned this twice in the document in both times it's about cardio nothing on lifting. There's another section addressed specifically to people who already meet the minimum with the same slight they say most adults should increase their aerobic activity to exceed the minimum level and move towards 300 minutes a week and then they say adults should also do muscle strengthening activities on at least two days a week. Not that they say adults should do more cardio than the minimums which we agree with but they don't say the same thing about lifting. I realize that no one really reads the guidelines but on the off chance that they do this leaves

1:08:09a lot to be desired. What you can't do is publish the thing as a starting point and then just stop one set of eight to twelve reps two days a week presented as the strength prescription instead of the beginning of the journey. People vary in how much training it takes to get to any given target some will clear it on the minimum dose others will need two or three times that to end up in the same place. So what if somebody needs considerably more training than is recommended to get their strength or their bone density to a level that improves their health. What if somebody wants to be healthier than the minimum will make them a guideline that names a target and a range handles that by itself because you train until you hit the target. But a guideline that only names the dose is incomplete. So let me do the thing I just described because it's easy to criticize a guideline and much harder to write one I do not envy that position. Nonetheless here's what I would write. The outcomes are a longer life less disease and still being able to do what you want at 80 the adaptations that get you there are muscular strength bone density and how your body

1:09:13handles fuel so here's the dose. For volume somewhere between eight and twelve hard sets per movement pattern per week push pull squat and hinge with a list of examples underneath each one that's about double what the guidelines ask for for load it should be heavy enough to clear the threshold bone actually responds to which the strain data puts somewhere around 65% of a one rep max. I'd say most of the training should be done between 65 and 85% of a one rep max which is about a five to twelve rep max load most sets should be challenging but not maximal where you could do two to four more reps if you had to. For type pick exercises that train all of the major muscle groups of the upper and lower body ideally most of your exercises would involve multiple joints which are called compound exercises machines dumbbells barbells body weight and other forms of loading all can work each with their own pros and cons pick exercises you like and can load sufficiently for progression as you get fitter your challenging sets will start to feel easier that's you getting stronger

1:10:17and as a result you'll have to add weight. This should happen periodically over time every few weeks on average and often faster for newer trainees add a small amount of weight three to five percent of the load being lifted for frequency split up training per your own preferences more frequent shorter sessions works just as well as fewer longer sessions and vice versa frequency is just how you distribute the work based on your availability. And then the targets which is the part the guidelines never include for strength a leg press around two and a half times body weight for men and two time body weight for women would be reasonable ideally we'd have more targets that capture more lists that people would potentially do there would also be health targets that are known to improve with properly programmed resistance training such as reduced blood pressure if it was elevated improvements in fasting blood sugar if it was elevated and so on if we're treating to target this time with lifestyle measures we have to say how to titrate the dose so there would be a section on how to add training load and explicit mention of known ceilings on various adaptations and how they relate to health along with permission to go further

1:11:21if someone wants to basically to avoid people saying silly things like lifting more than two hours a week is bad for you. For most people the existing guidelines will generate a modest increase in fitness and as a result a significant improvement in health still I think most people would get much closer to maxing out the benefits from exercise by doubling the guidelines though that's still an open question to where the real ceiling exists. Next week we're going to do the same thing with cardio where the data is better there are still some more heart issues to address and the sweet spot recommendation come from one guy sitting in a chair. For Barbel Medicine I'm Dr Jordan Feigenbaum we'll catch you next week and every week right here on the Barbel Medicine Podcast.