#8 - Can extreme exercise damage the heart? With Dr Benjamin Levine

hello and welcome to inside exercise today we've got the extraordinary ben levine from texas who has undoubtedly the best track record in sports cardiology and cardiovascular physiology he's done an amazing range of studies in terms of exercise effects on the heart space research looking at exercise at altitude and today we're talking about you know how exercise affects the heart and you know the sort of controversial question can too much exercise actually damage the heart we talk about how the most important factor for endurance exercise is your maximum stroke volume we compare and contrast the heart's

responses to endurance exercise versus resistance exercise we discussed the remarkable findings that three weeks of bed rest have more negative effects on the heart than 30 years of aging he talks about his sweet spot for the amount of training you need to do for cardiovascular health how important it is to start exercise before the age of 55 in terms of cardiovascular health how just normal walking isn't really sufficient to maintain your heart function and how in the vast vast majority of very highly trained endurance athletes exercise is still good for the heart and increases longevity

so enjoy this one hi ben how are you hey glenn nice to uh see you down under and this is coming here from uh extremely hot area of uh north texas oh wow okay it's kind of cool here it's obviously it's opposite people don't always think about that so we got it's summer for you winterfest hey i can't help noticing you at the cardiology there does the the heart love space we might talk about that later you know you've been all over that stuff as well um but we're going to talk largely about um you

know is is exercise good for the heart which i think we know it is but can extreme exercise actually cause problems for the heart so you know i think that's an interesting thing to discuss and you've you've done massive amount of work on that um but first of all i was just interested you know you're a medical doctor um you know and you do exercise research i'm wondering did you start off interested in exercise or you know interested in medicine how did you actually get into this so and i'm a cardiologist and cardiovascular physiologist and

in my youth in high school and college i was a competitive athlete i played tennis and i wrestled competitively at the d1 level um and so exercising competitive sports has always been part of my life um i never was good enough to make a living doing it um so and in fact when i was in in college i was a music major i was a classical saxophonist and uh ultimately i decided that the world did not need another mediocre classical saxophonist so i had to ask myself what kinds of things was i really interested that

was i passionate about and is there a way for me to make a living doing it and so i decided that i was perhaps would try to combine my interest in science and in sports and be a sports medicine doctor and that was my intention in fact i i went to harvard medical school and worked with lyle mckayley doing a little bit of research and when i went to my residency at stanford my original intention was to do three years of medicine and then orthopedic surgery but i really didn't like to operate and what really

excited me was understanding human performance physiology and so i had a lot of wonderful mentors there at stanford her paltrin the guy who first reported high altitude pulmonary edema in the english literature was one of my first attendings and he was a cardiologist and herb was a great mentor for me and i was also very fortunate to be able to work with bob debusk and bill haskell and at the time bill was one of the he was the president of american college of sports medicine and one of the unique things about cardiology is it's one

of the very few specialties in medicine where exercise is a critical component of both the diagnosis and treatment of disease so i went to bill and sat with him in his office and i said bill where could i go in the united states to do a fellowship in cardiology where i could get great research training in exercise science and great clinical training in cardiovascular medicine and he said he no then didn't blink an eye he said that he'd give his right arm to work with gunner bloomquist and jerry mitchell at ut southwestern in dallas so

i said okay why not and i had the very very great fortune of working with these two giants titans in cardiovascular physiology and medicine both of whom have passed as you know jerry most recently last year and i also had the opportunity to work with bank saltine i did a fulbright scholarship in in copenhagen and learned the copenhagen model of integrative and clinical physiology which i brought back with me to dallas and when even when i was a cardiology fellow started the institute for exercise and environmental medicine where i now work we're about to celebrate

our 30th anniversary and it's grown into the largest center for the study of human physiology in the united states so i i have you know one of the greatest jobs on the planet i get to merge my research interest in my clinical interest i do interesting science that pushes the envelope of human performance and apply my research institute to the care of in patients which is very satisfying and allowed has allowed me to build a career in that direction wow what a stunning what a stunning background i mean you said at one stage you were

lucky but you obviously made your own luck with some of those uh you had to have done well to get to each of those steps and you and you've obviously done well since so there's a lot of stuff there that you talked about so um you know pushing the envelope you've got the space stuff there i touched on earlier which which we might get to the altitude work you've done um obviously that the heart has been you know involved with that but if we just step back a little bit one of the changes in the

heart you know acutely and chronically with with say endurance exercise versus resistance exercise for example sure no i think it's an important question and the first thing i would say is there's no hard line in the sand between resistance or strength and endurance or dynamic exercise most exercises involve some combination of both we think about endurance primarily as the repetitive contraction of large muscle groups and as you do that and increase the metabolic demand in skeletal muscle it is the skeletal muscle that drives the cardiovascular response to exercise and particularly in the upright position you

pump blood back to the heart by contracting the skeletal muscle the heart has to dilate and get bigger in order to pump the blood that's coming back and indeed within the first even at low levels of exercise first 50 to maximum the heart expands to its maximal amount the end diastolic volume and it is that ability to dilate and accommodate a large amount of blood flow that distinguishes the elite endurance athlete from a sedentary individual if you think about it i don't know if your your audience will know what the thick equation is but oxygen

uptake v.o.2 is uh uh the best measure is a measure of the integrated uptake of oxygen and make it using it to create energy for physical work and oxygen i'm taking is a function of two things only two things the cardiac output which reflects the ability to deliver the blood and the arterial venous oxygen difference the ability to extract in the skeletal muscle cardiac output is a function of two things heart rate and stroke volume so the ability to take up and extract oxygen to do physical work is really only due to three things the

