0:00

Everyone. Has to get old some time.

0:02

but what if? at least for some

0:04

aspects of aging, we didn't have to

0:06

imagine if the loss of heart size

0:08

and the stiffness that often comes with

0:10

aging could be reversed, even well into

0:13

late middle age and not by a

0:15

little by a lot to days gas.

0:17

Dr. Benjamin Levine has shown that with

0:19

the right exercise protocol, people who are

0:21

sedentary most of their lives could reverse

0:23

up to twenty years of heart aging.

0:26

Doctor. Their been is one of

0:28

the world's leading expert and understanding

0:30

how the heart adapts under a

0:33

variety of conditions whether that's exercise,

0:35

elite athleticism, or hospital bed rest,

0:38

or even highly exotic conditions like

0:40

prolonged exposure to microgravity. He is

0:42

the founding director of the Institute

0:45

for Exercise and Environmental Medicine at

0:47

U Southwestern in Dallas, a leading

0:49

facility renowned for it's research and

0:52

cardiovascular physiology. His expertise also extends

0:54

into space Medicine, where he advises.

0:56

Nasa, underscoring his broad, deeply

0:58

fundamental understanding of how the

1:00

heart changes over time. Additionally,

1:03

he is a recognize authority

1:05

in sports cardiology consulting for

1:07

organizations such as The End,

1:09

C A N F L

1:11

N H L and various

1:13

professional sports leagues. The implications

1:15

of being able to reverse

1:17

any aspect of aging are

1:19

immense, but the key ingredient

1:21

truly is committing to the

1:23

process, doing their routines sometimes

1:25

boring. Stuff day in and day

1:28

out and sometimes embracing a little

1:30

challenge. To Dr. Levine's research highlights

1:33

the importance of ongoing commitment. It

1:35

is one of his landmark trials

1:37

that he is his team showed

1:40

that participants who had been sedentary

1:42

for most of their lives put

1:44

them on a structured, graduated training

1:47

regimen. This program culminated in five

1:49

to six hours of physical activity

1:51

per week, sustained over two years

1:54

participants to engage in a variety.

1:56

of exercises ranging from high intensity

1:58

interval training sessions like the Norwegian

2:01

4x4, to light aerobic activity on

2:04

recovery days and strength training. The

2:07

results were remarkable, demonstrating that it

2:09

is possible to reverse significant aspects

2:11

of heart aging with the right

2:13

commitment and exercise protocol. But

2:16

let's suppose for a moment our goal

2:18

isn't just to bail ourselves out at

2:20

the absolute last minute with some type

2:22

of Herculean effort and instead we ask

2:24

ourselves what we should have been

2:26

doing all along? What is

2:28

the right routine to age best?

2:31

From the start, Dr. Levine's research

2:33

also looked retrospectively at the hearts of

2:35

individuals based on their self-reported activity levels

2:37

over 25 years. It

2:40

was the committed exercisers alone, those

2:43

who consistently exercised at least 4-5

2:45

days per week who

2:47

saw significant benefits in staving off

2:49

the gradual increase in cardiac stiffening

2:51

and heart shrinkage seen later in

2:54

life. This highlights the importance of

2:56

exercise as part of your personal

2:58

hygiene and provides insight into how

3:00

much we should be exercising throughout

3:02

our life to maintain heart health.

3:05

However, as we push the boundaries of what

3:07

our bodies can handle, some

3:09

studies have raised concerns about the

3:12

potential risks associated with extreme exercise

3:14

such as high levels of coronary

3:16

artery calcification seen in marathon runners

3:18

and a greater risk of heart

3:21

arrhythmia known as atrial fibrillation in

3:23

veteran endurance athletes. Today,

3:25

Dr. Levine will help us explore

3:28

the balance between beneficial and

3:30

potentially risky physical activities, clarifying

3:32

how intense exercise regimens might

3:34

influence heart health differently and

3:36

what this means for those

3:39

who regularly engage in high

3:41

endurance activities. We delve

3:43

into whether the stabilization of plaque through

3:45

an exercise, an intense exercise, leads

3:48

to lower risk of cardiovascular events

3:50

despite the higher calcification levels

3:53

often reported. In this

3:55

episode, Dr. Levine and I also discuss

3:57

why 3 weeks of bed rest produces a functional

4:00

decline that is actually worse for fitness than

4:02

30 years of aging and

4:05

also how bed rest affects the size of

4:07

the heart mimicking aging, how to

4:09

make exercise a part of your personal hygiene

4:11

and some of Dr. Levine's key insights on

4:13

how to do that best. His

4:16

ultimate prescription for life, blending

4:18

resistance, aerobic endurance training and

4:20

more conventional programming like CrossFit

4:22

into one package to maintain

4:24

a youthful heart even into

4:26

older age. Whether CrossFit

4:28

counts as endurance training, resistance

4:30

training or both. Why

4:33

pure strength trainers should incorporate endurance

4:35

training and vice versa. The

4:37

number one sign you're over trained. Dr.

4:40

Levine's activity recommendations for recovery

4:43

days, practical lifestyle

4:45

protocols for lowering blood pressure, why

4:47

you shouldn't become an endurance athlete

4:49

just to live longer and so

4:51

much more. As a companion

4:54

to this episode, we've prepared a thorough

4:56

guide on omega-3 supplementation that I think

4:58

will be invaluable for anyone looking to

5:00

understand this complex topic more deeply. It

5:03

addresses the substantial benefits of

5:05

omega-3s for cardiovascular health confirmed

5:07

by numerous randomized controlled trials

5:09

and it also tackles the

5:11

nuances and potential risks, specifically

5:13

the recent discussions around omega-3s

5:15

and atrial fibrillation. In

5:18

the guide, you'll find a rigorous examination

5:20

of what makes a quality omega-3 supplement.

5:23

Options like purity, freshness, the bioavailability

5:25

of different forms and dosing strategies

5:27

that can elevate your omega-3 index

5:29

to a level linked through observational

5:32

trials with a significant increase in

5:34

life expectancy. We also

5:36

provide a critical analysis of

5:38

some of the top omega-3

5:40

supplement brands evaluating them based

5:43

on their performance and third-party

5:45

testing to ensure you're choosing

5:47

the most effective and safest

5:49

options available. I highly recommend

5:51

downloading this guide. It's available

5:53

for free at fmfomega3guide.com. Once

5:58

again, that's fmfomega3guide.com.

6:00

omega3guide.com. Now

6:03

let's get on to the core of today's discussion,

6:06

how exercise prevents and reverses aspects

6:08

of heart aging with Dr. Ben Levine.

6:12

I'm so excited to have you here, Dr.

6:14

Levine, and there's many, many things that I

6:17

really can't wait to talk about with you today,

6:19

but maybe we can start with bed

6:22

rest and the effects of

6:25

bed rest on cardiovascular

6:27

health. So you were part

6:29

of one of a very, I would say,

6:31

famous and informative studies, the Dallas Bed Rest

6:33

Study. Yeah, so actually I was

6:35

only 10 years old when that study was

6:37

first done, so my part arrived

6:40

much later. Thank you for that very

6:42

generous introduction. But the cardiovascular

6:44

community used to put people to bed

6:46

after heart attacks or things like that. That was

6:48

the standard of care. And

6:51

in the mid 1960s, my

6:53

mentors in Dallas, Jerry Mitchell,

6:55

Gunnar Blunkwist, and Banks-Sultene, some

6:57

of the most famous cardiovascular

6:59

physiologists ever, took five young

7:01

men and put them to bed for three

7:03

weeks, and then trained them for two

7:06

months. And frankly, almost

7:08

everything we've learned about the

7:10

cardiovascular adaptation to changes

7:13

in physical activity began with that study,

7:15

only five guys. And so,

7:18

like I said, I was only 10 years

7:20

old, so I didn't participate in that study.

7:22

But 30 years later,

7:24

we found those same five guys

7:27

and brought them back to Dallas to study them

7:30

and to compare the effects of 30 years

7:32

of aging with what

7:34

happened to them during bed rest.

7:36

And quite remarkably, not a single

7:38

person, not one, was in

7:41

worse shape after 30 years of aging

7:44

than they were after three weeks of bed rest when they

7:46

were in their 20s. So three

7:48

weeks of bed rest was worse for the

7:50

body's ability to do physical work than

7:53

30 years of aging. And

7:55

that observation really started us

7:57

on a whole series

7:59

of studies. studies trying to understand what's

8:02

the difference between a sedentary

8:05

behavior or

8:07

lying in bed or being physically

8:10

inactive and aging.

8:13

So when you say that 30 years

8:15

of aging was no worse than three

8:18

weeks of bed rest in terms of –

8:20

so what sort of physiological parameters are you

8:22

talking about? These were the five most

8:24

studied humans in the history of the world in

8:26

terms of all the studies that were done to

8:28

them. But the

8:30

sort of simplest is the maximal

8:32

oxygen uptake. That's the maximal amount

8:34

of oxygen that can be taken

8:36

in from the environment, brought into

8:38

the body by the lungs, transported

8:41

by the heart to the skeletal

8:43

muscle, and used to do physical

8:46

work. It's the exercise physiologist's marker

8:49

of fitness.

8:52

And so when we hear the

8:54

term cardio-respiratory fitness, that's what we

8:56

really mean. And

8:58

there are ways to estimate it. There are ways to measure

9:01

it directly. Many of

9:03

your audience will have seen or even participated,

9:05

had a mouthpiece in their mouth, and run

9:07

on a treadmill until they can't go anymore.

9:09

And that's how you measure the maximal oxygen

9:11

uptake. Back in

9:13

the 1960s, they did a lot of

9:15

other things. You should see the pictures

9:17

of these guys. They're catheters in the

9:20

arms, catheters in the bladder, catheters everywhere.

9:22

They measured heart size. There wasn't echocardiography

9:24

then. So they measured heart size

9:26

by x-ray. Now

9:29

that takes into account both the

9:32

muscle mass of the heart and its volume. And

9:35

the heart just shrunk and deadrest.

9:38

So the heart shrinks, the

9:40

muscles atrophy. And

9:43

that's probably the single most

9:46

important thing that happens, at

9:48

least to the heart. The

9:50

blood vessels adapt to meet

9:53

the demands it's placed on. So the

9:55

blood vessels kind of get a little

9:57

smaller. Also everything kind of contracts. probably

10:00

if I had to pick one thing that

10:02

would be the archetype of the bed

10:04

rest is the shrinking and atrophy of

10:07

the circulation including the heart. And

10:09

you said that they

10:11

were trained after bed rest. So

10:14

was this reversible? Well, that's really interesting,

10:16

right? Because out of those five guys,

10:19

three of them were just average Joes. You

10:22

know, they weren't athletic, they weren't sick,

10:24

they were just healthy college students.

10:27

Two of them were competitive athletes. One

10:29

was a semi-pro football player and

10:31

the other was a distance runner. They

10:34

all decreased by about

10:36

the same amount. They lost fitness.

10:40

But what was really interesting is that the

10:42

three guys who were relatively unfit quickly

10:45

returned to baseline and even got

10:47

fitter than they were beforehand. For

10:50

the fitter people, it took them

10:52

the full two months to

10:55

get back and even then they weren't quite back to

10:57

where they were. So

11:00

people whose bodies are adapted

11:02

and trained, they

11:04

lose the same amount, but

11:06

it may take them longer to get back.

11:08

And part of that may have to do

11:10

with the load that's placed on them. So

11:13

you have to kind

11:15

of build back up slowly after you've been in bed

11:17

for a while. And

11:20

it just takes, people forget how much load

11:22

they placed on themselves to get them back

11:24

trained. And you can't just pop into that

11:26

all of a sudden. You've got to build

11:29

up slowly when you've been in bed. And

11:31

we've learned a lot about this in the

11:33

COVID pandemic where people

11:36

went to bed and were placed in quarantine and

11:38

lost a lot of fitness. I

11:40

will tell you, to me, one of the

11:43

most compelling observations is what in

11:45

sticking with the COVID pandemic for a minute,

11:47

because really is the same concept.

11:50

So you've heard about long COVID, for

11:52

example, in people who have symptoms that

11:54

last more than three months,

11:57

12 weeks after their COVID infection.

