10 Good Reasons Not To Exercise?

Exercise may actually be bad for you! A professor says he stumbled upon this "potentially explosive" insight. The New York Times has been quick to peddle it. And couch potatoes descend on it like vultures on road kill. But professors can get it wrong, too. 

Before we judge the verity of the "exercise may be bad" claim, let's first look at how the media present it to us. We shall use the recent article in The New York Times, headlined "For Some, Exercise May Increase Heart Risk". The first paragraph confronts us with a journalist's preferred procedure for feeding us contentious scientific claims: presenting an authoritative author with stellar academic credentials and a publication list longer than your arm. While that is certainly better than having, say, Paris Hilton as the source of scientific insights, it is a far cry from actually investigating such claims. Which is what we want to do now.

The basis of the exercise-may-be-bad claim is a study which investigated the question "whether there are people who experience adverse changes in cardiovascular risk factors" in response to exercise [1]. The chosen risk factors in question were some of the usual suspects: systolic blood pressure, HDL-cholesterol, triglycerides and insulin. The research question: Are there people whose risk factors actually get worse when they change from sedentary to more active lifestyles? 

Sounds simple enough to investigate. Put a group of couch potatoes on a work-out program for a couple of weeks and see how their risk factors change. Only it is not that simple. In the realm of biomedicine, every measurement of every biomarker is subject to (a) errors in measurement and (b) other sources of variability. This makes it virtually impossible for you to see exactly the same results on your lab report for, say, blood pressure, cholesterol, glucose or any other parameter, when you get them measured two or more days in a row. Even if you were to eat exactly the same food every day and to perform exactly the same activities.  

Now imagine, if you conducted an intervention study on your couch-potato subjects and you found their risk factors changed after a couple of weeks of doing exercise, you could theoretically be seeing nothing else but a random variation caused by the error inherent in such measurement. 

To avoid falsely interpreting such a variation as a change into one or the other direction, it makes good sense to know the bandwidth of these errors for each biomarker, before you embark on interpreting the results of your study. Which is what the authors of this particular study did. They took 60 people and measured their risk factors three times over three weeks. From these measurements they were able to calculate the margin of error. Actually, they didn't do this for this particular paper, they had done this measurement as an ancillary study in the HERITAGE study performed earlier. The HERITAGE study had investigated the effects of a 20-weeks endurance training program on various risk factors in previously sedentary adults. Whether heritability plays a role in this response was a key question. That's why this study recruited entire families, that is, parents up to the age of 65, together with their adult children. 

I mention this because the paper, which we are deciphering now, is a re-hash of the HERITAGE study's results, to which the authors added the data of another 5 exercise studies. That's what is called a meta-analysis. In this case it covers more than 1600 people, with the HERITAGE study delivering almost half of them. 

Fast forward to answering the question of how many of those participants had experienced a worsening of at least 1 risk factor. Close to 10%. That is, about 10% of the participants had an adverse change of a risk factor in excess of the margin of error, which I mentioned earlier. I'm going to demonstrate the results, using systolic blood pressure and the Heritage study as the example. I do this exemplification for three reasons: First, blood pressure is the more serious of the investigated risk factors. Secondly, the HERITAGE study delivers most of the participants, and thirdly, the effects seen and discussed with respect to blood pressure and HERITAGE apply similarly to the other 5 studies and risk factors. 

But before we go there I need to familiarize you with a basic concept of statistics. It is called the "normal distribution of data". It is an amazing observation of how data are distributed when you take many measurements. Let's take blood pressure as an example. 

If you were to measure the blood pressure values for every individual living in your village, city or country, you could easily calculate the average blood pressure for this group of people. You could put all those data into a chart such as the one in figure 1. 

Figure 1

On the x-axis, the horizontal axis, you write down the blood pressure values, and on the y-axis (the vertical axis) you write down the number of observations, that is, how often a particular blood pressure reading has been observed. You will find that most people have a blood pressure value pretty close to the average. Fewer people will have values, which lie further away from this average, and very few people will have extreme deviations from the average. 

It so turns out, that when you map almost any naturally occurring value, be it blood pressure, IQ or the number of hangovers over the past 12 months, the curve, which you get from connecting all the data points in your graph, will look very similar in shape. Some curves are a bit flatter and broader, while others are a bit steeper and narrower. But the underlying shape is called the "normal distribution", and it means just that: It's how data are normally distributed over a range of possible values. The curve's shape being reminiscent of a bell, has lead to this curve being called the "bell curve". 

In statistics, especially when we use them to interpret study data, we always go through quite some effort to ensure that the data we measure are normally distributed. That's because many statistic tools don't give us reliable answers if the distribution is not normal.