heart rate the stroke volume and the total peripheral resistance now if you compare an elite athlete with a non-athlete the maximum heart rate of an elite athlete is if anything lower than a non-athlete right so heart rate is not what creates a great athlete and although athletes are able to increase the amount of oxygen they extract the avo2 difference a little bit better than non-athletes it's not a huge number it's not a huge amount and what absolutely clearly distinguishes the elite endurance athlete is the ability to pump a lot of blood and it's the stroke

volume so in fact one of the first studies that i got interested in was what how does an athlete pump so much blood right and one of the reasons that i was interested in that is because uh i wasn't working with grenobleisk in the in the space program and um fortunately for me unfortunately for the world while i was i lived in japan for a year just before i came to dallas the challenger accident occurred and so all space research was put on hold except that nasa continued to fund the investigative teams and gunner was

leading the work in cardiovascular adaptation and one of the things that that intrigued me was that pilots and astronauts were told initially not to do any endurance exercise because athletes are more prone to fainting i said well why should that be and so um we did some very bold experiments i put a catheter in the heart of elite athletes and some sedentary medical students and used that to measure the pressure inside the heart and look both simultaneously at the pressure and the volume and perhaps the best analogy to what i'm going to tell you is

with a rubber band right take a open up a box of rubber bands take a brand new you know stretchy rubber band and you stretch it and it snaps back right that's the elasticity of that rubber band now stick that in a drawer come back 10 years later and pull it in it doesn't stretch anymore it loses its elasticity and that's actually something that happens with aging and we'll get to that perhaps in a little bit but but the athlete then has to stretch the heart in order to um snap it back and so we

we measured the stretch ability the medical terms the compliance of the heart and a group of elite athletes and yes indeed their hearts were not only bigger but more compliant more stretchable more flexible so it allowed them as the blood comes back into it the heart can get really really big and pump that blood out and that was the single biggest distinguishing factor for the elite competitive athlete now um it turns out that that's a real advantage to being an athlete it's a little bit of a disadvantage if you're standing on you know quietly and

work for what we call orthostatic tolerance the ability to stand upright and i always tell you know my my trainees never put an elite athlete on a tilt table because they're going to faint every athletes elite athletes will think because their hearts are so compliant they expand during exercise and they shrink during why you're standing upright when the heart is unloaded so now as you do that what is it that that allows the heart to get so much bigger and that's an interesting question we make analogy to the volume loading that we see in some

disease states like when the heart valves don't function as perfectly as they could they regurgitate or they're insufficient the aortic valve or the mitral valve each time if the heart leaks a little bit the heart gets bigger and bigger and bigger and bigger and that's the volume load on the heart and that's what we mean that's what we see predominantly with endurance training it's more than that because the pressure goes up too the heart develops what we call eccentric hypertrophy it dilates and thickens right so um that is the primary process now remember patients who

have valves that don't work they develop the disease their hearts eventually stop working and that's because the volume load is every single heartbeat for their entire lives right for an athlete that volume load even if they exercise four hours a day it's still 20 hours a day that they're not exercising emphasizing that it is the recovery that is just as important to the heart as the volume load which stretches how causes the heart to add muscle cells in series and it's those flexible muscle cells in a connective tissue matrix that provides that structure to the

heart now there's one more thing we need to emphasize and that is the heart both chambers of the heart are encased in a sac called the pericardium and that pericardium provides structure it helps the right and the left ventricle coordinate and beat together but it also constrains the filling of the heart it's fibrous it's not as stretchable as the ventricles and one of my colleagues my good friend jim stray gunderson when he was a fellow with jerry mitchell did a study where he took a group of dogs beagles and he cut their pericardium and compared

them to a group where he did similar surgery and didn't cut the pair hang on you better watch out i've got my dog here so we've got i hope there's a happy ending hopefully he won't be able to understand the signs he's sitting on my lap but what i'll tell you maybe your dog would appreciate the fact that when the pericardium was cut the heart was able to expand even more and the cardiac output increased and the maximal oxygen uptake increased too so it's a couple of different things the heart has to become more compliant

the pericardium becomes more compliant and that's what allows the heart to pump a lot of blood so what about these um there's a lot of stuff that are unpacked that was that was great i just just let you let you go there because it was a great uh overview what about i was just thinking about that so when you cut the pericardium that you know the heart can pump more blood etc does it actually ever gets the point that these these you know incredible endurance athletes get get their heart actually gets to the point where

you know it's sort of like it's it's limiting in that that space always that the heart the pericardium has to stretch and and you know one of the things you might say to me you know one of your listeners might say will be wait a second levine maybe the heart is bigger than an athlete not because of their training but because you have to have a big heart to become a good athlete so which comes first and to answer that question we took a group of sedentary individuals and we trained them for a year to

become marathon runners and what we saw was the mass of the heart got much bigger the starling mechanism the ability to pump blood as you fill the heart got much better but and the heart got more compliant but not nearly as compliant as we saw cross-sectionally in our elite athletes and that's always intrigued me you know what is it that prevents somebody going on an endurance training program from achieving that those very large volumes that you see in an athlete and a couple of things occurred to me number one is it may take more than

a year to stretch that fibrous pericardium number two it may be that to get a truly elite athlete's heart you have to train while the heart is growing so as the pericardium gets bigger and the heart gets bigger that those things accommodate and grow together and that's the way that you get the truly large hearts and those elite athletes with 80 mls per kg per minute and then cardiac outputs are 40 liters a minute you know that which it's really difficult to get even in a young person if you put them on a dream 40