12:00

Well, you know, we were very worried when the

12:02

COVID pandemic hit about what was going to happen

12:04

to the athletes, because we were worried that they

12:06

were going to get infected. We know that COVID

12:08

could infect the heart. We were worried it was going

12:10

to cause sudden death. And so we

12:13

were very intensely monitoring all

12:15

the collegiate athletes. And

12:18

out of hundreds,

12:21

if not thousands, of collegiate

12:23

athletes who

12:25

had COVID and went

12:28

through a brief quarantine, how

12:30

many do you think had symptoms that lasted more than

12:32

12 weeks? 1,600

12:34

in Brad Pettock's study. What

12:37

percentage do you think? Make a

12:39

guess. 0.06%

12:42

to people, 2 out of 1,600. Why

12:48

is that? It's not that athletes are

12:50

resistant to long COVID. No,

12:52

it's because as soon as they got

12:54

over their quarantine period, because

12:56

they were in a competitive

12:58

environment, they quickly returned to

13:01

a trainer

13:04

monitored and implemented return to

13:07

play program. So

13:09

it's really important for

13:13

almost any condition, as soon as that

13:15

forces you to bed, that

13:17

you have to get up

13:19

and start moving and progress

13:22

your training to return to

13:24

your baseline state. And in

13:27

some cases, you can do even better. So

13:29

is the hypothesis that after

13:32

being, let's say, in COVID's case,

13:35

exercise may help protect

13:37

against having this long

13:40

COVID? Absolutely. Now,

13:43

let me caveat that by saying some people

13:45

get really sick with COVID. And

13:48

COVID can affect the heart and the lungs and

13:50

the mitochondria and the muscles in the brain. There

13:52

are all sorts of things, legions of things that

13:55

can be injured by the body with

13:57

COVID. So we're not talking about those

13:59

people. because that's a whole

14:01

different story. We're talking about people who

14:04

didn't get that sick and

14:07

had to be placed in

14:09

quarantine, which often resulted,

14:12

if not in frank bed rest, at least

14:14

dramatic reductions in their physical activity. Well,

14:17

the other thing is that there was a lot of public

14:19

health messages that were urging people

14:22

not to exercise. I know, I

14:24

know. Because it was somehow,

14:26

I don't even know exactly where that was

14:28

coming from, but it was potentially dangerous. Well,

14:31

that's what we were worried about with the

14:33

athletes, right? Because

14:35

we would check them for

14:37

troponin, which is a marker

14:40

of cardiovascular injury. We do

14:42

echocardiograms. We check electrocardiograms. That

14:45

was called the triad. I

14:47

was part of the sports cardiology

14:49

council that laid out

14:52

those guidelines of the COVID

14:55

triad testing. What

14:57

we learned since is that that really

14:59

wasn't that effective unless

15:02

the individual or the athletes had cardiopulmonary

15:05

symptoms. If they had palpitations

15:07

or exertional shortness of breath

15:09

or chest pain, those are

15:11

the people who really needed

15:13

more intensive evaluation to

15:15

make sure that their bodies, their hearts and their

15:17

lungs had not been injured by COVID. We

15:20

then went on to do cardiac MRIs in a

15:22

lot of people, a lot of

15:24

athletes who had abnormalities in this triad.

15:27

If they didn't have cardiopulmonary symptoms, they

15:29

didn't have anything wrong with their heart.

15:33

We were deathly afraid of this

15:35

because, for example, in

15:37

the military, the most common cause

15:39

of certain cardiac death during

15:41

basic training is myocarditis.

15:43

That's an inflammatory infection of the

15:46

heart muscle by a virus. That

15:49

remains and persists as a diagnosis,

15:51

as a cause of certain cardiac arrest

15:54

in young athletes. So once

15:57

this COVID pandemic started, we realized that it

15:59

affected the whole world. the heart, we said,

16:01

oh my god, you know, the

16:03

streets and the playing fields are going to

16:05

be littered with the dead bodies of young

16:08

athletes. Fortunately, that was not the case. But

16:10

we were worried about it. And I think

16:13

it generated tons of publications and guidelines and things

16:15

like that. And we learned a lot from it.

16:17

You know, it gets us back to this

16:20

bedrest model that you had started talking

16:22

about in the original Dallas bedrest and training

16:24

studies, what we put people to bed for

16:26

three weeks. And a

16:28

lot of our high resolution physiology

16:31

experiments have used that kind of

16:33

two to three week model. And

16:36

because at least in the in the early

16:38

90s, that was what we were doing in

16:40

spaceflight, right bedrest is a model for spaceflight,

16:43

because you remove the head to foot gravitational

16:45

gradient. So from head to feet, there is

16:47

no gravity. So that's very expensive

16:49

to do work in space. So we use

16:51

bedrest as that model. But we put people

16:54

to bed for a longer time than that,

16:56

we've put people to bed for two weeks,

16:58

six weeks, even 12 weeks

17:00

of bed rest. And this is like

17:03

literally bed rest, like not getting up,

17:05

you can't even get up to use

17:07

the toilet. That's we're talking strict bed

17:09

rest. And, and that, you know,

17:11

that takes a little practice for people, by the way.

17:14

So, so how much of I

17:17

mean, it is this bed rest,

17:19

a almost accelerated aging model and,

17:21

and how much of

17:23

cardiac aging? What

17:25

is cardiac aging? How much is due

17:27

to being sedentary? That's a million dollar

17:30

question, isn't it? We found that the

17:32

heart loses about 1% of its

17:34

muscle mass a week in

17:36

bed. So it just

17:39

when we monitor people for 12 weeks, the

17:41

heart just got smaller and smaller and smaller.

17:44

Now, obviously, it can't get continued

17:47

atrophy forever. And we sort of use

17:49

spinal cord injury as a model for

17:51

what that plateau is, you know,

17:53

how low can you go? And it's

17:56

about 25%. So

17:58

patients with spinal cord injuries have a about a 25%

18:00

reduction in the mass of the heart. We

18:04

see the same things in young women with

18:06

a disease called POTS, or the Postural Orthostatic

18:08

Tachycardia Syndrome. We can talk more about that

18:10

later if you want. I know that's not

18:13

your prime focus. If

18:15

we take people and look either

18:17

cross-sectionally, if we train them, we

18:19

can see, you know, at least a

18:21

15 to 20% increase in the size of

18:23

the heart. And

18:26

if we look cross-sectionally, comparing

18:29

elite runners to spinal cord injury,

18:32

it's a 75% change

18:34

in cardiac muscle mass.

18:36

It's adaptable, plastic, responsive

18:38

to changes in physical

18:40

activity. So, you know,

18:43

we asked just the question that you asked, Rhonda, how

18:46

much of what we see with normal

18:48

healthy aging is due to becoming secondary?

18:50

One of the first studies we then

18:53

did to follow up on the Dallas

18:55

Bedressing Training follow-up study

18:58

was we went out and recruited a group

19:01

of extremely healthy, but

19:04

sedentary older people. It's not

19:06

so easy to do, by the way.

19:08

You know, these are people who had

19:11

no chronic medical problems, were taking no

19:13

medications except for perhaps cholesterol lowering medication,

19:17

but just didn't do any regular physical

19:19

activity. And we compared

19:21

them to a group of elite

19:23

master's athletes. These were individuals

19:25

who trained virtually every

19:28

day for much of their

19:30

adult lives and were competitive

19:32

at the regional and national level.

19:35

And we used

19:38

a technique that we developed in

19:40

my laboratory to estimate and to

19:42

quantify the, let's

19:44

call it the flexibility or stretchiness

19:46

of the heart's muscle. The

19:49

medical term is compliance, but it's really

19:52

how much will the heart stretch? And

19:55

we all think about aging, you know,

19:57

you think about aging of the skin, for

19:59

example. right, that it becomes

20:01

less stretchy, you know, it

20:03

can stiffer. And the analogy

20:05

I like to give people is with a

20:07

nice brand new rubber band, right? Take

20:09

it out of the box, stretch it,

20:12

it stretches great, right? Stick it in

20:14

your junk drawer, right? And come back

20:16

20 years later and take it out

20:18

of the drawer and try to stretch it again. It

20:21

doesn't really stretch, it loses

20:23

that stretchiness. And there are a

20:25

number of specific biological reasons why

20:27

that might be and we can talk about

20:29

that. But that becomes

20:31

a really good marker for the

20:33

cardiovascular system. The compliance or

20:36

the ability of the heart to

20:38

stretch and accommodate blood, not just

20:40

the heart but the blood vessels

20:42

also, is a marker

20:44

of the youthful cardiovascular

20:46

structure. So we

20:48

stick a catheter in the heart, we put it

20:50

into a vein in the arm, we

20:53

then unload the heart,

20:55

we reduce its volume by using

20:58

a procedure called lower body negative

21:00

pressure. Basically you put someone in a

21:02

box sealed at the level of the hips, hook

21:05

it up to a vacuum cleaner and suck. And

21:07

we can literally pull all the blood out of

21:09

the heart. So we can make the heart smaller

21:12

and measure the pressure and its

21:14

volume using echocardiography. Then

21:17

we give them a volume load, we put an

21:19

IV in and we blast saltwater into the heart

21:21

and we make it bigger, as big as we

21:23

can get it. And then we

21:25

look at the slope, the stretchiness of the

21:28

heart. And what we

21:30

found is that when we compared

21:32

the seniors to

21:34

the healthy young individuals,

21:37

we noticed that not only did

21:39

the heart shrink but it stiffened,

21:42

right? And then when we

21:44

looked at the elite athletes, their

21:48

hearts were indistinguishable from healthy 30 year

21:50

olds. So a lifetime

21:52

of endurance training at

21:55

a level commensurate with the competitive athlete

21:57

was sufficient to prevent that

22:00

aspect of cardiovascular aging. Now

22:03

that's really interesting from a physiological perspective,

22:05

but it's not a very good public

22:07

health measure. We

22:10

can't really expect everybody to be

22:12

a competitive master's athlete. So

22:14

the next question we asked was, okay, how

22:22

much exercise does someone

22:24

need to do over a lifetime to

22:27

preserve their youthful

22:29

cardiovascular structure? So

22:31

we turned to our colleagues at

22:34

the Cooper Clinic and we partnered with them. Cooper

22:36

Clinic is a center in Dallas

22:39

developed by Ken Cooper, where

22:41

they have tracked physical activity and

22:43

physical fitness for 40

22:45

years. I mean, Ken

22:47

was very prescient in starting that database, and

22:50

we've learned a lot from that, and

22:52

looking at people and tracking their fitness and

22:54

their physical activity over a very long time.

22:57

And we said, okay, we want you to help

22:59

us find people who over 25

23:02

years and multiple visits to the

23:04

Cooper Clinic have said on their

23:06

questionnaire, yeah, I do no regular

23:09

exercise. And we call

23:11

those people centenary, and we would allow so

23:13

two, less

23:16

than two days a week of

23:18

regular physical activity centenary. Then

23:20

we took people, okay, who did two

23:22

to three days a week, consistently

23:25

over their lifetime, we call

23:27

that casual exercise training. Then

23:30

we looked at people who did four to five

23:32

days a week, we call that

23:34

committed training, and then

23:36

a whole other group of master's athletes

23:39

who are called competitive training. And

23:42

when we did the same techniques, we

23:44

measured their heart compliance and their vascular

23:46

compliance, and lo and

23:48

behold, two to three days of exercise over

23:50

lifetime had no effect at all. It

23:53

did not protect against that

23:55

aging effect. Four to

23:57

five days a week got us most of the way.

24:01

close to the competitive athletes, not exactly the

24:03

same, not all the way there, but pretty

24:05

close. So that

24:08

gave us the sense that the optimal

24:10

dose, if you will, physical

24:12

activity is four to five days a

24:14

week over a lifetime, making it's

24:17

got to be part of your personal hygiene. We can

24:19

talk about that a little bit later. Because

24:22

then the next question we had to ask was, all

24:24

right, we studied our master's athletes

24:26

and our healthy sedentary people at age 70,

24:30

and our youthful people were at age 30. So

24:33

when in the aging process does this begin?

24:37

So we partnered with the

24:39

Dallas Heart Study, a large community-based,

24:43

very highly intensive

24:46

epidemiologic study. And

24:48

we looked at people who were in their 30s, in their 40s, in

24:50

their 50s, in their 60s, in their 70s. And

24:54

we did the same studies on them. And

24:56

what we found is that the

24:59

heart starts to shrink in

25:02

that late middle age period. You

25:05

know, if you think about aging at,

25:10

so late middle age is kind of that 50

25:12

to 65 period. Early

25:15

middle age is at 35 to 50

25:18

range. So the heart

25:20

will get a little bit stiffer, but

25:24

it's in that late middle range that

25:26

starts to atrophy and get really, you

25:28

can see the most dramatic effects of aging.

