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.











European Journal of Cardiovascular Prevention & Rehabilitation, 19 (1), 73-80 DOI: Schnohr, P., Marott, J., Jensen, J., & Jensen, G. (2011). Intensity versus duration of cycling, impact on all-cause and coronary heart disease mortality: the Copenhagen City Heart Study(1), 73-80 DOI: 10.1177/1741826710393196

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