do you actually get up to four because i know so just step back a little bit so cardiac output at rest is about five liters per minute and you know with with uh you know maximum exercise like an untrained person might get up 15 to 20 you know liters a minute but you actually get i know 30 but they the best actually like 40 liters a minute yeah miguel in durian one liter bottles of coke or whatever yeah yeah the great cross you know bank saltine has studied the elite cross-country skiers in scandinavia and you

know some of the great uh endurance tour de france cyclists and it can get up to 40 liters a minute yeah i guess there's some genetics there as well so in terms of you know getting those big hearts those big cardio couples those big vo to max's is it true that the the sort of elite athletes would have started off with a bigger heart as well and then adapted you know we don't know that answer you know there are a number of people around the world who are have developed these longitudinal studies um looking at

kids before they become elite athletes the problem is it's hard to identify you know i think everybody knows that intuitively everybody knows that there are some kids on the playground who are faster and have more endurance and are stronger than others and there obviously must be some genetic components but i i think that it would be a mistake to assume that that is deterministic so if if you are have the gene whatever that is for to be an elite athlete and don't train you're not going to be a great athlete and conversely if you start

young and train hard there's no question that individuals like that can become elite athletes and that's the fallacy of looking for a single gene and thinking that we know enough about genetics to say okay you this genetic profile you should you know become a chess player and you with this genetic profile you should become an elite rower i think that's fundamentally false i think the more we know that the more we realize how complicated everything is um you know this is much more you know looking for one gene for diabetes or whatever it's not going

to happen it's a gene environment interaction just like everything else in life so i'm just talking about the the adaptations to exercise the heart so we're talking about like a volume load as you said so the heart stretching and getting a bigger left ventricle so bigger stroke volume and as you said that the heart rate max if anything goes down so uh the major increase in the vo to max is the stroke volume so what about with the resistance exercise so it's a very different i know you said all exercise is a bit of a

combination of you know things going on but you know they get these massive increases in blood pressure of you know just a step back a bit so you know normal blood pressure systolics are when the heart's pumping as it is 120 millimeters of mercury then during the resting phase it's about 80 now we're talking about during resistance exercise it can be 400 on 300 things like that so so naturally the hearts you know seeing a very different environment what's happening there and how does the heart adapt to that sort of load so so i think

it's it's also a very interesting question and lots of unknowns that we have so we we tend to think dichotomously of strength and endurance but let me give you an example rowing rowers have the biggest hearts of any athletes the largest hearts the most muscle mass that's because every time they pull on the oars there's a huge increase in arterial pressure from a combination of intense large mass muscle contraction and huge stroke volume so so rowers have both thicker hearts and dilated hearts you know aaron baggish and his team at harvard have studied the harvard

rowing team a lot and we've learned a lot about the adaptive process and those people it's a combined strength and endurance type training stimulus um and we phil clifford uh when he we were together in copenhagen stuck arterial catheters in with neil secker and elite rowers and they have mean arterial pressures of 250 millimeters of mercury so that's mean pressure right so so pressure goes up a lot during dynamic exercise um particularly when you have a large amount of muscle contraction you're right that you know during single one repetition max exercise arterial pressure goes up

very high you have to be a little careful about that though okay because markowski has shown that if you measure the transmural pressure across the heart um that is a difference from inside to outside the heart or from the heart to the aorta if that muscle contraction is accompanied by a valsalva maneuver a brief thousand minutes so basically holding your breath for you yeah or that that grunting you know when you contract in and you close your glottis and you raise the pressure and actually kind of cushions the heart and the proximal aorta now the

pressure outside the chest goes up a lot in the head in the distal arteries and the legs and the arms but inside the chest what the heart sees is not nearly not nearly as high as you might think just from the measurement of arterial pressure now it's much more complicated than that because that's a single one repetition same thing with uh the mcdougall study that you are quoting about the 400 millimeter of mercury systolic arterial pressure um done led by the late and great john sutton by the way of course um so um i think

that one of the reasons why we don't see the massive thickness and left ventricular hypertrophy in strength athletes that we see in patients with aortic stenosis for example where that that outlet from the heart is constricted in every single heartbeat it pumps against a very very high load those patients can get a lot of hypertrophy patients with are too high blood pressure hyper tension can get very hot thick hearts and again sort of like the analogy with the endurance athletes i gave you before those hearts are loaded with every single heartbeat when you're weight training

it's just not that much so it is true that way people who do entirely strength training with little endurance training will get something that's more like a concentric hypertrophy so the heart will get a little bit thicker but it won't dilate as much unless you include some kind of endurance exercise again i have to be very careful about this pure dichotomy it's not but in its most extreme forms so endurance running for example versus body building massive strength training weight lifters those hearts will look very different okay now i'm also aware that we talk about

the cardiovascular system that people tend to think heart heart heart so you know the vascular system is also adapting so you get um you know increases in compliance again so that so that maybe you can explain what compliance is um sure well the heart obviously has to pump the blood out into the arteries and the arteries are also very flexible and distensible and that's called the wind kessel effect you pump the blood out into the aorta it expands the valve closes and then that elastic aorta the liver continues to deliver that blood as it gets