Back to our famous study. What you see in figure 2 is how the authors present their results for the blood pressure response of the HERITAGE participants. 

Figure 2

For each individual (x-axis) they drew a thin bar representing the height of that person's change in blood pressure after 20 weeks of exercise. Bars extending below the x-axis represent reduced blood pressure, and those extending above the x-axis represent increased blood pressure. The bars in red are those of the people whose blood pressure increase was in excess of the error margin of about 8mmHg. 

Now, Claude Bouchard, the lead author of the paper, is being quoted in the NYT as saying that the counterintuitive observation of exercise causing systolic blood pressure to worsen "is bizarre". 

Here is why it is neither counterintuitive nor bizarre: When we accept the blood pressure values of our study population to be distributed normally, we have every reason to expect the change in blood pressure to be distributed normally, too. Specifically, since all participants went through the same type of intervention. 

Figure 3

If we now run a computer simulation, using the same number of people, the same mean change in blood pressure, and the same error values, then we can construct a curve for this group, too. Which is what you see in figure 3. Eerily similar to the one in figure 2, isn't' it? 

That's because we are looking at a normal distribution of the biomarker called 'blood pressure change'. It is an inevitable fact of nature that a few of our participants will change "for the worse". And I'm putting this in inverted comma because we don't really know whether this change is for the worse. 

After all, we are talking risk factors, not actual disease events. In the context of this study you need to keep in mind, that all participants had normal blood pressure values to begin with. The average was about 120mmHg. The mean change was reported as 0.2 mmHg. That's not only clinically insignificant, that's way below the measurement capability of clinical devices. 

When I started to dig deeper into this study, I found quite a number of inconsistencies with earlier publications. For example, in the latest paper, the one discussed in the NYT, the number of HERITAGE participants was stated as 723. In a 2001 paper, which investigated participants' blood pressure change at a 50-Watt work rate, the number was stated as 503 [2].  In the same year Bouchard had published a paper putting this number at 723 [3]. Anyway, the observation that the blood pressure change during exercise was significantly larger (about -8 mmHg) than the marginal change of resting blood pressure indicates that there probably was some effect of exercise. 

So, what's the take-home point of all this? With the "normal distribution" being a natural phenomenon that underlies so many biomarkers, it is neither bizarre nor in any other way astonishing to find "adverse" reactions in everything from pharmaceutical to behavioral interventions and treatments.  Whether such reactions are truly adverse can't be answered by a study like the one, which is now bandied about in the media. That's because risk factors are not disease endpoints. They are actually very poor predictors of the latter, as I have explained in my post "Why Risk Factors For Heart Attack Really Suck". 

So, keep in mind, that there is no treatment or intervention, which has the same effect on everybody. Pharmaceutical research uses this knowledge, for example, when determining the toxicity of a substance. This toxicity is often defined as the LD50 value, that is, the lethal dose, which kills 50% of the experimental animals.  Meaning, the same dose which kills half the animals, leaves the other half alive and kicking. 

And correspondingly, the same dose of exercise, which cures your neighbor from hypertension, may have no effect on you. Because you belong to those 10% who react differently. But are these 10 good reasons not to exercise? How to deal with this question will be the subject of my next post. Until then, stay skeptical. 

[tweet this].

1. Bouchard, C., et al., Adverse Metabolic Response to Regular Exercise: Is It a Rare or Common Occurrence? PLoS ONE, 2012. 7(5): p. e37887.

2. Wilmore, J.H., et al., Heart rate and blood pressure changes with endurance training: the HERITAGE Family Study. Medicine and Science in Sports and Exercise, 2001. 33(1): p. 107-16.

3. BOUCHARD, C. and T. RANKINEN, Individual differences in response to regular physical activity. Medicine and Science in Sports and Exercise, 2001. 33(6): p. S446-S451.

Bouchard C, Blair SN, Church TS, Earnest CP, Hagberg JM, Häkkinen K, Jenkins NT, Karavirta L, Kraus WE, Leon AS, Rao DC, Sarzynski MA, Skinner JS, Slentz CA, & Rankinen T (2012). Adverse metabolic response to regular exercise: is it a rare or common occurrence? PloS one, 7 (5) PMID: 22666405

Wilmore, J. H., Stanforth, P. R., Gagnon, J., Rice, T., Mandel, S., Leon, A. S., Rao, D. C., Skinner, J. S., & Bouchard, C. (2001). Heart rate and blood pressure changes with endurance training: the HERITAGE family study. Medicine and Science in Sports and Exercise DOI: 10.1097/00005768-200101000-00017

Bouchard, C., & Rankinen, T. (2001). Individual differences in response to regular physical activity Med Sci Sports Exerc DOI: 10.1097/00005768-200106001-00013

No Time To Exercise? You Are Not Alone!