25:31

So we said, okay, well,

25:33

is this all reversible? That was sort of the question

25:35

you asked me earlier. And so

25:38

we took our healthy

25:40

seniors and we trained them for a

25:42

year. We

25:44

used the same training program that

25:47

we used in a group of young people, trying to make

25:49

them endurance athletes. Well, I

25:52

know you want to chat about that a little bit also. But

25:55

we put them, we trained them hard

25:57

and they got fitter for sure. but

26:00

we didn't change the heart structure at

26:02

all, not even a little

26:04

bit. So once

26:07

you got to be age 70, it

26:10

was virtually impossible to change the

26:13

heart structure. That was very

26:15

disappointing because we really thought we were going to

26:17

be able to reverse it. And

26:19

when we trained our young people, we sort

26:22

of very marked and

26:24

very impressive increases cardiac size and

26:27

compliance and things like that. But

26:31

we said, okay, what if we made

26:33

a mistake? What if we started too

26:35

late? And what if we

26:37

didn't train them long enough? And what

26:39

if we didn't train them hard enough? So

26:42

we then said, okay, let's take a group

26:44

of those late middle-agers

26:46

in the sweet spot. Let's

26:49

train them hard, train

26:52

them increasingly fit over a year,

26:54

and then sustain that at

26:56

our perfect dose, that four to five

26:58

days a week. And we'll

27:00

do that for two years. And

27:04

lo and behold, we were able to reverse

27:06

the effects of sedentary aging by

27:09

sustained training at the right dose,

27:11

at the right time period in

27:13

the aging process. So

27:17

that paper, which is published in Circulation, got

27:19

a lot of press. It

27:22

still is among the top 10

27:25

papers for something called Outmetrics,

27:27

which is the interest within

27:29

the media and the public

27:32

and the professional community, the top

27:34

10 in the history of Circulation,

27:36

which is the American Heart Association

27:38

Journal. Incredible. How

27:40

much would you say

27:42

the heart aging was reversed

27:45

in these mid-late

27:48

middle-aged 50-year-olds? Yeah, 50-year-olds.

27:50

So the answer to that is

27:53

from the standpoint of the youthfulness,

27:56

the compliance of the heart, most of it.

28:00

So we didn't get quite back

28:02

to being a healthy theriole, but we got

28:04

pretty close. So, you know,

28:06

there are a lot of other things that

28:08

happen with aging that are not just related

28:10

to the sedentaryness

28:12

of the circulation, of course.

28:15

You know, one of the things that happens is you

28:17

get accumulation of

28:19

advanced glycation end products. You know what

28:21

those are? Those are, yeah,

28:24

so those are the things that, not

28:27

you Rhonda, but other people

28:29

stiffen your skin

28:31

and cause wrinkles. We

28:33

measure it in diabetics with

28:35

hemoglobin A1C. It's

28:37

a natural biologic chemical

28:40

reaction called the maloid reaction. Your

28:42

audience is probably more familiar

28:44

with it from basting a turkey. What

28:47

do you think causes the crinkling and stiffening

28:49

of a skin when you base a turkey?

28:52

It's this reaction, this complexing

28:54

of glucose, sugars, with

28:56

carbohydrate, with collagen.

28:59

And it happens in the skin, it happens in

29:01

the blood vessels, it happens in the

29:03

heart. So we actually

29:05

gave a drug,

29:07

which doesn't exist anymore. I have the

29:10

last of it in my laboratory that

29:12

breaks advanced glycation end products. And

29:14

we gave it to another group of healthy

29:17

sedentary seniors. And one group just

29:19

got the advanced glycation

29:21

end product inhibitor. One

29:23

group got a placebo. Another

29:26

group did a year of training, just

29:29

training. And another group did

29:31

the advanced glycation end product

29:33

and training. So four groups. Just

29:37

taking the advanced glycation end product inhibitor

29:40

didn't do anything. It worked

29:42

in animals. We saw a

29:44

marked improvement in rats. Nobody

29:46

really cares that much about that

29:49

because we're not rats, but it

29:51

didn't help the sedentary humans. And

29:54

once again, we saw that a year of

29:56

training didn't do anything. But

29:59

When we added the... Training and they

30:01

advanced guy case and product inhibitor.

30:03

We have the equivalent of about

30:05

a sistine year reduction in the

30:08

appearance, vascular seeds of the circulation

30:10

in seven year olds in in

30:12

seventy or that. Says the

30:14

City advanced the kitchen and. Products It's

30:16

interesting because it's very as you

30:19

mentioned, tied to blood glucose regulation

30:21

and of course people with type

30:23

two diabetes or the extreme case

30:25

where Arab type one. Is lot like

30:28

they're not able to regulate their blood glucose. And

30:30

have probably the most. Risk

30:32

of having higher levels, advanced classes and

30:35

products and in a vast damage. At.

30:38

The So you mentioned. That the heart aging and

30:40

you talked about. Both the i

30:42

don't know She started with what When the

30:44

starts with the stiffening you said it is

30:46

stiffening until about middle age and then it

30:48

starts to shrink to the is that correct

30:50

address. So. The question is, it's

30:53

interesting, that and. You

30:55

are able to. Reverse.

30:57

This you know, cardiac aging in

30:59

these you know, late, late. Middle.

31:02

Age as dry on a little easier

31:04

like you know. So fifty to sixty

31:06

five sets are late middle age torso.

31:09

It So what you're You're already stiffening the blood vessels

31:11

at that. Point: You're probably

31:13

having some stiffening. That's

31:15

exactly is it's not

31:17

fully ensconced. You know

31:19

it's still reversible. By.

31:21

Then. Set. Up and says

31:24

so. The question is a be interesting to see

31:26

if there were like a subset of people to.

31:28

That let's say had. Low Very

31:30

low Hp When A when C

31:32

or something that did respond I

31:34

was it's a good question. Rondonia

31:36

As you think about it seem

31:38

a globe which is what we're

31:40

talking about. Movie measure Hemoglobin A

31:42

One See that in a last

31:44

one hundred and twenty days rights?

31:46

It doesn't. Those red cells don't

31:48

last forever right? So so that

31:50

that's why seem a woman a

31:52

one see as such a good

31:54

marker of diabetic control and blood

31:56

glucose his messenger Go those instantaneously.

31:58

Hemoglobin A One. See as

32:01

measuring the average over the

32:03

last few months because that's

32:05

how long hemoglobin last, but

32:08

college in last forever. So

32:11

once you've got cheated, it's done.

32:13

and that's why it's in a

32:15

measuring Graduated him of products in

32:17

the skin or in the vascular

32:20

shirts is a marker of something

32:22

over an even longer time scale.

32:24

You know? We we hoped to

32:26

be able to break all those

32:29

to be nice with you. I'm

32:31

not sure that we did this.

32:33

The animal date is very compelling.

32:35

We did not actually take cardiac

32:38

biopsies to prove that we had

32:40

broken. The advanced like a

32:42

son and products, right? We

32:44

just use the physiological consequence

32:46

and so one could argue

32:48

that we didn't even do

32:50

what we thought we did.

32:52

But I think I was

32:54

impressed enough by the combination

32:56

of exercise, training and breaking

32:58

their. An. Age Ease

33:01

of use that acronyms for

33:03

simplicity sake. That

33:06

I do think a play some role

33:08

as Odyssey. Not the entire issue I

33:10

be the says breaking them by themselves

33:13

didn't do anything but the combination of

33:15

the stretch. Of

33:17

the blood vessels and the

33:19

hard during exercise is perhaps

33:22

in stance or was perhaps

33:24

enhanced by breaking their desk

33:26

like is. So

33:29

what would you say to someone

33:31

who is in their seventies and

33:34

sedentary. And once to. Train.

33:36

Forty five days a week and said

33:38

you're talking about this two year study

33:41

A minute and I've I've looked as

33:43

I've read the methods such as soon

33:45

as it's a quite impressive I mean

33:47

this Sieber in other doing a lot

33:50

of physical activity and including a vigorous

33:52

intensity exercise in our weather during in

33:54

a very intense exercise at least once

33:56

maybe twice a week and. So

33:59

so what? you say to someone who's in their 70s,

34:01

I mean, how can they

34:03

improve their cardiovascular health? So

34:06

I'm not saying that we should throw our hands

34:08

up and saying, oh, it's too late because that's

34:10

clearly not true, right? I will say

34:12

if you hope to overcome 70

34:15

years of bad behavior, of

34:17

bad diet and sedentariness and

34:20

smoking, you can't make

34:22

that up with a couple of years

34:24

of exercise training when you turn 70. That

34:27

being said, there are a lot of

34:29

other benefits to exercise training that are

34:31

not related to cardiac structure, right? You

34:34

improve endothelial function. What I

34:37

mean by that is that

34:39

the arteries have a lining

34:41

inside them that is,

34:43

it's not like a lead pipe. It's

34:45

actually alive. It's biological. And

34:48

it allows for that smooth flow

34:51

of blood to, and then as

34:53

you need more blood, like during

34:55

exercise, those blood vessels start

34:58

to expand. So

35:00

the endothelium relaxes and

35:03

opens up the blood vessels and it's

35:06

damaged the endothelium with cholesterol

35:08

and hypertension and

35:10

smoking over years that causes

35:12

atherosclerotic disease. So

35:15

it's a very important biologic

35:17

phenomenon that is clearly improved

35:19

by exercise training at

35:22

any point in life. So

35:24

I think that's really helpful. I think we

35:27

know that exercise training alters

35:30

the autonomic control of the

35:32

circulation. The autonomic nervous

35:34

system is that part of the brain

35:36

and the nervous system that regulates those

35:39

things that we don't have to think

35:41

about. Like you're not sitting here saying,

35:43

what's my heart rate? Is it 60? Is

35:45

it 50? How do I make it 62? That

35:47

just happens in the background, right? The

35:50

autonomic nervous system has a break,

35:53

which is the parasympathetic nervous system.

35:55

You've heard the term vagal

35:58

responses and an accelerator. That's

36:00

the sympathetic nervous system. And

36:03

you're constantly balancing break and accelerators

36:05

throughout your life. During

36:07

exercise, you take your foot off the

36:09

brake, you withdraw the vagus nerve, and

36:11

you increase the sympathetic nerve. That's

36:13

what speeds the heart rate during exercise.

36:16

And that comes from signals and skeletal

36:18

muscle. That's how your brain

36:20

knows what to do during exercise.

36:23

So we know that if you –

36:25

this is going to be a little bit – I'm

36:27

going to take a step back for one second. We

36:29

know that if you have an

36:32

acute heart attack, and if I – in

36:34

a dog, if I tie off a coronary

36:36

artery with a little snare

36:38

while they're running on the treadmill, some

36:40

dogs will develop ventricular fibrillation and have

36:42

a cardiac arrest. And they'll do

36:44

it every single time. And if

36:47

we resuscitate them, and then

36:49

we put them on the treadmill and

36:51

stimulate the vagus nerve to the heart

36:53

and tie off the coronary, none of

36:55

them have ventricular fibrillation. They don't die.

36:59

And if you train them before

37:02

you tie off the coronary artery without

37:04

even stimulating the vagus nerve, you have

37:06

the same effect. So

37:09

the ability to increasing

37:11

in vagus tone or

37:14

neural activity in that parasympathetic

37:16

nerve may be very

37:19

protective against sudden cardiac death.

37:21

And those things will happen even if you start training

37:24

in your 70s. And

37:27

lastly, of course, is people get fitter. We

37:29

know I can make them fitter, right? I told you that.

37:32

And that's good. That's important because unfortunately

37:35

with aging, you get less

37:37

fit. Even if you're

37:39

a master's athlete, you get less fit. I

37:42

would be a fool if I sat here in

37:44

front of you and told you that exercise training

37:46

can completely prevent the

37:48

aging process. I wish that it could, but

37:51

it doesn't. But

37:53

one of the most important things is that

37:55

it preserves your aerobic

37:58

power, this VO2 mag.

38:00

And so think about a cliff,

38:04

right? And you're heading towards

38:06

that cliff with aging. And

38:08

that cliff is where the

38:10

maximal effort that you have

38:12

in your body that you can do is what

38:15

you need to do activities of daily living. That's

38:18

in that three to four metabolic

38:20

equivalent. That is the amount of

38:22

oxygen you need to just sit

38:24

here quietly. Three and a

38:26

half mLs of oxygen per minute per

38:28

kilogram of body mass. And

38:31

once you get to that, you're really kind of

38:33

in trouble, right? Because then everything you do in

38:35

life is a maximal effort. Well,

38:37

if that point is here, and you're

38:40

a master's athlete, and you're up here

38:43

when you're young, right, and you train all

38:45

your life, you stay above that

38:47

really well. If

38:49

now you're unfit, and you

38:52

don't exercise your life, and you're heading

38:54

towards that cliff, what you want

38:56

to do is change that trajectory, and

38:58

either push it up or flatten the

39:00

curve a bit, so that

39:03

you prolong that period before you

39:05

become disabled. And that

39:07

comes down to both endurance training

39:09

and strength training, because you need

39:11

both of those to be

39:14

able to maintain functional capacity. I

39:16

this is great. I do want to get it

39:18

a little bit more into both of those, the

39:20

cardiorespiratory fitness and what it means for longevity. But

39:23

just before a couple more questions on your

39:26

intervention study, exercise dose intensity.