smaller and smaller into the circulation out into the muscles and so that we call that ventricular arterial coupling how the heart and the blood vessels interact with each other and um we know more about let me use the aging analogy if if if you don't mind so because i've been very interested in the aging process as well in part again because of my uh experience at ut southwestern in dallas i know you're going to say i think what we tend to do is as we get older we can take more interest in aging i've been

interested in this for a while and i'll tell you why so one of the most famous studies in our field was done in the 1960s it's called the dallas bed rest in training study and gunner blunquist jerry mitchell bank saltine bob johnson put carlton chapman put five young men only five they put them to bed for three weeks and then train them for two months and almost everything we know about the adaptive capacity of the circulation really began with that very famous study 78 pages in circulation published in 1967. now i was only 10 years

old when they did that study so i had nothing to do with it but when i came to dallas in the mid 90s we found those same five guys and brought them back to dallas now 30 years later and one of the most important observations we repeated those same studies and we found that not a single person not one was in worse shape uh after after uh 30 years of aging than they were after three weeks of bed rest in their twenties so three weeks of bed rest that's the opposite of the training right it

was worse for the bodies of functional capacity than 30 years of aging why is this interesting and how does it get us perhaps to the space model is because one of the major things we see with aging is people become more sedentary and one of the best analogs for space flight is putting people to bed it increases confinement and it eliminates the head foot gravitational gradient just like you've been up in space and so what we found is we see exactly the opposite effect to the heart when we put people to bed than we see

with exercise training the heart atrophies it gets smaller the muscle mass gets less by about one percent a week one percent a week and if we look cross-sectionally at let's say someone who's been a spinal cord injury right hasn't moved in two years they have about a 25 percent reduction in lv mass ventricular left ventricular mass yeah if you look at um a elite runner they have about a 50 increase in left ventricular mass so if you look at that range 75 of the heart's muscle mass is plastic adaptable responsive to changes in physical activity

so we started by saying okay how much of what we have always attributed to aging maybe was really related to sedentary behavior so we part of my long-standing nih grant was we took a group of elite masters athletes people who had trained for decades and were highly competitive at a regional and national level and then we selected a group of similarly aged about age 70 people who had no medical problems no hypertension no diabetes they could have a little bit of cholesterol but never been hospitalized hard to find them by the way and we catheterized

them and we found that aging healthy but sedentary aging leads to atrophy and stiffening of the heart and lifelong pattern of exercise training completely prevented that process really quite dramatic and we did the same thing with the blood vessels we measured the stiffness of the blood vessels and aging caused stiffening of the blood vessels and impaired coupling from the heart to the blood vessels and lifelong training preserved aortic compliance and that coupling process yes that's that's amazing i think the heart's one situation but all sorts of things metabolism you know muscle mass bone etc this

study after study finds that you know is it the aging or is it just the inactivity so and you know usually it sort of tends to come out that that if you're active then you can maintain most of these things it's not like you can stop aging of course but you can maintain a lot so that's an interesting point because you know with studies you know often people are saying okay what's the effect of training but but you've also got the effect of inactivity so you also you kind of need in these studies you need

to have like inactive group a normally active group and then a trained group right to actually get the full idea of what's going on well so so you're right and as part of this discussion about can you do too much exercise you know i just told you that we identified a group of elite masters athletes who train you know 10 15 hours a week and are highly competitive their hearts look like healthy 20 year olds i mean it's quite dramatic but that's not a very good public health measure right and so we had to ask

how much exercise do you need to do over a lifetime to preserve the function of the heart so we collaborated with my colleagues at the cooper clinic been a wonderful collaboration that's been very productive for me over many years and we identified people who over a 25-year period had reported the same amount of exercise every time they went to the cooper clinic doctors and we divided them into four groups one group was sedentary that is no regular exercise and then we recruited another group of competitive athletes six or seven days a week and highly competitive

in competitions then we selected people who did two to three days a week on average over a lifetime we call those people casual exercises and then a group that did a little bit more three four or five days a week we called them committed exercisers and what we found we catheterized them and measured their cardiac compliance and their vascular compliance well it turns out that two to three days a week of casual exercise had no impact at all on the structure of the heart and blood vessels four to five days a week got you almost

as much as the elite athletes not quite but clearly four to five days a week was that that um sweet spot of how many days a week and that's my exercise prescription for life when i patients ask me what should i do doc i say well first of all it depends on what your goals are right you want to be an elite athlete you got to train to be an elite athlete that's one different dose if you want to train for health then i say chain four or five days a week and i want you

to do one day a week that's so that lasts at least an hour that's a long session and it should be fun i don't care what it is it could be playing tennis it could be going dancing with your spouse could be taking a long bike ride i don't care but it needs to last at least an hour and it needs to be fun at least two to three days a week should be of moderate to vigorous intensity that is at least hard enough that you are breathing a little harder get a little sweat on

your brow you can talk but you can't sing it's called the talk test right um about 30 minutes can do in front of the television while you're watching you know however you want to handle that work that into your life and then one day a week of something more intense and i i'm a big fan of the 4x4 the norwegian ski team workout the uric whistle off four minutes at nearly 95 percent of maximal followed by three minutes of recovery repeated four times and that combination of duration frequency and intensity and then i think people

should do at least one or two days of strength training it doesn't mean they have to lift weights they could do tai chi they can do strength yoga they can do pilates anything that works on strength and balance and that's my prescription for life for optimizing cardiovascular health there you go well that's that's pretty interesting in several ways first of all i guess it's a little bit surprising so two to three days of exercise was was no better than sedentary yeah and at least for cardiac structure so so i think that's important obviously there are