Lack of time is the most often cited excuse for not exercising. I deliberately chose the word "excuse" over its less judgmental alternative "obstacle". Simply because I cannot see an "obstacle" when I compare two simple metrics: the hours people spend watching TV and the minutes needed to maintain one's health with exercise. With high intensity interval training, or HIT, health enhancing exercise can be compressed into an amazingly short amount of time. When done right. [tweet this].

According to the Nielsen "Three Screen Report" Americans spend 5.1 hours daily in front of their TV. But they admit to "only" half that time, according to a survey of the Bureau of Labor Statistics. To be fair, I take the survey's figure of 2.7 hours for the comparison with the American College of Sports Medicine (ACSM) current guidelines for quantity and quality of exercise [1]. The ACSM's recommendations of 2.5 hours exercise PER WEEK vs. 2.7 hours in front of the TV PER DAY. Cut your 162 minutes of daily TV watching by just 21 minutes, and it still leaves you with more than 2 hours for mind numbing soaps.  

On a cautionary note to my fellow German readers: don't think for one minute that our TV habits are in any way better than those of our U.S. friends. According to statista's "Daten & Fakten zur Mediennutzung" we spend on average 220 minutes in front of the dumb tube. So, either we have, for once, outdone our U.S. friends, or their self-admitted 2.7 hours are an understatement. Anyway, those figures tell you why I talk about excuses and not obstacles.

But I'm a realist. Whatever my view on the issue of having time, it won't change other people's views. Which is why my colleagues in public health have begun to look into ways of how to get the same health punch out of dramatically shorter exercise routines. And, as I mentioned in my previous post, the solution might have been found. It is called high intensity interval training, or HIT.

HIT is an exercise routine, which consists of brief bouts of vigorous activity, alternating with "active recovery" periods of more moderate intensity.  Until very recently, researchers focused on the comparison of HIT with the conventional continuous endurance exercise of moderate-to-vigorous intensity, which is what those public health guidelines are all about. Most studies comparing those two exercise alternatives matched them for energy expenditure. Since energy expenditure is higher during the intense bout the overall time needed to expand the same amount of energy is shorter in HIT than in continuous exercise. 

Latest research efforts, however, try to answer the question whether those high-intensity bouts might even compensate for an overall lesser energy volume. In other words, could we reduce not only the time spent on exercise but also the total exercise volume simply by doing HIT? Which means, reducing the time required for doing exercise even further? The latest study, conducted by Katharine D. Currie and her colleagues seems to suggest just that [2]. Before I go into the details, let me explain why I find her line of investigation very appealing and important.

The overall purpose of exercise is to maintain functional health. The reason why exercise is key to human functional health is because humans are made to move. Only, today they don't move anymore. That's why my primary interest in exercise is about its link to health. Anything else, such as weight loss, is secondary. Because, if I can improve health by exercising, I have achieved my objective.  Regardless of whether weight loss has materialized as a side effect or not. Weight loss for its own sake without any improvement in health is a purely cosmetic issue, which doesn't interest me that much.

One of the main health issues attached to exercise is arterial function. It's impairment is the first step that leads to atherosclerotic plaque build-up in your arteries and ultimately to heart attack or stroke. The entire process typically lasts decades, and our current portfolio of risk factors, such as high cholesterol, alert us way too late to this situation. I have written about this in my earlier post "When Risk Factors For Heart Attack Really Suck". Which is why I believe that arterial function is THE benchmark for testing the efficacy of exercise: It's an extremely sensitive early warning signal and a reliable tool to measure the effect of your exercise efforts. This is what Currie and colleagues had in mind. They wanted to see how a low-volume HIT routine affected the arterial function and fitness of 10 participants with existing heart disease.

Participants were tested individually for their fitness on a cycle ergometer. The researchers used the results of the fitness test to set the parameters for the two exercise routines, which all participants had to perform. The endurance protocol was set at 55% of each participant's peak power output as determined during the fitness test. In the endurance exercise bout, participants had to cycle at this intensity for 30 consecutive minutes.

The HIT protocol consisted of 10 1-minute bouts of exercise at 80% of peak power output, separated by 1-minute bouts at 10% of peak power output. That's 30 minutes of continuous exercise vs. 19 minutes of HIT, not considering warm-up and cool-down which were the same for both protocols.
Interestingly, while all participants completed the HIT protocol, 2 participants were unable to last through the endurance protocol. Arterial function improved after both exercise protocols similarly, despite the fact that the total work performed in the endurance protocol was significantly greater than in the HIT protocol.