39:29

So what about people

39:31

that, let's say they're

39:33

they're exercising, they're doing the committed

39:35

exerciser, right? They're four to five days

39:37

a week. Yeah. But they

39:39

think, well, I don't, you know, I'm exercising

39:42

frequently, I don't need to get my heart rate

39:44

up to a high intensity, you know, vigorous, whether

39:46

you're like 80, 85% max heart

39:49

rate. What do you think

39:51

about that is important? Because in your study,

39:53

at least in the two year intervention,

39:56

people were definitely doing vigorous intensity

39:58

exercise in addition. So

40:00

that's, I think, one of the more

40:03

challenging questions to sort out, right? Because

40:07

if you were – I know you were listening

40:09

carefully and reading carefully. I'm very quite impressed by

40:11

how prepared you've been to come

40:14

to this interview. But we

40:16

only stratified people by

40:18

frequency. That's, you know,

40:21

two to three, four to five, or six to seven. We

40:23

didn't stratify them based on how many

40:25

interval sessions they did or how long

40:27

was their long run. You

40:30

know, those are factors that

40:32

the other components of dose

40:35

includes not just frequency but

40:37

intensity and duration. And

40:39

you can imagine trying to quantify that over 25

40:42

years is kind of tough. People

40:44

can tell you, yeah, I trained Tuesdays and Thursdays.

40:46

I went out for a walk. You know, I

40:48

did my Zumba class. But if you ask them,

40:50

well, how hard did you work and what was your heart

40:52

rate and how long – you know, that's a little harder

40:54

to manage. So I think

40:58

that there clearly are advantages

41:00

to higher intensity exercise. There

41:03

are also greater risks. So

41:06

we know that exercise by

41:08

itself does tragically increase risk

41:12

for anybody at any time. And

41:15

that's greater risk with higher intensity.

41:17

Now that risk is relatively small.

41:20

And it depends on how fit you were to begin with. What do

41:22

I mean by that? Well, you

41:25

know, the classic scenario is, you

41:27

know, Detroit, Michigan, big

41:29

snowstorm. You know, the

41:31

dad goes out, hasn't done any exercise and

41:33

needs to shovel the walk, and he has

41:35

his cardiac arrest. Barry Franklin published those data

41:37

many years ago. And what

41:40

we know from a number

41:42

of studies is that that

41:45

risk of exercise is

41:47

dramatically higher if you're

41:49

unfit. So

41:51

it may go up a hundredfold

41:54

above background of

41:56

risk of exercise if you don't do anything. If

41:59

you're very fit – It may only go up 10% or 20%. Still

42:03

goes up, but it doesn't go up

42:05

by that much. So maintaining

42:07

fitness reduces the

42:09

consequences of intense activity.

42:13

But I think that we all

42:15

have bursts of

42:17

exercise during our lives, whether that be

42:19

running up the stairs, trying to catch

42:21

a bus or a train, running

42:25

after a kid, whatever. And

42:28

I think that we also know

42:30

that high intensity training relatively

42:33

has relative advantages over

42:35

lower intensity training for

42:38

improving maximal aerobic power. If

42:42

you're gonna ask me what does high

42:44

intensity training mean, that's a whole nother

42:46

discussion. I know you met with my

42:48

friend Marty Gabbala and had a discussion

42:50

with him many a few months ago.

42:52

So when

42:54

I think about aerobic power, I

42:56

like to think about Jan

42:59

Haff's 4x4, which

43:01

is the old Norwegian ski team

43:04

workout. Four minutes at 95% of max,

43:07

followed by three minutes of recovery, repeated

43:09

four times. Even if

43:12

you don't have a heart rate monitor on, it's basically

43:14

as hard as you can go for four minutes. And

43:16

at the end of that four minutes, you need to

43:18

be ready to stop. And

43:20

then at the end of the three minutes of recovery,

43:22

you need to be ready to go again. And

43:25

that's how you judge that intensity completely independent

43:27

of heart rate. And I think that if

43:30

I compare, you know, a 30 minute

43:33

moderate intensity session

43:35

versus a 30 minute 4x4, clearly

43:39

the 4x4 will have a

43:41

greater benefit on improving aerobic power

43:44

session per session. That

43:46

being said, over time, I

43:49

think there are great benefits to doing

43:52

more moderate intensity exercise. Also, it's lower

43:54

risk, it's easier to do. It's

43:57

emotionally easier for

43:59

many people. people. Others

44:01

love doing short duration burst activity. They say,

44:03

oh my god, I can get, I mean,

44:05

I can get the same benefit by only

44:07

exercising for four minutes, as opposed to 40

44:10

minutes, I'll do it. So it's very

44:12

individual. And at the end of the

44:14

day, certainly when

44:16

you look at a competitive athlete, no

44:19

athlete does just one thing. That's why

44:21

a lot of the studies in this

44:23

field are a little bit artificial. Because

44:26

I say I'm going to do only

44:28

moderate intensity training. There's a whole new

44:31

burst of enthusiasm for zone two training.

44:33

I mean, gosh, I've had about 10

44:35

interviews about what is zone two training.

44:38

For your audience, typically,

44:41

that means exercising hard enough

44:44

that you get a little sweat on your brow, you can

44:47

still talk but you're a little short

44:49

of breath. And I like to

44:51

tell people you can talk but you can't sing. That's

44:54

a good indicator of that higher

44:56

level of zone two training. So

44:59

the ideal strategy then

45:01

is to incorporate all kinds of

45:03

training. That's what the human body

45:05

is best at adapting to. It

45:08

doesn't really adapt very

45:10

well to doing the same thing over

45:13

and over and over again. You

45:15

will not get fitter if you do

45:17

that. And in fact, in our two

45:19

year training study, if

45:21

you read below the lines

45:23

a little bit, we

45:26

markedly upscaled people. These were completely

45:28

sedentary and we worked them very

45:30

hard for a year, including

45:33

multiple high intensity sessions,

45:35

prolonged sessions. But then

45:37

we said, all right, I want you to sustain that

45:39

for a year. So we dropped them to only one

45:41

interval session a week and one long session a week.

45:44

And we didn't increase the dose.

45:47

We didn't increase the frequency or

45:49

duration or intensity over

45:52

that last year. And you know what? They

45:54

didn't get any fitter. And their

45:56

hearts didn't get any bigger. The only thing

45:58

that got bigger was the atria. And we can

46:00

chat about that when we get to talking

46:02

about toxicity of exercise training. So

46:06

to come back to our point,

46:08

the human body doesn't adapt very

46:10

well to doing the same thing over and

46:12

over again. And so

46:15

my prescription for life, if you

46:17

will, is one that mixes things

46:19

up. So I suggest to

46:21

people that you spend at

46:23

least one day of a long session that

46:26

lasts at least an hour. And

46:28

it should be fun. I don't care what it

46:30

is. It could be going

46:32

square dancing. It could be a long walk with

46:34

your spouse or a long bike ride. It could

46:36

be some other class that you take, but it

46:38

needs to last over an hour and at least

46:40

to be fun. The second

46:43

thing you need to do is do one high

46:45

intensity session a week. I

46:47

like the 4x4. I

46:50

think it's very effective. There's great data

46:52

about it from the Norwegians. But

46:56

I don't care if you did 2x6 or

46:59

if you're a Marty Gabbal fan, if you

47:01

did 30 seconds times 8, it doesn't

47:04

really matter. Just do one

47:07

thing at high intensity and then do

47:09

two or three sessions of

47:11

that moderate intensity at least 30 minutes,

47:14

getting the talk test, and then supplement

47:16

that with one or two days of

47:18

strength training. And what I

47:20

mean by strength training, it doesn't mean you have

47:22

to go to the gym and pump iron. It

47:25

could be Pilates. It could be strength yoga, anything

47:27

that requires training of strength and skeletal muscle. And

47:30

if you do that over your whole life, I

47:33

think that's the best strategy

47:35

for preserving cardiovascular

47:37

health. Now,

47:39

if you tell me you want to run an Ironman,

47:42

you got to train different than that. Okay?

47:45

And that's a really important thing for

47:47

your audience to understand. Training

47:50

for health versus training

47:52

for performance. Every

47:56

coach knows how to train for performance. And

47:59

so... If that's your

48:01

objective, if your goal is

48:04

to have a competitive performance

48:06

objective, then you have to train

48:08

differently. If you tell me your

48:10

goal is I just want to preserve my health

48:12

and stay fit and have a good life, then

48:15

you don't need to train 30 hours a week. But

48:18

if you want to compete in Kona, you need to train

48:21

20 to 30 hours a week or you're not going

48:24

to be successful. I

48:26

think you've got to clearly

48:28

identify what your goal of

48:31

your fitness is and your goal

48:33

of your overall health and

48:35

that's what will guide your training program

48:37

over your life. Let me just

48:40

add one more thing. I can see the questions

48:42

circling around in your head. I

48:45

can't remember. I'll pop. We'll come back to

48:47

it later. Definitely a lot of questions and I'm trying

48:49

to figure out where to go first. I think the

48:53

cardio respiratory fitness and the

48:55

VO2 max and lots

48:58

of questions with that starting with you

49:01

talking about what your goal is. Do

49:03

you want to be a master's athlete? Do

49:06

you want to train for health and longevity?

49:09

I loved the way you explained the

49:11

cardio respiratory fitness and function, how it keeps

49:13

going down with age and how you want to stay

49:15

above this level. If you start way

49:17

up here, it's easier to go down. It's

49:23

going back to that same analogy like contributing to

49:25

your retirement fund. Dr. Brad Schoenfeld

49:27

talked about this in the podcast with muscle mass. It

49:30

applies to so many different areas and

49:32

cardio respiratory fitness is another one. If

49:34

you're starting way up here, then the

49:36

decrease with age, it's not

49:38

going to be as big of a deal functionally. Why

49:41

do you think cardio respiratory fitness

49:43

does correlate with longevity? The higher

49:45

the VO2 max, which is a

49:47

marker of cardio respiratory fitness, the

49:49

lower the mortality risk. I'm

49:52

going to remember your question. I remember what

49:55

I wanted to say. Let me go back to that. The

49:58

one thing I want to say is that But exercise

50:01

needs to be part of your personal hygiene.

50:04

It can't be something that you just add on at

50:06

the end of the day when

50:08

you're tired and you don't

50:10

really want to do it. It has to be part of

50:12

your life like brushing your teeth,

50:15

taking a shower, changing your underwear, having

50:17

breakfast. These are things you do to stay

50:20

healthy and exercise is one of those. The

50:23

mindset of people who sustain

50:25

exercise over a lifetime and

50:28

who are able to do

50:30

this over and over again

50:32

and who are able to stay fit

50:35

and healthy is that it's part of their lives. It's

50:38

not something they just add on. Right.

50:40

So you brush your teeth twice a day

50:42

because you don't want cavities. Well, you exercise

50:45

because you don't want cardiovascular disease. I mean,

50:47

there's other reasons you exercise too. But

50:50

yeah, I love that part of your hygiene where

50:52

it's not just, oh, it's the thing I have

50:54

time for. Oh, shouldn't I have to go on

50:57

the moon? Right. No, you

50:59

do it. It's like just like your best for teeth.

51:02

So the VO2 max and longevity

51:04

correlation, why

51:06

do you think VO2 max correlates

51:08

with longevity? So first

51:10

of all, I think it's important to

51:13

realize that correlation is

51:15

relatively weak. I mean, obviously,

51:17

when we're talking about

51:19

the effect of aerobic

51:21

power on longevity, there's

51:24

a number of reasons why I

51:26

think that relationship exists. First

51:29

of all, if you're not sick, it's

51:31

easier to exercise hard and preserve your

51:33

aerobic power. So there is

51:35

a bias associated

51:37

with looking at those

51:40

factors regardless of how well you try

51:42

to control for them statistically. That

51:45

bias exists. There's nothing you can do about

51:47

that. It certainly helps to be well enough

51:50

to continue to train and be fit. So

51:52

if you get cardiovascular

51:54

disease or cancer

51:57

or neurologic disease, it's harder to

51:59

sustain. your fitness. And

52:01

so just be a little bit

52:07

more careful. famous

52:11

equation called the thick equation,

52:13

which relates VO2, that's the

52:16

volume or the ventilatory

52:20

oxygen uptake. I

52:22

started this podcast by talking about what

52:25

that means, but it's

52:27

a function of two things, the cardiac

52:29

output, that's how much blood the heart can

52:32

pump, and the AVO2

52:34

difference, the arterial venous oxygen difference,

52:36

which is how much oxygen is

52:38

extracted in the skeletal muscle. The

52:40

cardiac output is also a function

52:42

of two things, heart rate

52:45

and stroke volume. Stroke volume is the amount

52:47

of blood that the heart can pump per

52:49

beat, so the heart relaxes,

52:51

and when it's done relaxing, that's

52:54

the end diastolic volume, the time

52:56

when the heart is completely relaxed

52:58

at its biggest, and then

53:01

it contracts and pushes that blood out,

53:03

that's the end systolic volume, and

53:07

the difference between those two is

53:09

the stroke volume. And

53:11

so the stroke volume times the

53:14

heart rate is the cardiac output.