other benefits of physical activity i'm not saying there's no benefit at all there are autonomic changes there are metabolic changes there are other things that are good for you but if you're trying to protect the structure of the heart and blood vessels and keep them youthful two to three days a week is not enough what about i guess you looked at blood pressure was there was there blood pressure improved by that well remember that life was bad to start with but yeah so we we excluded patients with hypertension so thank you sure um but even

just in a non hypertensive person do you think two to three days of exercise because i i was tending to think i'm into uh glucose metabolism mainly in insulin sensitivity now we tend to think about each bowel of exercise increases in some sensitivity to like 24 to 48 hours so so you think well you could probably get away with three or four days a week anyway yeah i guess it's getting worse four days we we did two to four days four to five or six to seven yeah obviously there's no hard line in the sand

and you know you could ask me you know what about intensity what about duration exactly and those are hard to track over a lifetime you know what i mean so people can tell you yeah i did you know my i went monday wednesday friday and you know played tennis on the weekend and it's but it's hard to say you know when i was in my 20s i went this hard and this long you know that was too much for us to be able to quantify it's very quick but with confidence based it on frequency it

reminds me when i've had a lot of people in to do video to max's for example and they you know you talk to them on the phone oh yeah i do a lot of exercises you get them in their video to max it's like just crap then you say hang on what's and they go oh well actually i've you know the last month i've only done much and whatever so it it must be very hard to quantify over time it is it is hard but you know i will tell you that when we looked at

the vo2 max based on free purely on frequency over a lifetime in 70 year olds um it was a r squared of 0.99 perfect r squared it's amazing now you know that one question you might ask is well if you've been sedentary can you fix it right can you reverse it and so we took our sedentary 70 year olds and we trained them for a year to try to get them fitter and to change their cardiac compliance and although we did increase their vo2 max we couldn't touch their cardiac or vascular compliance didn't change at

all after a year of exercise and that even even if we gave them a drug called algebrium a drug that breaks advanced glycation end products um the the the complexing of glucose to collagen which is as you know what causes hemoglobin a1c it's that the mallard reaction and on on hemoglobin only lasts 120 days but collagen lasts forever so when you make that complex there are many people who think that is part of the aging process we gave them a drug to break that and if we gave them just the drug nothing happened if we

did exercise training nothing happened if we gave them both exercise training and the drug we were able to make about a 10 or a 15-year reduction in the effective cardiac compliance but maybe the question is you need to start earlier or train harder right so the next thing that we did was first had to say when in the aging process does this stiffening occur so we work with the dallas heart study and we looked at over a hundred patients we catheterized over 100 patients and we divided them into decades um right we did youth which

is under 35 early middle age 35 to 50 late middle age 50 to 65 older than 65 we actually divided them by decade and it turns out that what happens is as you age up until about 55 the heart actually stiffens the slope of that pressure volume curve shifts upwards after you get to about 55 it doesn't get a lot stiffer it just shrinks than atrophies so we figured okay maybe that sweet spot was right there in late middle age and so we took a group of middle-aged individuals and now we trained them for two

years and we were able to reverse the effect of a few decades of sedentary behavior aaron howden published that paper in circulation a few years ago and it's among the most highly uh viewed papers in the history of circulation wow okay the other thing i was thinking was um you know obviously we're 100 gatherers not that long ago so the idea was that we would be active you know every day doing a little bit um but i was you know noticing that you said again with your study where you looked at the you know two

to three days and whatever and then you suggested what sort of exercise you were suggesting i guess a little bit harder than a lot of people would like to think you know a lot of people would like to think that they could just go out for a walk and again i know you talk about cardiac structure not necessarily like metabolic health but you think sort of going out for just for walks i mean i know you can do brief walks you think that that probably isn't enough really for you to make confidence it's not enough

yeah okay it doesn't induce enough of a cardiac load to cause a cardiac adaptation or to prevent the effects of aging okay and then again what about the blood vessels so we talked a little bit about that so you know you said you get compliance so it is a thing called endothelial uh function you know so function is a is a challenging topic glenn and a lot of that we understand what it is but the way we typically measure in research studies by doing flow-mediated vasodilation of the forearm that's not endothelial function right we know

that what happens in the forearm is not the same what happens in the coronaries and i i think that it's probably the best way for us to measure it simply in clinical practice but you know for example reiner hembrecht in germany has done some beautiful studies actually doing cardiac catheterizations and measuring uh blood flow changes with acetylcholine or um down the coronary arteries and we know that that you can improve endothelial function the ability to vasodilate in response to flow or metabolic stress very nicely with exercise training and i think the dose is a little

bit different than what is required to change cardiac structure one of the first editorials i ever wrote which i wrote with jerry mitchell in the early 90s in circulation about a paper bill haskell published where he took a group of elite ultra endurance runners and brought them to the stanford cath lab and gave them nitroglycerin and what they found and compared them to a group of let's say patients who were referred for cardiac calf with chest pain but had normal coronaries the elite athletes at rest the size of their blood vessels are about the same

but when they gave them nitroglycerin the athletes dilated much more than the non-athletes so i think sustained exercise training is good but even exercise training for example after a heart attack and cardiac rehabilitation is one of the key factors that improves blood flow to the heart so if you're asking about the dose of exercise you've got to answer the question what outcome are you interested in are you interested in cardiac and vascular compliance are you interested in function are you interested in metabolic health are you interested in obesity are you interested in blood pressure control