Now, 10 participants is a rather small number of subjects for such a study. The problem with a small number is insufficient statistical power to detect a difference in arterial function between the two protocols, if there was a difference. Which is why we will be looking forward to seeing larger trials investigating this question using more participants.

The researchers also show one thing which is always close to my heart but which is rarely reported in study publications: the very different outcomes between individuals. After the endurance exercise one participant saw a dramatic improvement in arterial function, 4 participants had a more modest improvement, and the remaining 5 no improvement. Following the HIT routine, there were 2 participants with a dramatic improvement of arterial function, 2 with a more moderate improvement, 1 whose arterial function actually got worse and the remaining 5 with no change. Unfortunately the researchers do not tell us whether those who improved or didn't improve in one routine showed corresponding effects in the other routine. My guess is, for at least some of the participants, the reaction will have been different. But even if that was not the case, we can see again, that the presentation of group results masks the fact that different people react very differently to the same type of intervention. I have presented an example of this effect in my earlier post "Am I shittin' you? Learn to be a skeptic".

A similar degree of inter-individual difference was seen in a study which used the same protocol of low-volume HIT, but this time on healthy sedentary adults. The question was whether 2 weeks of performing the HIT routine 3 times per week would improve the participants' ability to burn fat instead of carbohydrates. This so called oxidative capacity is a marker of metabolic health and gives you a clue about your diabetes risk. True enough, the results support the idea, that this minimal amount of exercise can substantially improve metabolic function. But again, the wide standard deviation of the group results points at substantial differences between the individuals [3].  

These inter-individual differences make prescription of exercise always a trial-and-error effort. As much as you would like to hear from your coach or doctor that a specific type of exercise will have a specific effect on your health, nobody can give you that certainty. In fact, if you encounter a coach who talks certainty, you know a coach whose knowledge is too limited to make him recognize his own limitations. That's something to be wary about.

Now, what if you would like to try HIT for yourself? How would you design a HIT routine? Before I give you a few pointers, let me warn you first: Do not take my advice as a medical recommendation. You follow it at your own risk. If you have been sedentary, and you have any doubt as to whether exercise at high intensity is good for you, seek medical advice first.

Obviously the best way of designing a maximally effective HIT routine is to go through a fitness test first. Ideally, one which tests things like your maximal oxygen consumption. The gold standard is the cardiopulmonary exercise test during which gas exchange is measured together with heart rate or ECG. The measured values will allow your coach to tailor the intensity of the intervals to maximum effect. But there is a simple do-it-yourself way, too. Here is how it works:

In exercise research we know that people's perception of exertion correlates quite reliably and closely with biomarkers of exertion (e.g. heart rate, oxygen consumption). We call this subjective perception the "rate of perceived exertion" or RPE. And we have scales for you to express this RPE. The most commonly used one is the Borg scale of perceived exertion. I personally prefer the OMNI version because its 0-10 scale is so much more intuitive than Borg's 6-20 scale. 

The picture to the right is a copy of the OMNI scale.

It doesn't matter whether you run or cycle or do any other type of endurance exercise. What you would describe as "extremely hard" (9-10) is the most strenuous intensity at which you can currently perform your exercise. Regardless of your personal maximal oxygen capacity. That means, an Olympic marathon runner has his 100% max at 10 and so do you as a couch potato. Even though both of you have vastly different capacities. Since we want to exercise at 80% of that capacity it doesn't matter what it's absolute value is. The only thing that matters is that we hit the 80%. Which is what these scales are so good for.

At the left end (0) of the scale you find the descriptor "extremely easy", which is the way you would describe an exercise that you could perform for very long durations without any distress. The point is to get your exercise intensity during the high-intensity intervals to where you would describe the feeling as "hard", that is, at a 7-8 out of 10. That point correlates pretty closely with the 80-85% of maximal effort used by the researchers. The period of active recovery, which separates two high-intensity intervals, should get you to a perception in the range of 4-6.

Keeping this scale in mind you can now perform your own interval training with whatever exercise you fancy, whether its cycling, running, skating, swimming, or whatever. From experience with our own study participants I find a HIT routine of 1-minute high-intensity intervals, separated by 4-minute active recovery intervals, the most agreeable to start with. If that's too tough, cut the high-intensity interval down to 45 or 30 seconds. Try to get 3 to 4 high interval bouts into one exercise. And don't be frustrated if initially you can manage only two. Do this 3 times a week, always with one day between 'HIT days', and you'll find your fitness level responding very fast to this minimal effort. Increasing this effort will be no problem. You can play around with different ways of doing that. Shortening the active recovery period is one way. Stringing more intervals into your exercise bout is another. The variations are limitless.

