If you don't die from an accident, a serious infection or a
cancer, you'll live as long as your arteries let you. And how long they let you
is all in your hands. I know this sounds over-simplified, but it's biomedical
knowledge in a nutshell. Lets look at what happens in and to your arteries and
what that means for keeping them in mint condition.
The endothelium is a one-cell-thin layer which has often
been likened to the teflon coating on your non-stick pots and pans. The only
true part of that analogy is the non-stick part. It prevents cholesterol and
fat from docking on to endothelial cells and gradually growing into
atherosclerotic plaques. When they rupture, blood clots form and those clots
might cause a heart attack or stroke. I say "might" because not all
plaque ruptures turn into such dramatic events, but we will get to this later.
Many people think that a chronic overdose of cholesterol or
fat, or simply aging, are the causes of atherosclerosis. That was the working
hypothesis of scientists 50 years ago. But it doesn't jibe with the observation
that half of all patients with confirmed atherosclerotic lesions, have
cholesterol values within the normal range [1]. That's because plaques grow WITH
cholesterol, any amount of cholesterol, but they start growing ON inflammation.
Chronic inflammation, to be precise. And chronic inflammation grows on your
physical activity habits. Or rather the lack thereof.
Inflammation in itself is nothing bad. It's a process by
which cells rid themselves of invaders. Only when inflammation becomes chronic
do we have a problem. To avoid chronicity, endothelial cells have a mechanical
switch. Or, as we call it in biomedicine: a mechanoreceptor. Those receptors
respond to pulsatile blood flow. That is, if those receptors are being hit
often, long and strong enough by blood waves gushing through the artery, they
trigger an anti-inflammatory cascade of hormonal reactions. If we don't keep
hitting those receptors, the cascade turns pro-inflammatory and the career of
the atherosclerotic plaque begins. The extremely complex biochemical happenings
do not concern us here. What concerns us is that this pounding of the endothelial
cell receptors doesn't come from sitting around, or from playing golf or from
walking through the park. It only comes from vigorous physical activity. Which explains the growing evidence for
the relative benefits of more intensive vs. less intensive physical activity.
One example is a recent study by researchers who had followed
close to 20000 adults aged 20-90 for almost 20 years, monitoring their cycling
habits and their health [2]. The study took place in the
Danish city of Copenhagen where 5 Million people own 4 Million bicycles. Male
study participants who reported habitual cycling at the highest of three
intensity levels lived on average 5.3 years longer than their peers in the
lowest intensity group, independent of the duration of cycling. Of course, this
was a prospective cohort study, which only allows us to talk association but
not causality. But its findings match nicely with the expectations we have from
our knowledge about the anti-inflammatory effects of higher-intensity exercise.
Specifically, that high-intensity exercise inhibits the oxidative processes
which precede and coincide with inflammation in the endothelial cells [3]. These effects were either
absent or negligible in exercise of moderate intensity. By the way, this second
study had been performed in women. I point that out, just so that you don't
think what applies to male Danes may not apply to women.
Now, what's the good news in all this for those devotees of
the minimalistic physical activity lifestyle, otherwise known as couch
potatoes?
The good news is, that you don't have to spend hours in
endurance exercise. In my lab we have seen significant improvements in fitness
and health with thrice weekly 20-minutes high-intensity interval training
(HIT). In our HIT routine our participants spent those 20 minutes with 4
consecutive intervals, in each of which they ran or cycled for 4 minutes at
moderate intensity, followed by a 1-minute all-out sprint, with no break
between intervals. A recent review confirmed the benefits of HIT [4], which accumulate with a
significantly smaller time commitment to exercise, than what is required for
conventional endurance exercise.
There is more good news. Remember that I mentioned that the
rupture of an atherosclerotic plaque "may" cause a heart attack or
stroke. That's because we know a couple of interesting and encouraging things
about such plaques. First, plaques may be of a "vulnerable" or of a
"stable" type. The stable ones don't rupture easily but the
vulnerable ones do. Secondly, not all those plaque ruptures end in a heart
attack or stroke. Most ruptures actually don't. And we can't predict exactly
which ones will cause problems, and when. So there is a large element of chance
in all this. Third, plaques can change their status from vulnerable to stable
or vice versa within weeks or months.
The good news in all this is that it is in your hands, or
rather in your exercise, whether your existing plaques become more stable, and
whether you decrease or increase the chance of a heart attack or stroke. All it
takes is the intensity of your exercise.
The bad news, those insights take away your excuse of lack
of time. Think about it, what are 60 minutes a week for HIT, when the average
German spends 4 hours PER DAY watching TV, and the average American tops that
with another 2 hours a day.
So, when you want to know whether your physical activity
habits qualify as a lifestyle or a death style, keep the simple reasoning in
mind: exercise determines the health of your arteries, and the health of your
arteries determines your longevity. And the shortcut to the latter goes via HIT.
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