and that dose may be very different exactly so you mentioned the flow-mediated dilatation which may not be the the best way of measuring endothelial function and i've read that as well we've i don't know if you know but we've done studies where we've um you know you mentioned nitroglycerin so you know we're talking about nitric oxide um causing relaxation of blood vessels just wondering is one of the things that's been discussed with diabetes is it the is it the inner cell layer of the of the blood vessel so the endothelium which is you know sort

of going astray or is it the smooth muscle so the actual muscle with it which is affecting the the stretch and contraction of the vessel do you know how does exercise affect those so blood vessels think it i think it does both but i think what exercise is most effective at is causing vasodilation and arteriole or vasodilation what regulates the blood flow is the resistance vessels and and and endurance athletes are able to dilate to an extraordinary degree and accommodate a huge amount of muscle of a blood flow in 50 times resting values it's really

quite dramatic so that's more than just flow-mediated vasodilation which is a function of the large conduit vessels but much of the the resistance occurs in the resistance arterioles and those they dilate dramatically in athletes now we we haven't talked so much about whether you can do too much exercise and i think that the the reason that i wanted to set the stage is i want to make it clear to the audience that a sustained dose of high intensity exercise regular exercise we know for sure that in the vast majority of people it's good for you

right you know phil clark from australia maybe you know phil did this very interesting study looking at um uh thousands of fifteen thousand medalists olympic medalists from you know the beginning of of the olympic movement until the you know the 2010 1896 to 2010 and compared their conditional survival to people in the population and if that kind of exercise was bad for you we'd see olympic athletes dropping like flies but no that's not what happened in fact survival was better in olympic athletes now there are lots of other good things that happen if you're an

olympic athlete so then they divided it up into the pure strength training and pure endurance type events and the effect was not as compelling in the strength athletes but very compelling in the endurance athletes so i i think that there are you know we we haven't talked about risk of arrhythmias and stabilization of electrical pathways that's probably a little too complicated for your audience but i i think that this field um was was uh turned on its side a little bit and began with the group from germany who looked at a number of marathon finishers

in their 50s and looked first at the presence of coronary calcium as a sign of atherosclerosis and then at the presence of delayed enhancement by cardiac mri so if you um can you just explain delayed enhancement sure if you take cardiac mri and inject gadolinium which is a contrast agent that it shows up on an mri and if the heart's been injured or scarred you can see it and um they looked at a bunch of marathon runners who had done multiple marathons and compared them with a group from the heinz nixdorf recall study and a

small number of them had a little bit of scarring both that looked like it was related to from the heart arteries ischemia caused and by sort of diffuse injury none of it reached classic values of statistical significance but it simply raised that concern i will say in our master's athletes we never saw it but but the person who's really done the most elegant work in this field is andre lagersch from melbourne and andre when he was a fellow with hein hybocal and then has evolved this this really important research program in melbourne has shown that

in fact it's the right ventricle that is most susceptible to fatigue and to injury so the right ventricle is the thin walled ventricle it's the one that pumps the blood to the lungs it's not under as much pressure we talked a lot about pressure in the beginning the pressure in the lungs are much less and so the size of the right ventricle is much less but relative changes during exercise are much greater so if your blood pressure goes from 120 to 180 and that's you know a small rise compared to if it goes from 20

to 60 a three-fold rise excuse me so in some people who do an extraordinary amount of exercise the right ventricle can get not only fatigued but injured and they can develop arrhythmias that put that look for all the world like life-threatening arrhythmias and that's called an exercise-induced right ventricular cardiomyopathy andrei really has anyone who's interested should just look up lagersh and uh right ventricular cardiomyopathy and i think you'll find an interesting question i'm pleased you said that because he just yesterday agreed to come on the podcast well andre i won't i won't then steal andre's

um andre yeah thunder but i will i will though say this because i think that there are some other groups then that we've learned that exercise can be dangerous probably the archetypal one is people who have a genetic disease of the desmosome the part of the heart that links and holds the muscle cells together and that's a genetic disease it's called right ventricular cardiomyopathy and we know from work done by the johns hopkins group um that if those patients who look fine and we know are carriers of the gene because we've studied them as part

of a family member if they train hard to become an athlete they have a much more rapid development and progression of their disease to life-threatening arrhythmias and death so having an underlying genetic abnormalities of the right ventricle is clearly dangerous we haven't yet identified if there is a another currently unrecognized gene or set of genes that put people at risk for this exercise induced right ventricular cardiomyopathy but all of us in the sports cardiology world have seen it and you know andre is the person who can discuss it with you at great length there are

other genetic cardiomyopathies that involve structural proteins the lamin ac protein is another good example and our italian colleagues have shown that carriers of that gene who participate in competitive sports have a much more rapid progression to heart failure and death so there are other genetic cardiomyopathies hypertrophic cardiomyopathy is one example where we don't yet know we in fact it may be that exercise is protective for them and we're currently doing some studies looking at high intensity exercise in patients with hcm charlene dave and sarah surberry published the reset trial showing that moderate exercise was safe

leslie linewein in colorado has used an animal model of hcm showing that if you create a transgenic animal that has that abnormality and you exercise train it when it's as it's growing they never develop the phenotype it's protective so we're still learning about that dynamic interaction between uh your inheritance and exercise training i don't know if you want to talk about atrial fibrillation or you want to do that there's actually a few things i wanted to bring up so so the concerns i guess that have been expressed here and there uh atrial fibrillation uh calcification