If there is one particular biomarker which you want to improve, be it blood pressure, blood sugar or arterial function, get it tested before you start and then a couple of weeks after you have persisted with the weekly HIT routine. To see the health effects of your efforts can be a strong motivator to go on, or to do even more. To get from 20 minutes three times a week to 20 minutes daily will be a huge improvement. It still leaves you with plenty of TV time, and probably with enough time to wonder how you could have ever thought of time being an obstacle to exercise.

You'll probably not be tempted to do what I did 10 years ago: I threw out my TV and never replaced it. Which is why I can now work, study, exercise and write a blog. Which also means that to compensate for my zero TV time, somebody must spend a lot longer in front of the TV than the average 2.7 hours. Could that be you? Or someone you know, who would benefit from reading this?  [tweet this].

1.    Garber, C.E., et al., Quantity and Quality of Exercise for Developing and Maintaining Cardiorespiratory, Musculoskeletal, and Neuromotor Fitness in Apparently Healthy Adults: Guidance for Prescribing Exercise. Medicine & Science in Sports & Exercise, 2011. 43(7): p. 1334-1359 10.1249/MSS.0b013e318213fefb.

2.    Currie, K.D., R.S. McKelvie, and M.J. Macdonald, Flow-Mediated Dilation Is Acutely Improved following High-Intensity Interval Exercise. Medicine and Science in Sports and Exercise, 2012.

3.    Hood, M.S., et al., Low-volume interval training improves muscle oxidative capacity in sedentary adults. Medicine and Science in Sports and Exercise, 2011. 43(10): p. 1849-56.

Garber, C., Blissmer, B., Deschenes, M., Franklin, B., Lamonte, M., Lee, I., Nieman, D., & Swain, D. (2011). Quantity and Quality of Exercise for Developing and Maintaining Cardiorespiratory, Musculoskeletal, and Neuromotor Fitness in Apparently Healthy Adults Medicine & Science in Sports & Exercise, 43 (7), 1334-1359 DOI: 10.1249/MSS.0b013e318213fefb

Currie KD, McKelvie RS, & Macdonald MJ (2012). Flow-Mediated Dilation Is Acutely Improved following High-Intensity Interval Exercise. Medicine and science in sports and exercise PMID: 22648341

Hood MS, Little JP, Tarnopolsky MA, Myslik F, & Gibala MJ (2011). Low-volume interval training improves muscle oxidative capacity in sedentary adults. Medicine and science in sports and exercise, 43 (10), 1849-56 PMID: 21448086

How to Live Longer And Exercise Shorter?

Let's face it, if exercise was really that much fun, everybody would do it and we wouldn't be fat, diabetic or die of heart disease. So when your doctor tells you that you better start exercising, your immediate question might be: how much do I have to do? The answer is, it depends. It depends on whether you want to hear the polite version or the truth.  [tweet this].

The polite version goes something like this:  As long as you do some exercise, you will see some health benefits. When your doctor gives you this advice, he probably has studies in mind like the one performed by Hamer and colleagues [1]. They show us that as few as 1-2 exercise sessions per week protect against heart disease. I don't really buy it, and neither should you. Here is why:

The researchers took data from 23,747 people of the English and Scottish health surveys and grouped them into one of two groups, depending on the status of their metabolic health. The latter was defined along the risk markers of high blood pressure, low good cholesterol, diabetes status, high waist circumference and inflammatory status. People who had less than 2 of those risk factors made it into the metabolically healthy group, the rest into the unhealthy group. 

Since these surveys had also asked people to self-report their physical activity levels, the researchers were able to investigate, how exercise volume correlates with health outcome. And, lo and behold, over the average follow-up period of 7 years those among the metabolically unhealthy people, who reported exercising just once or twice a week, had the same risk of developing heart disease as the metabolically healthy people. I'm not trying to discredit this study. It is a valid method to look at associations between exercise and health. But we have to keep in mind that it only answers the question whether PA, at this low volume of 1-2 times per week, is associated with heart health. What the study doesn't tell us is, whether this association is of a causal nature. In other words, it really does not tell us whether low-volume PA "...is protective in men and women with clustered metabolic abnormalities" as the authors suggest.