53:16

Now let's look at an elite

53:18

athlete versus a sedentary person. An

53:20

elite athlete can extract more oxygen

53:23

than a sedentary person, but

53:26

not so much more. It's

53:28

not a lot more than

53:31

a sedentary person. And

53:34

the heart rate, the max heart rate

53:36

of an elite athlete, if anything, is

53:38

lower than that of a sedentary

53:40

person. So the biggest difference

53:43

between being sedentary and have high

53:45

levels of aerobic power is

53:48

having a big stroke volume. So

53:50

having a heart that is nice and

53:52

stretchable and compliant, that can relax

53:54

to a large amount, that let your muscles

53:57

pump blood back to it, and can... contract

54:00

strongly and vigorously and pump that

54:02

blood out into the blood vessels.

54:05

That is the biggest adaptation that

54:07

allows you to be an elite athlete.

54:09

Well, that goes back to your,

54:12

you know, how exercise improves cardiac

54:15

structure and function because the heart's

54:18

not atrophying, it's getting bigger

54:20

and it's not stiffening, it's

54:22

being more stretchable. Exactly. Exactly.

54:24

So I think that there

54:26

are clear advantages into heart

54:28

structure and vascular function by

54:30

sending all this blood out

54:32

and pumping large amounts of

54:34

blood. In a

54:36

healthy vascular

54:38

system, the aorta and

54:40

the large blood vessels accommodate

54:43

that blood. It's called the

54:45

wind kessel effect. When the

54:47

heart pumps the blood into

54:49

the aorta, it expands. That's

54:51

why it needs to be

54:54

nice and compliant. And

54:56

then in between heartbeats, it releases that

54:58

blood into the rest of the circulation.

55:01

So that sustained dilation

55:03

is what requires

55:05

a flexible arterial system

55:07

as well as a flexible heart.

55:10

And the heart and the blood vessels are coupled together

55:12

very tightly. That's called ventricular arterial

55:15

coupling in the physiology world. But

55:18

they need to be coupled. And I

55:20

think having a nice regular

55:25

flexible aorta becomes really essential. Of

55:27

course, if you've got aortic diseases,

55:30

Marfan syndrome, for example, genetic diseases

55:33

of the blood vessels, then exercise

55:35

can be quite dangerous for some

55:37

of those people. And the aorta

55:39

can tear. That's called an aortic

55:41

dissection. So we know that exercise

55:43

clearly does drive more blood out

55:45

into the aorta. So

55:48

I think that the advantages

55:50

and the reasons why high

55:52

aerobic power improves mortality is

55:54

it preserves vascular structure, improves

55:57

endothelial function, optimize

56:01

autonomic tone preserves

56:03

the mitochondrial function. The

56:05

mitochondria are those little

56:08

energy producing organelles,

56:11

subcellular things within your skeletal muscle,

56:14

within your cardiac muscle, even within

56:16

your brain which utilize all that

56:18

oxygen. So it preserves

56:21

the energy producing architecture

56:23

of many of your

56:26

organs. And all those

56:28

things are advantageous in leading to

56:30

mortality. Now, or

56:33

preserving of mortality. Now,

56:36

you know, you have to ask yourself what kills

56:38

people? Right? Well, one thing

56:40

that kills people is cardiovascular disease.

56:42

And again, I wish I

56:44

could tell you that exercise completely protects

56:47

you from cardiovascular disease. It does not.

56:50

Athletes get hypertension, they have high

56:52

cholesterol, there

56:54

are genetic effects that influence the

56:56

development of cardiovascular disease. So exercise

57:00

will not provide

57:03

immortality, right? But it

57:05

will help you manage

57:07

those diseases of

57:10

human life. There

57:12

is some evidence that exercise can

57:14

be protective against certain kinds of

57:17

cancers. That

57:19

evidence has been challenged recently but

57:21

I do think the overwhelming weight

57:23

of the evidence is that it

57:25

reduces the risk of breast

57:28

cancer and colon cancer. And

57:30

how it does that, I'm not 100% sure,

57:33

but I think increasing blood flow

57:35

on a regular basis is

57:38

beneficial. And it of

57:40

course by utilizing energy, it helps

57:43

to prevent diabetes. And if you have

57:45

diabetes, it helps to manage diabetes. It

57:48

increases blood flow to the brain and

57:51

has some modest effect about

57:53

preventing dementia. It will

57:55

not prevent you from getting Alzheimer's disease.

57:57

If you're genetically inclined, I wish we

58:00

completely understood why people get it.

58:02

We don't. But it certainly will

58:04

reduce that risk. So I think

58:07

it is a combination of

58:09

the physiologic adaptations to exercise

58:12

at every step of that oxygen

58:14

cascade, the heart muscle, the blood

58:17

vessels, the mitochondria, the sustained

58:19

high rates of energy expenditure

58:21

of multiple

58:24

organs that help to protect

58:26

and improve mortality with higher

58:28

levels of fitness. You've,

58:31

I'm sure, seen this drama study in

58:33

2018 that was published in Looking at

58:36

Cardiorespiratory Fitness and Mortality. And the

58:40

interesting thing to me about that study

58:42

wasn't so much that, okay, well, if you're

58:44

low cardiorespiratory fitness, you have a five-fold increased

58:46

mortality rate over people that are more elite.

58:49

So they're in the top 2.3% of cardiorespiratory

58:53

fitness. But what was so interesting to

58:55

me, and again, you mentioned

58:57

reverse causation. So that's obviously people that

58:59

are more fit are able to exercise

59:02

more with that in mind. The

59:05

fact that when all these

59:07

other, you know, diseases or negative habits

59:10

were looked at, for example, smoking, it was,

59:14

at least by the data and the hazard ratio,

59:16

it was clearly worse to be in the low

59:19

fitness groups. So the bottom 25% of the population

59:23

that was looked at, it

59:26

was, they had a higher risk of mortality

59:28

being in that low fitness group

59:30

than smoking. Right. So be a

59:32

little bit careful about that. For

59:34

your audience, what's been being what

59:36

often is reported in literature is

59:39

relative risk, not absolute

59:41

risk. So there is

59:43

a protection of one compared to

59:45

the other. But for example,

59:47

if being low fit were to be a low

59:50

absolute risk, then a little

59:54

bit of protection doesn't, you know, if let's

59:56

say your risk of dying in the

59:58

next 10. years is

1:00:01

1%, okay? And

1:00:03

I reduced that risk by 50%, 1.5 hazard

1:00:10

ratio. I've only reduced your risk by 0.5%.

1:00:12

So the absolute benefit is relatively

1:00:16

small. So you sent

1:00:19

me that paper and I of course

1:00:22

I was aware of it. It's by

1:00:24

my good friend Dermot Thielen when he

1:00:26

was at the Cleveland Clinic and his

1:00:28

team there. So I know the data

1:00:30

well. We knew about that when we

1:00:32

put together the scientific statement for the

1:00:34

American Heart Association suggesting the cardio respiratory

1:00:37

fitness be included as a vital sign.

1:00:39

You know the same thing as your blood pressure

1:00:41

and your body weight when you go to see your

1:00:43

doctor, you're supposed to get and have them ask you

1:00:45

what's your fitness level. There are

1:00:47

ways to do that within the electronic medical

1:00:49

record now. Simple Liz

1:00:51

Joy and Bob Salus

1:00:54

when they were both presidents of the American

1:00:56

College of Sports Medicine have pushed the exercise

1:00:59

vital sign which is very

1:01:01

simple. How many days a week do you exercise?

1:01:04

Enough to get a little bit of sweat

1:01:06

on your brow and make you a little short of breath.

1:01:09

And how long do you do it? Multiply

1:01:11

frequency times duration, get your physical

1:01:14

activity vital sign. So your doctor

1:01:16

should be asking you that or if he isn't,

1:01:18

he or she isn't, you should tell them. But

1:01:24

so when you come back down to that

1:01:26

Cleveland Clinic study, remember there are two things.

1:01:28

First of all, these

1:01:31

were people who referred for exercise

1:01:33

testing. These were not healthy people.

1:01:35

Okay, these are people all who

1:01:37

had some complaint. Some of

1:01:39

them had valvular disease, some of them had heart

1:01:41

disease. None of them were

1:01:43

a fitness test on a competitive athlete.

1:01:46

And if you look at elite

1:01:48

fitness level, they are

1:01:50

nowhere near elite. The peak

1:01:52

VO2 in the young people

1:01:54

was 50 ml per kg

1:01:56

per minute. I mean

1:01:58

that's 50% less than

1:02:01

a competitive athlete at that level. So

1:02:04

calling them elite was a little bit disingenuous

1:02:07

in my mind. They were

1:02:09

the top percentage of people referred for

1:02:11

exercise testing, but they're nowhere

1:02:13

near elite. These are not people

1:02:15

doing 10, 12, 15 hours

1:02:18

of exercise a week. This

1:02:21

is 50 mLs per minute

1:02:23

per kilogram. That's an average

1:02:25

fit. Good fit, but good fit

1:02:27

young person. So

1:02:33

by looking at percentages of

1:02:35

predicted of healthy

1:02:37

people, you can get a

1:02:40

little bit of a different perspective. So I

1:02:42

don't think you should take the message home

1:02:44

that there's no upper

1:02:47

limit and you can just keep on training and

1:02:49

you'll keep getting better. I

1:02:51

do think the message that fitness is

1:02:54

as important as other cardiovascular risk

1:02:56

factors is critical. And I

1:02:58

think that's a very important take home message. I

1:03:01

don't put too much stock in comparing

1:03:04

relative risk scores. I don't think that's

1:03:06

helpful without knowing the absolute risk data.

1:03:09

But my friend Steve Blair used

1:03:11

to say, I'd rather be fit and

1:03:14

fat than lean and sedentary. Yeah,

1:03:16

it sounds like the measuring

1:03:18

your cardiorespiratory fitness is

1:03:21

at the very least a good biomarker of

1:03:24

your health. And like you

1:03:26

said, relative risk. Well, so you're talking

1:03:28

about a 30-year-old. Yeah, their

1:03:31

risk of death is quite low. But when you start

1:03:33

to get to 70, you got a 75-year-old male, their

1:03:37

VO2 max, that absolute

1:03:39

risk matters more, right? Because they

1:03:41

do have a higher risk of dying from

1:03:44

heart disease or whatever, right? Age-related diseases.

1:03:46

We're not going to get rid of

1:03:49

that. We're not going to extend the

1:03:51

human lifespan forever. But you're

1:03:53

right. I think that, and we made a strong case

1:03:55

for that in our scientific statement.

1:03:58

I do is

1:04:00

as important as smoking and as hypertension

1:04:03

and they have different treatments,

1:04:05

right? So I

1:04:07

think the other thing to be careful about

1:04:10

is there is some data from

1:04:12

the Cooper Clinic mostly but also

1:04:15

from others. Jonathan Meyers at the

1:04:17

VA in California has shown that

1:04:20

if you measure

1:04:22

fitness at one particular point

1:04:24

in time, people who gain

1:04:26

fitness gain

1:04:28

advantage equivalent

1:04:30

to people who have sustained fitness and

1:04:33

people who lose fitness lose that

1:04:36

advantage. There are much fewer studies

1:04:38

of changes in fitness over time

1:04:40

as there are about a single

1:04:43

point measure. So you have to

1:04:45

it's the data are not as

1:04:47

robust as what happens if you

1:04:50

stop smoking or what happens if you treat high

1:04:52

blood pressure or what happens if

1:04:54

you treat high cholesterol. Those

1:04:56

data are hundreds of thousands

1:04:58

of people, really high

1:05:01

quality clinical trials treating

1:05:03

these diseases. So we

1:05:06

know what the outcome is.

1:05:08

I know less about what

1:05:10

happens if I take a 50 year

1:05:13

old and I train them and I increase

1:05:15

their VO2 max by 10 or 20 percent,

1:05:18

what does that do to their subsequent

1:05:21

mortality? I don't know that

1:05:23

as well. There

1:05:25

are data there. I

1:05:27

think they're encouraging but

1:05:29

they're not as certain for

1:05:31

example. So I know for sure

1:05:36

that I need to lower your blood pressure if it's too

1:05:38

high and I

1:05:40

think our targets are getting progressively

1:05:42

lower. Same thing with cholesterol.