okay let me deal with those two things quickly let me deal with that calcification first because i've spent a lot of time studying that again with our colleagues at the cooper clinic and we have the advantage of having a huge database 25 000 people who we've quantified physical activity over decades and measured their coronary calcium and let me just tell you cut to the chase right the first thing is there is a slightly greater about a 10 risk greater risk of having a high coronary calcium score in people who do a lot of exercise so

can we just step back so we're talking about the calcium in the best cells of the coronary arteries is that right so talking about spark formation thing can we just explain that a little bit sure so so as atherosclerosis develops and heals it there it it does it by a process of calcification so so actually we're not worried about the calcium itself calcium calcified blood vessels don't rupture they don't cause heart attacks they don't kill people but it's the company that it keeps so um the presence of calcium in the blood vessels that we can

measure by a cat scan tells us that the atherosclerotic process is there and the more calcium you have the more atherosclerosis you have again it's not the calcium that's the problem but it tells you a good index of the volume of atherosclerotic plaque and there have been some cross-sectional studies in marathon runners for example and and even in younger individuals suggesting that athletes might have more calcification than not um and one study from sanjay sharma's group in the uk suggesting that yeah they have more calcium but if you use coronary ct angiogram which is a

different kind of a technique they can look at both the calcified and the non-calcified plaque the athletes had really more calcification but not more non-calcified plaque so they were at they could be considered at less risk but none of those studies looked at outcomes and that's where the cooper clinic data came in and we divided um individuals into low levels of activity moderate levels of activity and very high levels of physical activity so less than an hour a week versus more eight hours a week okay at the high end and we divided them into those

at a coronary calcium score less than 100 and that's a range where we don't worry about it so much and those at more than 100 that's when the risk of events starts to go up and there was absolutely no difference based on physical activity of the volume of coronary calcium so no evidence that exercise training increases the coronary calcium score what it did was increase the risk of having a higher calcium score that's a subtle difference but more importantly most importantly for the athletes that had low levels of calcium the people who did a lot

of activity there was a 25 reduction in mortality and events so being highly physically active if you've got a little bit of calcium was protective right and conversely let me just make sure i got that right it's um yeah so if i'm sorry let me say that again for those who had a coronary calcium score less than 100 that's a level that we don't worry about so much the high physical activity people um which is about 75 percent of our total cohort of 22 000 people had a 50 reduction in their rate of death or

having a cardiovascular mortality so that's hugely advantageous not disadvantageous yeah what about those those individuals who had a high coronary calcium score about 25 of our total cohort not only did they not have an increase in risk those who did eight hours a week of exercise it was a 25 percent lower risk didn't quite reach statistical significance so so my feeling is that number one higher amounts of physical activity do not cause associated with higher levels of coronary calcium and it doesn't increase mortality if anything it reduces mortality yeah okay great and the thing that

jumped out at me is and we and you sort of touched on it there was was even if there is higher because you see calcium calcification and you you know you i think you coined the term heart of stone you know from the rolling stones and i wrote that editorial yeah that sounds scary right but the point the thing that jumped out at me is is that the calcification of a plaque is sort of makes it stable and what you don't want is the sort of mixed unstable plaques they are the ones that become loose

and cause um you know heart attacks and strokes and whatever so that so that's that was really interesting now i wanted to say that there was a study done by the copenhagen city study that generated a lot of press by schnoor back in 2015 looked at runners and and they implied they implied that people who did a lot of running they called them strenuous joggers had a higher mortality than those who did only moderate jogging well what did they base that on right they based that on two deaths in 36 individuals and it wasn't even

close to statistical significance and they don't know why those people died i mean i don't know maybe they got hit by a car so the idea that strenuous jogging increases mortality at least based on that study is simply antenna and as you say there's all the studies the studies with all the olympic athletes that have a better health span a bit of lifespan it kind of reminds me a bit of um this is probably before a lot of people's time but remember jim fix played a big role in the running boom back in the 70s

he died on a heart attack while running so people said well you know running must be bad for you but the problem is his coronary arteries were like 99 percent occluded and then if you guys so a bunch of things that jim that people don't know about jim fix right so jim wrote the complete book of running and um but what most people don't know jim died at the age of 53 from a heart attack while running but before he took up running jim was obese dyslexic with a cholesterol over 300 he's a smoker and

he had a very strong family history his father died at age 43 so one could argue that that jim's exercise training gave him an additional 10 years of life so i think jim fix is not the archetype of this particular well i just think that's that's the sort of thing people jump on though right you know like oh i thought i thought exercise is good for you but jim fixed out of a heart attack while running you know and it's like hang on a minute he did not have a good background and his coronary arteries

were included and whatever and some people some people die while you know getting hit by a car while running so exactly but i guess it's fair is it fair to say though i mean exercise is undoubtedly good for you but if you've got 99 percent occluded arteries coronary arteries and then you start doing vigorous exercise that's putting your heart at a lot of strain right yeah no i think that that's true and and i think that running with uh ischemia that's the imbalance between supply and demand is not good for the heart and we there

is some data suggesting that that can actually induce scarring so i i think it's important that your audience not ignore symptoms tightness pressure uh while exercising particularly one that gets worse when you're running and gets better when you stop don't ignore that that's something that should be evaluated by a physician for sure can we just go back uh to the atrial fibrillation story sure these studies with skiers and they found that um the ones that did the most exercise had more atrial fib maybe if you just explain what atrial fibrillation is quickly and then yeah