If studies like the one of Hamer and colleagues are used to entice the couch potatoes to pick up exercise, even if it is only once or twice a week, then, by all means, that's a good start. In public health we love this type of message for a simple reason:  We can throw it at the media in the hope of encouraging sedentary people to take up exercise. If the message is effective, there will be fewer heart attacks and early deaths. What we deliberately do not tell you, though, is how effective this exercise is for YOU. We have a number for that. It is called the 'number needed to expose' (NNE). It tells you how many couch potatoes need "to be exposed" to a change in exercise habits in order to prevent one single case of heart attack or death. In the case of Hamer's study that number stands at more than 40. Meaning, for every 40 people, which we convince, we can prevent 1 death from any cause. Good for us. But probably not good enough for you. If you take up our advice, the 1 in 40 simply means a 2.5% chance that this avoided death would have been yours. Not very motivating. Which is why you don't read so much about these numbers.

Now, if you were my client, I would ask you, whether you were interested in getting the best out of the limited time you are willing to invest in exercise. Which brings us to the second version of the answer, which I promised you in the beginning of this post: the truth.

Evidence is accumulating that the intensity at which you exercise is far more important for your health than the total volume of exercise. In an earlier post (Shortcut to Longevity) I introduced the results of the Copenhagen City Heart Study, which showed an association between heart disease mortality and the intensity, but not the volume, of habitual cycling. Of course, what applies to the Hamer study, applies to this study too. An association is not necessarily of a causative nature. But if we take it as an indication that exercise intensity is so important, isn't that bad news and bad news for the couch potato? Not only does he have to exercise, he also has to exercise hard? No, this is where the good news are: There is method of milking this high-intensity effect to the point where it saves you oodles of time.

It is called high intensity interval training, or HIT for short. This acronym should get you excited, because it super-charges the benefit:time ratio of exercising. In fact, if done correctly, you can expect to improve your fitness and endurance to the same extent as you would with traditional continuous endurance exercise while spending 90% less time on exercise [2]! But let's take it a step at a time.

What is HIT? As the name implies, HIT sessions consist of alternating intervals of vigorous and moderate intensity exercise. One-minute intervals of sprinting, interspersed with 3 minutes of jogging at a moderate pace, would be one of a virtually infinite number of variations of HIT. Do this for 16 or 20 minutes thrice a week and I promise you, within 2 weeks, you'll be excited about the noticeable progress you make. That's 60 minutes a week! Should be possible for the tightest of time budgets. After all, time is the most often cited obstacle to taking up exercise. Understandably, because there are only 24 hours in a day, of which statistically, every German spends 4 hours in front of the TV and every American 6 hours. Which really leaves us so little time to do something meaningful, aside from working and sleeping. If that comes across as sarcastic, I'm guilty as charged.

Anyway, I haven't answered the next logical question, whether HIT also translates into real health benefits. You bet it does. In fact those benefits are so profound, that even heart attack and heart failure patients are now being put on HIT routines. Wisloff and colleagues randomized 27 heart failure patients into 3 training groups [3]: a HIT group which walked three times a week four 4-minute intervals at close to maximal heart rate, with 3-minute intervals of walking at 50% to 70% of maximal heart rate between the high intensity intervals; a moderate-intensity exercise group which walked thrice weekly continuously for 47 minutes at 70% to 75% of maximal heart rate; and a control group which met every 3 weeks for a 47-minute walk. After 12 weeks, the control group showed no improvement in fitness, measured as maximal oxygen uptake. The moderate-intensity group had improved fitness by 14%, whereas the HIT group, which had spent 50% less time on exercise, had an improvement of 54%. Moreover HIT improved arterial function, cholesterol and heart function, significantly better than the continuous moderate-intensity exercise protocol.

In another study, diabetics were put on a HIT protocol consisting ten 60-s sprints interspersed with 60-s moderate-intensity cycling. After only 6 sessions, participants' glucose metabolism had improved substantially and so had their muscles' oxidative capacity [4]. Unfortunately, this study was not controlled, meaning there was no control group to compare the relative benefits of HIT vs. continuous moderate intensity exercise. Which shows, we are still in the early days of finding our ways to optimal protocols for different people with different health issues.

In my lab, we wanted to know whether the high benefit:time ratio of HIT, together with its quickly noticeable results, would entice couch potatoes to do more than a prescribed weekly minimum of three 20-minute hit sessions. After 6 months 76% of our 120 study participants had acquired the habit of exercising more than 150 minutes per week. When they started on our program they had all been sedentary and mostly overweight, but they were otherwise healthy. Over the 6 months they not only improved their fitness substantially but also reduced their weight and improved their risk factors for heart diseases and diabetes [5].

I prefer telling a couch potato that, to gain a health benefit,  (a) he or she has to do exercise, that (b) the exercise has to be of sufficient intensity, and that (c) this benefit can be his or hers at a modicum of time spent on exercise. I prefer that to making polite noises about the benefits of very little exercise, no matter what intensity and volume, because the benefit I would be talking about wouldn't be the benefit she or he is thinking of. 