1:05:45

I know for sure that treating it

1:05:47

will lower your risk of having a

1:05:49

heart attack for example or having cardiovascular

1:05:51

outcomes. So I

1:05:54

do think that measuring your fitness

1:05:56

gives you a leverage to say

1:05:59

okay let's improve that fitness and

1:06:02

there are many reasons to do it beyond

1:06:04

mortality. You know,

1:06:06

I view lifespan as only

1:06:08

one objective of

1:06:10

healthcare. Healthspan

1:06:13

is at least if not more important. Certainly

1:06:15

that's true for me. Right. I

1:06:19

also think that you mentioned the

1:06:24

changes in VO2 max and so like if

1:06:26

you're not, you know, improving, you know,

1:06:29

at a certain point like you mentioned earlier

1:06:31

about like people that are doing the same

1:06:33

thing, for example, they're not really improving their

1:06:35

cardiorespiratory fitness and I'm wondering if

1:06:37

that also goes back to this non-response,

1:06:40

like what is this non-response

1:06:42

where people will, they'll meet the

1:06:45

requirements for, you know,

1:06:47

physical activity guidelines, they're doing two and a

1:06:49

half hours of exercise a week and

1:06:52

yet they can't improve their cardiorespiratory

1:06:54

fitness. So I think there

1:06:56

are a couple of things to think about there. Number

1:06:59

one is if

1:07:01

those people were doing nothing, they would be a lot

1:07:04

less fit. Okay. That's for

1:07:06

sure. And I can

1:07:08

make almost anybody fitter

1:07:10

and there's a little bit

1:07:13

of disingenuousness about the non-responders

1:07:15

also. It's non-responders to

1:07:17

the dose that they've been given.

1:07:20

So same thing like saying, you telling me, look,

1:07:22

you know, when I take one Tylenol, it doesn't get

1:07:25

rid of my headache, but if I take two, it

1:07:27

gets rid of my headache. My husband, he does

1:07:30

fine with just one Tylenol, right?

1:07:32

So I think there is a dose response

1:07:34

of exercise just like there is for any

1:07:36

other medication. That's one of

1:07:39

the rationales behind Bob Salus' exercise

1:07:41

is medicine. And so

1:07:44

Carson Lundy and his group in Copenhagen

1:07:49

have shown very clearly that

1:07:51

if you take someone who's

1:07:53

a non-responder, non-responder in quotes,

1:07:56

and increase their training dose, they

1:07:58

all improve. So I

1:08:01

don't think, I'm sure

1:08:03

there must be some people who are

1:08:05

non-responsive, but in our study, in

1:08:07

Erin Houden's study, Erin now

1:08:09

is a player and cardiovascular

1:08:13

expert at the Baker Heart Institute in

1:08:15

Melbourne, Australia. In her study

1:08:17

about the two-year training in the 50-year-olds,

1:08:20

we had zero non-responders, zero.

1:08:24

Right. But you were also adding

1:08:26

in, I think, some of those non-response, like you

1:08:28

said, the dose changes or the intensity of the

1:08:30

add-in, some high intensity, all of a sudden they're

1:08:32

responding. Exactly. So again, going back

1:08:35

to your point where, you know, mixing it up and, you

1:08:37

know, you do want to continually challenge yourself, right? I mean,

1:08:39

you don't want to just do the same thing every single

1:08:41

day. Right. And I think that there's a number

1:08:43

of benefits to that. We're talking now as a,

1:08:45

you know, how do you adjust your

1:08:48

hygiene, right? I'm not necessarily

1:08:51

saying that you want to do things

1:08:53

to steadily improve your fitness progressively over

1:08:55

a lifetime. I think that's almost impossible

1:08:57

to do. You want to

1:08:59

achieve a level of fitness and sustain that

1:09:01

over life. That's a difference.

1:09:04

And we're coming back then to the

1:09:06

performance versus the health benefits of exercise.

1:09:09

So I think doing the same thing over and

1:09:12

over again is, for

1:09:14

some people, they love it. They find that very

1:09:16

satisfying. And doing that and preserving

1:09:18

their fitness, I think, is important. For

1:09:21

some people, it gets boring and

1:09:23

they want to mix it up, you know,

1:09:25

and they want to change what they're doing.

1:09:27

And that gives them more joy and it

1:09:29

also helps them stay compliant

1:09:31

with physical activity over a lifespan.

1:09:34

So I think those and

1:09:36

my own biases that the different

1:09:38

kinds of exercise have different roles

1:09:42

in improving and preserving

1:09:45

fitness over a lifetime. I

1:09:47

mean, if you want to run your 5K faster, you

1:09:50

got to train harder. You know what I

1:09:52

mean? But if you go, look, I'm happy

1:09:54

with my 30-minute 5K and I don't care

1:09:56

about running that faster. I just want to

1:09:59

stay well. then increasing the

1:10:01

dose has less benefit for

1:10:03

you. So

1:10:09

you're mentioning the stroke volume being really important

1:10:11

for cardiorestory fitness. I mean, is that the

1:10:13

limiting factor? Like is that how, what

1:10:16

is the limiting factor for improving your

1:10:18

VO2 mux? Right, so I think that

1:10:20

for a lead competitive athlete,

1:10:26

the stroke volume and the cardiac output

1:10:28

are the limiting factor. And

1:10:30

I know this because, I mean, if I

1:10:33

blood dope them and I give them

1:10:35

more blood, their muscles can accept that just

1:10:37

fine and they get faster, right?

1:10:39

So it's just the ability to get that

1:10:42

blood to the muscle that's important. The muscle

1:10:44

has a lot of reserve. And

1:10:46

you know, obviously there comes a point where you

1:10:48

can't make the heart any bigger. But

1:10:51

I do think that that is the

1:10:53

primary difference between the elite of the

1:10:56

elite and the sub elite. Now that's

1:10:58

different if you told me I've got

1:11:00

a 50 year old

1:11:02

guy who wants to start training or

1:11:05

a patient with hypertrophic

1:11:07

cardiomyopathy, a genetic

1:11:09

disease of the heart muscle. James McNamara

1:11:12

at our institution has been studying how

1:11:14

you make, those people fit or

1:11:16

they've been told their whole lives don't train. Because

1:11:21

earlier data suggested that patients with that

1:11:23

kind of genetic disease were at risk

1:11:25

for dying during exercise. Turns

1:11:27

out that now the evidence in the

1:11:29

last couple of years have become much

1:11:31

more obvious that those

1:11:33

types of individuals can safely train.

1:11:35

And in fact, regular physical

1:11:38

activity and fitness is critical to their

1:11:40

survival. Some animal data

1:11:42

suggesting that if they train when they're young, it may

1:11:45

even prevent the full expression of the disease.

1:11:48

We're working on that right now. But

1:11:51

those kind of individuals, particularly some

1:11:53

who may be limited by cardiac

1:11:56

limitations will improve their ability of

1:11:58

the muscle to experience. oxygen.

1:12:01

And I think when you get to the top

1:12:05

of the slide, you can see that the oxygen is optimized.

1:12:08

Maximum lung function, maximum cardiac function,

1:12:11

maximum muscle function, and they are

1:12:13

all linked together in the entire

1:12:15

oxygen cascade.

1:12:18

For people who are sub-elite, who have not

1:12:22

raised each particular part of that physiological

1:12:26

process to their limits, can improve

1:12:30

VO2max by increasing oxygen extraction.

1:12:32

They can increase the number and size of mitochondria.

1:12:37

They will increase their AVO2 difference. They

1:12:39

can't increase

1:12:42

it forever. So you increase that,

1:12:44

and particularly if you've

1:12:46

got a cardiac limitation. If you're

1:12:49

sedentary and don't have one, you

1:12:51

may increase both in

1:12:54

parallel. But it's the cardiac limitation

1:12:56

that gets, differentiates the highest levels

1:12:58

of aerobic power,

1:13:02

fitness, from the less lower. And let me give

1:13:04

you an example. We tried, we took a group

1:13:06

of young people,

1:13:11

because I wondered how much

1:13:13

of this extraordinary

1:13:17

aerobic power is genetic and how

1:13:19

much is trainable. So we

1:13:21

took a group of sedentary young people, in their 30s, and I

1:13:23

trained them to be marathon

1:13:26

runners. I trained them to

1:13:28

be successfully complete, either a marathon

1:13:31

or a 100 mile bike ride. And

1:13:35

we made them a lot fitter, some

1:13:37

of the largest gains in heart size

1:13:39

and fitness than anyone's ever seen, including

1:13:43

long duration, two hour, up to

1:13:45

two hour runs on the

1:13:47

weekend, multiple workouts, high

1:13:50

intensity sessions over the week.

1:13:52

I threw everything I could

1:13:54

at them. And frankly I

1:13:56

couldn't make their mates as big as our

1:13:58

competitive athletes. You know, I just

1:14:01

like the lifelong competitive athletes. No,

1:14:03

no, these are young people. These are

1:14:05

30 So well lifelong up until then

1:14:07

right so high-level competitive athletes. I

1:14:10

just couldn't get the heart size the same They

1:14:12

got a lot bigger but not the

1:14:14

same. I've wondered why that is

1:14:19

One thing to remember is that

1:14:21

the heart is constrained by a

1:14:23

stiff Fibrous sack called

1:14:25

the pericardium and the

1:14:28

pericardium is really important It

1:14:30

it allows the right and the

1:14:32

left ventricles to function together Remember

1:14:35

the right ventricle pumps blood to the lungs the

1:14:37

left ventricle pumps it to the body and

1:14:39

they work in concert so

1:14:42

that pericardium preserves

1:14:44

that ventricular interaction

1:14:46

in a positive way and it may

1:14:49

be that Training for one

1:14:51

year or maybe even two

1:14:53

years isn't enough to stretch

1:14:55

that pericardium The myocardium scotum

1:14:57

muscle is very adaptive the

1:14:59

pericardium less so It's

1:15:02

also possible That

1:15:05

you have to train when you're growing to get

1:15:07

the biggest bang for your buck That

1:15:10

you know, obviously the pericardium Constraints

1:15:13

the heart of a baby as much

1:15:15

as it does the heart of a

1:15:17

elite athlete and as the heart grows

1:15:20

and adds Myofibers

1:15:22

this the muscle fibers within the

1:15:24

heart the pericardium adapts and remodels

1:15:26

to accommodate that It

1:15:29

may be that those things have to rise together

1:15:33

In order to get the truly biggest

1:15:35

hearts of the most elite athletes I

1:15:38

don't know that there are some studies

1:15:40

ongoing, you know in Europe and in

1:15:42

the US to try to address that

1:15:44

You know class and then Andre LeGares

1:15:46

have the pro at heart study that

1:15:48

are looking at young athletes I don't

1:15:50

know that anyone's looking at kids that are starting

1:15:52

when they're 12 though I just in lolly and

1:15:54

in sprook is trying to do that a

1:15:57

group in Norway is trying to do that So I

1:15:59

think they that we are as

1:16:02

a community trying to get that it's hard to

1:16:04

study kids, you know, but I guess I

1:16:09

suspect that you've got to

1:16:11

train when you're growing to get the

1:16:13

maximal ability. You

1:16:15

know, Antonio Policia from the

1:16:18

Italian Olympic Committee, really the one

1:16:20

could argue the father of the

1:16:22

whole concept of sports cardiology in

1:16:25

the world, has studied

1:16:28

athletes who have participated

1:16:30

in multiple Olympics, up

1:16:32

to four or even five Olympics. That's

1:16:34

a lot of Olympics, you

1:16:36

know, and what he shows is that if

1:16:39

he looks at their heart size over

1:16:41

12 or 16 years of

1:16:43

sustained high intensity Olympic competition, it

1:16:45

doesn't get a lot bigger, you

1:16:48

know, and so these are people who

1:16:51

have acquired that fitness to get to

1:16:53

the Olympic level and then

1:16:55

to sustain that over time, it's

1:16:58

not that they're progressively getting bigger,

1:17:01

they're sustaining and preserving their fitness

1:17:03

and their heart size, but

1:17:05

there may well be a limit

1:17:07

to what that how big that

1:17:09

can be. Of course, I mean, you're limited by

1:17:12

the size of your body, right? The heart can't

1:17:14

just go continue to get big forever. So

1:17:17

obviously, there's an upper limit to that at some

1:17:19

point. Can you

1:17:21

sort of differentiate between so I've heard

1:17:23

you talk about I mean, this is at

1:17:25

that you're talking about the adaptations to endurance? Yes,

1:17:28

type of aerobic exercise. Yes, versus

1:17:30

I mean, Olympic athletes that are

1:17:32

more strength training, right? So in

1:17:34

terms of this adaptation of the of the

1:17:37

heart getting bigger? What

1:17:40

add up how that how are the adaptations different? Well,

1:17:42

so I'm going to give you the traditional thought,

1:17:44

and then I'm going to tell you that that's

1:17:46

not probably 100% right. So

1:17:49

the traditional thought, what has

1:17:52

been called the Morgan Roth hypothesis is

1:17:54

that strength training, which

1:17:57

does not increase Venus

1:17:59

return. that is the

1:18:01

blood returning to the heart. It

1:18:04

doesn't increase stroke volume very much

1:18:06

because it imparts a

1:18:08

huge afterload, a rise

1:18:10

in pressure during

1:18:13

a static strength contraction.