so atrial fibrillation is the most common arrhythmia in the world particularly it's a rhythmia middle-aged men and women with hypertension and essentially the atria are the collecting chambers and they prime the ventricles um and they have multiple different purposes but they're at the top of the heart and the heart fills into the atria they they have they feel like a reservoir and then they prime the pump um just before the heart contracts and so they have a really important function and the body's pacemaker sits in the upper right hand corner of the right atrium and

that's what initiates the regular heartbeat it turns out that that many different cells within the atria can take over and have their own electrical activity and when that happens that the electrical activity can get very chaotic and the heart can be irregularly and fast it can reduce performance it can make you feel bad it can increase the risk of stroke and so there's a lot of work done trying to prevent it and treat it that's not really the topic of this of this discussion but i think there's little doubt that doing a lot of of

endurance exercise increases the risk of afib there's dozens of studies um meta-analyses and i think our feel it's the one thing that there's very little disagreement about that increa that endurance athletes are have about a five-fold increase above the population of atrial fibrillation non-competitive athletes probably not really nice study from tromso norway followed people um you know for 30 years 25 years and looked at their risk of atrial fibrillation and moderate or high levels of of physical actually doing no physical activity increase the risk of atrial fibrillation so it's sort of a u-shaped curve so

low is high risk moderate high levels are probably the nadir extreme exercise vigorous exercise starts to increase that risk and and they didn't by about twofold or so um not as much as the elite athletes which is about a five-fold increase now andre you should let andre talk to you dr laguerre about his damn model he and guido classen have published a beautiful study showing why that is during exercise the the valves between the atria and the ventricles close up and they because you want the blood to come out the aorta and the pulmonary artery

and as you increase the heart rate you increase the amount of time that the body spends with those valves closed at the same time you're pouring blood into the atria so the atria distend and they get stretched and we actually did in the study that i mentioned to you before we train middle aged people for two years we looked at their different components of their heart size and after one year we trained them with gradually increasing duration frequency intensity for about a year and then we kept them stable for the second year and what was

really interesting is their vo2 max and their left ventricular size kept getting bigger for that first year and then when we kept the dose the training load the same the o2 max didn't increase more and left ventricular size didn't increase more so just doing the same thing over and over again didn't dilate the ventricle but it did dilate the atria the atria continued to rise so the atria are thin walled and they're more likely to dilate with exercise than the ventricles and that's what increases the risk of atrial fibrillation and that doesn't necessarily increase um

disease risk anyway right because i thought one of the studies showed that the athletes that had the atrial fibrillation actually had lower risk of stroke and uh yeah well you know the risk of stroke with afib i think is something that that you have to consider carefully so the things that increase the risk of stroke are having known cardiovascular disease having hypertension having diabetes having um being much older particularly uh in with being female so that's that's called the chad's vasque ii score again beyond the scope of this particular discussion but you know an an

older athlete with hypertension and atrial fibrillation yeah i think you have to worry about stroke it's a devastating outcome so i just mentioning uh woman there females there i i couldn't help noticing as well that the study with the skiers found the ones that did the most exercise had the most atrial fibrillation but that was the males but in the females they didn't find that do you yeah and i think that there's a number of different reasons why that might be first of all there are a lot fewer number of females in the study so

it's a little bit harder to know i think they looked at over decades when women were not doing as much exercise as men i think modern data might show something different than women don't get the same hypertrophic stimulus that men do and we've demonstrated that that's another study by young investigator aaron howden now from melbourne showing that women don't hypertrophy as much to training as men do so they might be protected against that dilation to some degree actually just just getting back i've been meaning to ask about this extreme exercise sort of what's the definition

i guess do we have data on the real extreme exercises so you know people that are doing the the iron person behind me now now remember iron man extreme duration exercise is done at low intensity not at high intensity right we do know the ultramarathons in bill haskell study for example had improved laser dilator function and we did present at the american heart a couple of years ago an interesting study where we took the same cooper clinic group and we looked at those not just who did more than 3 000 but did more than 10

000 met minutes a week that's 30 hours a week we didn't have that many of them you know we had 66 that's three times the number in the in the schnorr study of course and you know how many cardiovascular deaths there were zero it's premature to worry about extreme exercise at least for coronary calcium okay right well hey i'm a big fan of exercise so so i'm more than happy to take the bottom line here that um exercise is good for people we could start nitpicking and saying what about this what about that and whatever

but for the 99 of people or more surely exercise is good for you good for the heart and take my uh my my prescription for life to heart that's the best way to keep your heart and vasculature healthy make it part of your personal hygiene not something that you add on but part of your life can i ask you one last thing here i saw something the other day saying that exercise cannot overcome a bad diet and i saw something i think you mentioned something about that in one of the papers i read i'm interested

in that so if you eat a crappy diet but you exercise you know with your sweet spot or you know the intensity duration etc what do you think happens there right so so i i what i think is that you can't expect exercise to be a miracle it's not so exercise is one part of overall cardiovascular health so if you're yeah i think that regardless of what your diet and your body weight and your other risk factors are exercise is better than no exercise but you can't expect being fit to overcome cigarette smoking and you

know a bad diet is a tough thing to talk about but high cholesterol levels cigarette smoking diabetes all those things will not be overcome by exercise so exercise is only one component of a healthy lifestyle perfect all right that makes sense let's have people have a normal mixed diet healthy diet fruit and vegetables exercise and live happily ever after literally okay at least not live well until your time comes yes so that improve your health span and hopefully your longevity okay well thank you very much for your time it's been fantastic and i'll catch you

later bye-bye my pleasure