In the next post I will show you how to design your own HIT routine, how to find the optimal intensities and what to keep in mind when you bring such a routine into a hitherto sedentary life.

Seeing you again coming Monday.

1.    Hamer, M. and E. Stamatakis, Low-Dose Physical Activity Attenuates Cardiovascular Disease Mortality in Men and Women With Clustered Metabolic Risk Factors. Circulation: Cardiovascular Quality and Outcomes, 2012.

2.    Kent, W., The effects of sprint interval training on aerobic fitness in untrained individuals: a systematic review. British Journal of Sports Medicine, 2011. 45(15): p. A8.

3.    Wisloff, U., et al., Superior cardiovascular effect of aerobic interval training versus moderate continuous training in heart failure patients: a randomized study. Circulation, 2007. 115(24): p. 3086-94.

4.    Little, J.P., et al., Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes. Journal of Applied Physiology, 2011. 111(6): p. 1554-1560.

5.    Kraushaar, L., Improving the Efficiency of Lifestyle Change Interventions for the Prevention of Cardiometabolic Disease, in School of Public Health Medicine2010, University of Bielefeld: Bielefeld. p. 239.

Hamer, M., & Stamatakis, E. (2012). Low-Dose Physical Activity Attenuates Cardiovascular Disease Mortality in Men and Women With Clustered Metabolic Risk Factors Circulation: Cardiovascular Quality and Outcomes DOI: 10.1161/CIRCOUTCOMES.112.965434

Kent, W. (2011). The effects of sprint interval training on aerobic fitness in untrained individuals: a systematic review British Journal of Sports Medicine, 45 (15) DOI: 10.1136/bjsports-2011-090606.26

Wisloff, U., Stoylen, A., Loennechen, J., Bruvold, M., Rognmo, O., Haram, P., Tjonna, A., Helgerud, J., Slordahl, S., Lee, S., Videm, V., Bye, A., Smith, G., Najjar, S., Ellingsen, O., & Skjaerpe, T. (2007). Superior Cardiovascular Effect of Aerobic Interval Training Versus Moderate Continuous Training in Heart Failure Patients: A Randomized Study Circulation, 115 (24), 3086-3094 DOI: 10.1161/CIRCULATIONAHA.106.675041

Little, J., Gillen, J., Percival, M., Safdar, A., Tarnopolsky, M., Punthakee, Z., Jung, M., & Gibala, M. (2011). Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes Journal of Applied Physiology, 111 (6), 1554-1560 DOI: 10.1152/japplphysiol.00921.2011

Guess who is hiding the magic pill to longevity?

Imagine a medicine which protects you against cardiovascular disease, cancers, diabetes, depression and dementia. A medicine which works best when taken regularly and long before any symptoms of any of those diseases appear. A medicine which is cheaper than any supplement or aspirin. Would you take it?

Then why don't you? The name of that medicine is exercise, and ...

...OK, OK, I hear you saying "not again, I have heard that mantra before. Tell me something I don't know!" Which is exactly what I want to do: To tell you something you AND I don't know, because nobody seems to have the answer to the sixty-four-thousand dollar question: Why don't we take this medicine?

Now here is this hot item called swarm intelligence, the phenomenon which, we are being told, makes a horde of blooming idiots come up with solutions worthy of an Einstein's. That should work just fine for us. So, let's put it to the test. I'll tell you first a few facts and my thoughts, after which it is your turn, and then we can look at the results over the next few days, or so.

Now, just so that we all start form the same page, let me recap the effects of exercise. 

Exercise & Heart Disease

Exercise, done right, has been found to reduce the risk of dying from any cause by at least one third with a 9% reduction for every one hour of vigorous exercise performed per week [1]. To be fair, studies which calculate such risks are inherently flawed. They assess exercise through questionnaires, which makes it difficult to reliably judge the amount and intensity of exercise, and whether people stick with a given exercise level and for how long. That's why I like to look at the exercise-health correlation using fitness as the marker. Because fitness is a direct consequence of exercise, and it is something we can objectively measure in the lab.

A fit 45 years old man has only one quarter the lifetime risk of dying from cardiovascular causes compared to his unfit peer [2]. And 20 years later, at the age of 65, being fit means having only half the risk of an unfit 65-year old. So much about exercise and the number one killer of men and women alike, cardiovascular disease. How about the runner-up: cancer?

Exercise & Cancer

The association of fitness with cancer is not as well researched as with cardiovascular disease. But the available data clearly point to a substantial effect. In a study performed in 1300 Finnish men who were followed for 11 years, the physically fit ones, when compared to their least fit peers, had a 60% reduced risk of dying from non-cardiovascular causes, which means mostly cancer [3]. An almost identical value of risk reduction for cancer death had been found in a 16-year study of 9000 Japanese men aged 19-59 [4]. The ones in the highest quartile of physical fitness had a risk of dying from cancer that was 60% lower than the risk of their peers in the lowest quartile.