1:18:18

Any idea how much the blood pressure goes

1:18:20

up during exercise? Do you know this? Which

1:18:22

kind of exercise? Strength exercise. If

1:18:24

I were to have you do it. Definitely hypertension.

1:18:26

I mean 180. So if you're gonna do, if

1:18:29

I take a competitive

1:18:31

athlete and I do a 90% one

1:18:33

repetition max squat or what do you

1:18:35

think the systolic blood pressure gets to?

1:18:39

Oh like a multi-joint squat like 200 higher.

1:18:42

Keep going. 250. Keep going. 300. Keep going. 400.

1:18:44

400 millimeters of mercury. And John Sutton and his colleagues

1:18:49

put arterial lines and showed that many

1:18:52

years ago. So you generate

1:18:54

that kind of pressure by

1:18:56

intense muscle contraction which contracts

1:18:58

the blood vessels. So now

1:19:01

you're driving stroke volume into

1:19:03

a very small much smaller

1:19:05

space than you did

1:19:07

before. There's massive sympathetic activation

1:19:09

from something called the exercise

1:19:11

pressor reflex which is a

1:19:15

function of both the relative intensity and

1:19:17

the total maximal muscle contraction.

1:19:21

And so that raises arterial

1:19:23

pressure very high during

1:19:25

the contraction. Right? And

1:19:27

so to adapt to that in order

1:19:29

to reduce the load on the heart,

1:19:32

the heart has to thicken because the

1:19:35

wall stress, the stress on the heart

1:19:37

muscle is increased by

1:19:40

the bigger the heart is but is decreased

1:19:42

the thicker the heart is. So traditionally

1:19:45

purely strength trained athletes

1:19:48

tend to have thicker

1:19:50

hearts and what

1:19:53

we call concentric hypertrophy as

1:19:56

opposed to dilated hearts which we

1:19:59

call eccentric. hypertrophy. And

1:20:01

athletes who do almost exclusively

1:20:04

endurance training, runners,

1:20:06

swimmers, cross-country

1:20:08

skiers in the

1:20:11

days before skating technique,

1:20:13

they have massive increases

1:20:15

in blood flow. So

1:20:18

the adaptation of the heart is to get bigger

1:20:20

to accommodate and then sustain

1:20:22

those big stroke volumes. So

1:20:25

that's the sort of traditional view. The

1:20:28

endurance athlete has a bigger heart which

1:20:30

is eccentrically remodeled. I mean if I

1:20:32

just stretched it without making the heart

1:20:35

thicker, the walls would get

1:20:37

smaller. That's not what happens, right? The

1:20:39

heart adapts, gets bigger and

1:20:41

more muscular, but the walls don't get thicker.

1:20:43

A strength trained athlete,

1:20:45

the heart doesn't dilate, the walls

1:20:48

just get bigger. And it's the

1:20:50

eccentric hypertrophy that's important for stroke

1:20:52

volume and thus, cardiorespiratory

1:20:55

fitness? Exactly, that's correct.

1:20:57

Now it turns out that it's

1:21:00

not probably not so simple. And

1:21:03

it's not so simple for a number of reasons because

1:21:06

even during dynamic

1:21:08

exercise, when you

1:21:10

contract your muscles and run, you're

1:21:12

actually accruing blood flow during

1:21:14

those two. And many

1:21:18

sports like rowing, for example,

1:21:21

are an intense combination of both

1:21:24

static and dynamic or

1:21:26

strength and endurance type activity. So

1:21:29

rowers, every

1:21:31

time they pull on the oars, they

1:21:33

use a massive amount of skeletal

1:21:36

muscle that's contracting. But

1:21:38

they're also doing that in a rhythmic

1:21:40

basis like a runner or a swimmer.

1:21:43

So they're doing both strength and endurance

1:21:45

and they have the biggest hearts of

1:21:47

any athletes. The biggest hearts

1:21:49

that you ever see are in the rowers.

1:21:52

And now in some skiers.

1:21:55

So, you know, skating

1:21:57

technique in skiing is huge

1:22:00

strength as well as endurance

1:22:03

component. You know and in the four

1:22:05

I guess

1:22:07

gosh 1984 for a 40 years we've been classifying sports into

1:22:10

their static

1:22:17

versus dynamic exercise

1:22:19

and we create a little

1:22:21

matrix you know low medium and

1:22:24

high endurance low medium and high

1:22:26

static so a nine box

1:22:28

factor. And in

1:22:30

the Bethesda guidelines for managing of

1:22:32

athletes with heart disease we put

1:22:35

sports in these different bins. We're

1:22:38

revising those guidelines right those scientific

1:22:40

statements right now and we're

1:22:42

going to change how we display that.

1:22:44

We've eliminated the individual boxes and we

1:22:48

say there are increasing amounts of

1:22:50

endurance requirements in the sport and

1:22:52

increasing amount of strength requirements in

1:22:54

the sport but

1:22:56

it's not so simple I can't just put

1:22:58

them into little bins because I mean

1:23:01

even golfers strength train right

1:23:04

and even some strength trained athletes will

1:23:07

do aerobic exercise. So

1:23:09

you know most football

1:23:11

American football players don't

1:23:14

do anything more than 10 seconds never

1:23:17

you know I tend

1:23:19

to recommend to the trainers that

1:23:21

even the strength trained those athletes

1:23:24

will be better off if we

1:23:27

incorporate some higher intensity

1:23:30

they're the perfect people to do not

1:23:32

just a 10 second effort which is all they ever

1:23:34

do but do a one minute or

1:23:37

a two minute I mean how long do multiple

1:23:39

multiple play series

1:23:42

take last in

1:23:44

a football game for example American football

1:23:46

game. I think they need

1:23:49

to do four by fours or two by

1:23:51

twos and that's what's going to allow them

1:23:53

to sustain their fitness and not get tired

1:23:55

when you know they're they're playing fast on

1:23:57

the sport. So I think

1:24:00

We realize that sport is

1:24:02

not so simple. I

1:24:04

mean, even within a

1:24:06

sport, the goalies are different

1:24:09

than the fallbacks.

1:24:15

In American football, the defensive backs are

1:24:17

different than the linemen. It's

1:24:20

just really different. So we

1:24:22

can't just bin sports. In

1:24:26

all sports, people will train with

1:24:28

strength and even runners are training

1:24:30

with weight training and doing

1:24:32

strength training. Even runners are

1:24:34

doing strength training these days. To

1:24:37

try not to bin them, but I'm going

1:24:39

to bin them. So I say purely strength

1:24:41

trainers. There

1:24:45

does seem to be an argument then that they

1:24:47

should definitely incorporate some endurance

1:24:49

training if not for the stroke

1:24:51

volume increase and eccentric hypertrophy

1:24:54

and the effects on cardio risk-break fitness.

1:24:58

So I think that for

1:25:01

strength trained athletes, it's

1:25:03

a mistake not to do any

1:25:05

endurance. We can argue

1:25:08

about what endurance means, whether the two

1:25:10

minutes or four minutes or 40 minutes

1:25:12

is endurance. And I think that there are different

1:25:15

ways to skim the cat, so to speak. Certainly

1:25:19

for long-term health, that becomes

1:25:21

critically important. Jonathan Kim

1:25:23

and Lantas worked very closely with

1:25:26

the National Football League to

1:25:28

help retired NFL players figure

1:25:31

out how to change their training and their eating

1:25:33

and their habits to preserve

1:25:36

their health over their

1:25:38

lifetime. So their football careers just aren't that long.

1:25:41

So I think

1:25:43

you're right that for performance,

1:25:45

maybe not for Olympic weightlifting,

1:25:47

but for other

1:25:51

strength sports, I think there's

1:25:53

no question that endurance

1:25:55

is important. And for sports that require

1:25:57

repetitive bursts of strength, that's a big

1:25:59

deal. I think some

1:26:02

type of endurance training

1:26:04

of some degree, whether

1:26:07

that be high intensity, four by

1:26:09

four is there something is critical

1:26:11

for performance and will enhance

1:26:13

performance. When

1:26:15

we talk about cardiovascular health, that's a

1:26:18

little bit of a different story. And

1:26:20

I think that it is important for

1:26:22

overall cardiovascular health, in fact essential to

1:26:25

include that over time. And

1:26:28

again, I'll come back to the point that

1:26:30

no good athlete does just one thing. I

1:26:34

think that's where our studies

1:26:36

kind of are a little

1:26:38

bit too

1:26:41

isolated because in order to do

1:26:43

the research, you've got to focus

1:26:46

on and ask one simple question. But

1:26:48

training is not that simple in

1:26:50

real life. Right.

1:26:52

There are people that are much more

1:26:55

focused on resistance training and strength

1:26:57

training that are not athletes. They're

1:27:00

just interested in health. And

1:27:02

some people wonder, well, I'm getting my

1:27:04

heart rate up to almost

1:27:07

maximum heart rate when I'm doing my compound

1:27:10

lifts, my deadlifts

1:27:12

or my squats. And how

1:27:14

much of that counts towards am

1:27:16

I getting this improvement in

1:27:18

this eccentric hypertrophy and stroke

1:27:20

volume or do I

1:27:23

need to then incorporate some other types

1:27:25

of training as well. Right. So

1:27:28

I think you're articulating the CrossFit

1:27:30

concept basically. And so I

1:27:32

think that I'll

1:27:36

tell you that it kind of depends. So

1:27:38

I think that if

1:27:41

you ask what happens to

1:27:43

the heart rate

1:27:45

and cardiac output during a purely

1:27:48

strength activity, there are things

1:27:50

that drive the heart rate

1:27:52

that are controlled differently in

1:27:55

a strength activity and an

1:27:57

endurance activity. Let

1:27:59

me. dig into that if that's

1:28:01

okay. There's a little bit of

1:28:03

science here. Please do. All right.

1:28:05

So let's first talk about something

1:28:07

called the exercise presser reflex. So

1:28:10

simply it's easiest to study by

1:28:13

doing just a hand grip exercise.

1:28:15

Okay, but it would be true for any,

1:28:17

if I squeeze my hand, okay,

1:28:20

that's the same as, you know, doing a

1:28:22

short static exercise, do a hand grip. And

1:28:25

I do it at, let's say,

1:28:27

30% of a maximal

1:28:29

contraction and I hold it. Okay.

1:28:33

Heart rate will steadily rise. Blood

1:28:36

pressure will steadily rise. If

1:28:39

I put a little needle in an

1:28:41

efferent sympathetic nerve, as it passes by

1:28:43

the figular head, that's called micro-neurography, I

1:28:46

can actually record signals from the

1:28:48

brain to the blood vessels, which

1:28:50

cause vasoconstriction throughout the body. Okay.

1:28:53

It's a brain driven

1:28:56

process, which comes from feedback

1:28:58

from skeletal muscle. How do I know that?

1:29:00

Let's say I do that and I can't

1:29:02

do it anymore. And I take a blood

1:29:04

pressure cuff and I blow it up on

1:29:07

the arm and I

1:29:09

trap all the muscle,

1:29:11

all the metabolites, you

1:29:13

know, the things that are

1:29:15

happening in the muscle that are

1:29:17

causing fatigue, that are utilizing that

1:29:20

energy. And I trap them there.

1:29:23

And then I stop exercise.

1:29:25

I let

1:29:27

go. Heart rate comes

1:29:29

all the way back to baseline

1:29:31

immediately, but blood pressure

1:29:33

stays up and the sympathetic nervous system stays

1:29:35

up. And that is

1:29:37

the essence of the exercise

1:29:40

pressor reflex. The heart

1:29:42

rate is, now you can ask me,

1:29:45

is the heart rate controlled by the

1:29:47

brain then? Because I've stopped exercising, right?

1:29:49

So the brain's no longer trying

1:29:51

to make something happen. That's called

1:29:53

central command. Or is it

1:29:55

happening because the muscle tension, nothing to

1:29:57

do with metabolites because I stopped exercising.

1:30:01

Well, to address that, one of

1:30:03

my mentors, Jerry Mitchell, went to

1:30:05

Copenhagen and put some – Neil

1:30:07

Secker injected some curare into

1:30:10

the nerves, which

1:30:12

paralyzes them. And

1:30:14

they had them look at a screen, and

1:30:17

they said, I want you to try to squeeze

1:30:20

as hard as you did before, but

1:30:22

because the hand was paralyzed, they couldn't contract the

1:30:25

muscle. But they could try really

1:30:27

hard, and heart rate went up even higher, even

1:30:30

though the muscle was not contracting. So

1:30:33

we know that this vagal

1:30:36

withdrawal and sympathetic activation comes

1:30:40

to a – some – the heart rate

1:30:42

in particular comes from the central command. The

1:30:45

sympathetic activity also is

1:30:47

stimulated by what's

1:30:50

called group three and group four, hydrogen,

1:30:54

smaller, unmyelinated fibers – fibers

1:30:56

that are not insulated –

1:30:59

that carry signals from the muscle to

1:31:01

the brain and say, something's wrong, let's

1:31:03

alert, let's get that blood pressure up,

1:31:06

increased nerve activity constricting the blood

1:31:08

vessels. So that's

1:31:10

called the exercise press reflex. The

1:31:12

harder you squeeze, the

1:31:15

longer you do it for, okay, and

1:31:19

the more amount of muscle mass, the

1:31:21

bigger the blood pressure response. So

1:31:24

that's one component, okay. How

1:31:27

is the heart rate regulated during

1:31:29

dynamic exercise, during running, for example?

1:31:34

Well, it turns out that it is

1:31:36

almost certainly coming from an energetic

1:31:39

signal in your skeletal muscle.

1:31:42

How do I know that? Well,

1:31:45

some patients have diseases

1:31:48

of the mitochondria. They're

1:31:50

called metabolic or mitochondrial

1:31:52

myopathies. And one of

1:31:54

my colleagues at the Institute for Exercise

1:31:57

and Environmental Medicine, Ron Haller, studied the

1:31:59

– And he was a neurologist that

1:32:01

studied those patients. He's since retired. He's not

1:32:03

dead, just retired. And

1:32:06

what he found is when those

1:32:08

patients started to exercise, their

1:32:10

cardiac output went through the roof.

1:32:13

Their venous blood looked red because

1:32:16

they couldn't extract the oxygen. They had a

1:32:18

problem in the muscle. But

1:32:20

they would, you and I might

1:32:22

increase the cardiac output by about

1:32:25

five liters for every liter of

1:32:27

oxygen uptake. These people were

1:32:29

increasing up by 10 or 20 liters. So

1:32:32

even just walking down the hall is

1:32:34

maximal exercise to them. And

1:32:37

what that tells us, it is a

1:32:39

signal that we need energy. We

1:32:42

need oxygen delivered and fuel

1:32:44

that drives the heart rate

1:32:46

response and the cardiac output

1:32:48

response during endurance exercise. So

1:32:52

those are two fundamentally different things. One

1:32:55

increases the heart rate during a muscle

1:32:57

contraction from central command. The

1:33:00

other drives cardiac

1:33:03

output to match venous

1:33:05

return. The more the complaint of

1:33:08

the heart, the more blood could come back, the more

1:33:10

it can pump out. And those

1:33:12

two things are happening to a

1:33:14

greater or lesser degree with any

1:33:17

combination of movements. That's

1:33:19

why I mean it's no longer so simple

1:33:21

to talk about just strength or just endurance.

1:33:25

And then that gets me back to the

1:33:27

question we started with. Why are you training?

1:33:29

What's the purpose? Some people tell

1:33:32

me they want to look good. They want their muscles

1:33:34

to be big. They want

1:33:36

to have relatively little muscle

1:33:38

fat. They want to

1:33:40

be strong. I say, well, then you kind of do a lot

1:33:42

of strength exercise. If

1:33:44

what you want is to perform

1:33:49

during a CrossFit competition, you kind of do

1:33:52

CrossFit work. I think CrossFit is

1:33:54

very interesting to me because

1:33:56

it's a combination of

1:33:58

repetitive strength

1:34:00

type maneuvers, but

1:34:03

they also include repetitive muscle contraction.

1:34:05

So I think that

1:34:08

kind of exercise

1:34:10

does have both

1:34:12

an endurance and a strength component.

1:34:15

Mike Emery from Cleveland Clinic now

1:34:17

is a huge fan of

1:34:20

the CrossFit type training and

1:34:23

believes that it will get

1:34:25

you a combination of eccentric

1:34:27

and concentric type hypertrophy. And

1:34:30

again, it's where this

1:34:32

Morgan-Roff hypothesis kind of falls apart

1:34:34

because it's not one thing or

1:34:36

the other. It's kind of a

1:34:38

combination of both. I

1:34:41

don't think you can lift free weights

1:34:44

and expect that,

1:34:46

yeah, I slam down the weights on the floor,

1:34:49

walk around in between my sets that you're going

1:34:51

to get an endurance

1:34:53

type trained heart that

1:34:56

requires a more

1:34:58

sustained repetitive contraction and

1:35:01

more dynamic type exercise to

1:35:03

engage. I know that's

1:35:06

a little complicated, but does that help? Wonderful,

1:35:08

wonderful. I mean, I also love that you

1:35:10

did bring up the CrossFit, you know, that

1:35:12

they, I've been doing CrossFit for the last

1:35:14

few months. And also

1:35:16

there is an incorporation of a lot of

1:35:18

high intensity. There's rowing, there's jumping rope, there's

1:35:20

getting on the bike. So it is, you

1:35:23

know, like you said, it's not, you know, you

1:35:25

can't just put strength training and resistance training in

1:35:27

one bin and endurance in another, but just with

1:35:30

a lot of these programs now that are available

1:35:32

like CrossFit, Orange Theory, it's another one they do,

1:35:34

you know, they have something very similar. But

1:35:37

you're right, just like if you're just raising the dumbbells

1:35:39

and doing, you know, there's

1:35:42

not as much of the endurance kind of

1:35:44

training there. It's good to talk

1:35:47

about the science there on that. I

1:35:50

kind of want to go back to the blood

1:35:53

pressure thing as well because there

1:35:55

was an interesting study that

1:35:57

was recently published that made a lot

1:35:59

of headlines. on these isometric types

1:36:01

of exercises, right? The static hold

1:36:03

and being better at improving blood pressure.

1:36:05

What is the best exercise to

1:36:08

improve blood pressure, right? I mean that's...

1:36:11

So you know, when we take

1:36:13

care of patients with hypertension, the

1:36:15

first thing the community tells us

1:36:17

to do is lifestyle

1:36:20

modification, reduce intake of salt, reduce

1:36:22

intake of alcohol, make sure you're

1:36:24

getting plenty of sleep and increase

1:36:26

exercise. And I

1:36:29

will say that traditionally my

1:36:32

approach has been that dynamic

1:36:34

exercise is best because that

1:36:36

causes relaxation of

1:36:39

blood vessels. That's how

1:36:41

you get the blood to the exercising

1:36:44

muscle and we'll do one more

1:36:47

little science thing, okay? Because

1:36:49

the body has both a

1:36:51

general alerting response as

1:36:54

a function of the exercise pressor reflex and

1:36:57

a local response. So

1:36:59

when I'm exercising hard, the

1:37:03

muscles that are contracting are

1:37:05

relaxed. Blood

1:37:07

vessels everywhere else are contracted. It's

1:37:10

really interesting. So if I'm running,

1:37:12

the blood vessels in my

1:37:14

arms are contracting as they are in

1:37:17

my kidney and my gut. And that's

1:37:19

why you sometimes will get catastrophic gut

1:37:23

ischemia during extraordinary endurance

1:37:25

exercise because you

1:37:27

just don't have enough blood in your circulation

1:37:30

to maintain your blood pressure if

1:37:32

you've got a lot of skeletal muscle that's requiring

1:37:35

blood. It's one thing that the locals

1:37:38

call it the saltine hypothesis

1:37:40

about the cardiovascular limitations exercise

1:37:43

because if you add arm

1:37:45

exercise, while you're doing

1:37:47

intense flex exercise, you start

1:37:49

to constrict the blood vessels even in the legs

1:37:52

because you simply cannot sustain

1:37:55

your blood pressure with all the blood

1:37:57

vessels relaxed, even with a max blood pressure.

1:38:00

cardiac output. So

1:38:03

the blood vessels have to

1:38:05

constrict, but they constrict from

1:38:07

this general alerting increased sympathetic

1:38:10

activity, but in the muscles

1:38:12

you get something called functional

1:38:15

sympatholysis. What that means

1:38:17

is the muscles are releasing metabolites

1:38:21

as not just

1:38:23

from the muscle but from the blood vessels and

1:38:25

from the red blood cells themselves ATP

1:38:28

and ADP are

1:38:30

dramatically potent

1:38:32

vasodilators. So

1:38:35

you get constriction in one place

1:38:37

and dilation in another place and

1:38:40

it is the regular contraction, the

1:38:42

need, the release of those metabolites,

1:38:45

the driving of the cardiac output

1:38:47

response that causes

1:38:49

relaxation of the blood vessels and that's

1:38:51

what I want in hypertension. I want

1:38:54

the blood vessels to be relaxed. Remember

1:38:56

we started this by saying blood pressure. I didn't,

1:38:58

maybe I didn't. We talked about the Fick equation.

1:39:00

Blood pressure is also a function of two things.

1:39:04

Two things only, cardiac output

1:39:06

and vascular resistance, right?

1:39:08

We talked that cardiac output is heart

1:39:10

rate and stroke volume, so blood pressure

1:39:12

is the triple product of heart rate,

1:39:15

stroke volume and vascular resistance with probably

1:39:17

resistance being a major, very major component.

1:39:20

So what I

1:39:22

typically think is

1:39:25

that people need to do

1:39:27

sustained endurance activity to dilate

1:39:29

those blood vessels, cause that

1:39:31

relaxation and let those blood

1:39:33

vessels start to relax as a the

1:39:35

best way to reduce blood pressure. I

1:39:39

don't know what to make about the

1:39:41

static training study.

1:39:44

It's just one study. It's really

1:39:47

contradicts a lot of other data in the

1:39:49

literature. I don't think

1:39:51

that people say, oh, let me quickly

1:39:54

switch to doing

1:39:56

planks and leg sits against the

1:39:58

wall just because this one study showed

1:40:00

a low blood pressure. For

1:40:02

the most part, unfortunately, if

1:40:05

you have hypertension, and I've already

1:40:07

done your lifestyle modification, you're

1:40:10

probably gonna need medication to drop your

1:40:12

blood pressure. Hypertension

1:40:14

is a cardiovascular

1:40:17

disorder, and we've

1:40:19

learned that a lot of people are

1:40:22

gonna develop it. And so I

1:40:24

think the lifestyle stuff

1:40:27

is the foundation. I

1:40:30

don't think it's gonna make a huge difference

1:40:33

whether you do, whether

1:40:35

it changes my prescription for life, that

1:40:38

remains the same, and I

1:40:40

think having a strong component

1:40:42

of endurance exercise, but

1:40:44

incorporating strength, because that's important

1:40:47

for life and function

1:40:49

as you get older. I

1:40:52

think all of that is really important,

1:40:54

and it's not gonna change my prescription.

1:40:57

I do have specific approaches

1:40:59

to hypertension in physically active

1:41:01

people, but I

1:41:04

will remind your audience that

1:41:08

many people are salt-sensitive and reducing

1:41:10

salt intake, and the diet is

1:41:12

important if you have hypertension, and

1:41:14

maintaining a high potassium intake is

1:41:17

also important. And

1:41:19

then watch your alcohol, because

1:41:21

I think sometimes doctors don't tell you that,

1:41:24

but that too much alcohol

1:41:26

intake is a very strong

1:41:30

contributor to hypertension, and

1:41:32

making sure you've got good sleep and don't have

1:41:34

sleep apnea. So sleep apnea

1:41:36

is another thing. If your spouse or

1:41:39

partner snores, and

1:41:42

has hypertension, talk to

1:41:44

a sleep doctor. That may be something that's

1:41:46

a little easier to manage, and

1:41:49

will cause dramatic reductions in

1:41:51

blood pressure. So

1:41:53

along with those, you think

1:41:56

it's possible with

1:41:59

lifestyle intervention? reverse

1:42:01

hypertension? I think in some cases

1:42:03

in mild hypertension, I think that

1:42:05

that's true. If you've got

1:42:07

hypertension in a young person under the age of

1:42:10

40, I think you need

1:42:12

to look for other causes. I don't

1:42:15

think we look hard enough often enough.

1:42:18

Probably the single most important is

1:42:20

to measure a renin and an

1:42:22

aldosterone, to