The fact that fitness correlates so strongly with the risk of dying from cancer might tell us that the intensity of exercise plays a large role. In a study, which followed 2560 men for close to 17 years, the intensity of physical activity was clearly related to cancer mortality. But only in those who were physically active for at least 30 minutes per day did the higher intensity of exercise lower the cancer death risk by close to 50%. Do less than those 30 minutes, and high intensity might not get you away from cancer death. Obviously, low-intensity exercise does neither increase your fitness level nor does it decrease your risk of dying from cancer. The message to all those who play 18 holes on a daily basis: Get a (sports-)life!

Exercise & Dementia

Even less well examined than the exercise-cancer association is the exercise-dementia association. But also here we begin to see a remarkable effect. Results from the first relatively small trials show that physically active elderly have substantially reduced risk of Alzheimer and other forms of dementia, possibly in the range of a 50% risk reduction [5]. 

Why Don't We Exercise?

Ok, so here we are. Obviously, man is made to move. And whether you call exercise medicine or whether you call the lack of exercise a pathogen - which is clinician speak for something nasty that makes you sick - we already know a lot about how exercise does its work biochemically. That's beyond the scope of this post.

What interests me here is the question which I have asked at the beginning of this story: Why do we not take this "medicine" which is free-of-charge and which has a stronger effect than any of those pills for lowering cholesterol or blood sugar or blood pressure?

As researchers we have made no progress at all in answering this question.

The psychologists outdo each other with the creation of behavioral models, which give their inventors a lot of stature, but which have failed to get us one inch closer to the answer. Just to give you an impression, there is the Health Belief Model, the Theory of Reasoned Action, the Theory of Planned Behavior, the Transtheoretical Model of Behavioral Change, the Social Cognitive Theory, the Protection Motivation Theory, the Health Action Process Approach, and probably a few new ones in the making. Their common denominator: no reliable answer to our question.

That's why I would like to try swarm intelligence. If the "swarm" of readers of this blog post, that is you and me, is large enough, we might just come up with an answer that is worth pursuing in a more methodical way.

So, I'll go ahead and tell you a few suspicions which I have. And then, at the risk of baring my soul to the point where you might not find me a likable person, I will tell you what motivates me to do an early morning 90-minutes exercise session almost every day of the week.

But first the suspicions which I have why so few people get themselves to do even the bare minimum of exercise:

1.     Is it because we can't see, I mean literally see, the effects? Would some sort of visual feedback about the benefits and effects of exercise inside your body motivate you to exercise?

2.     Is it because we rather react than act? That is, we only do something to cure a disease once it's manifest rather than prevent it? But then, why do we have intelligence and one of its nifty byproducts called foresight in the first place?

3.     Is it because we are so focused on a pill or an operation as the only tools, which work against a disease, that we simply can't appreciate the value of something so simple and cheap as exercise?

4.     Why do we use the lousy excuse "no time" when we have several hours to spend in front of the TV EVERY day? Regardless of how busy we are with our work?

These are just a few questions which come to mind. They amount to asking why we don't exercise. 

But it will be equally helpful to ask the question: what is it, that KEEPS YOU exercising? 

Because from those who do, we can learn, how to motivate those who don't. Provided we get an honest answer. My suspicion is, the answers which we get in research, are mostly edited for "political correctness". The couch potatoes hide behind the time constraints, because being busy is not perceived as a character flaw, being lazy is. And what could possibly be a character flaw of the exerciser?

Well, I give you mine. The instinctive gratification with which my inner brute views the overweight person in front of me at the check-out queue or in the waiting room, the gratification that comes from being reminded of his risk for disease and suffering being a lot greater than mine (in German we have that word "Schadenfreude"), the gratification that comes from telling him, in my mind only, of course, "I have that strength of will that you don't". 

That's a gratifying incentive, to be sure. But it's not the only one. The main reason why I run every morning, no matter what the weather or the size of the hangover from Saturday's evening (yeah, it happens to all of us) is, that I have seen enough people who suffered a stroke or a heart attack. And I have seen their remorse of not having done enough while there was still time. I fear that. That's what keeps me running.

And what is it for you? Honestly. Let's hear it, and let's see whether we find a common thread, which research has overlooked so far. Remember, as a swarm we are supposed to be far more intelligent than as individuals.

1.           Samitz, G., M. Egger, and M. Zwahlen, Domains of physical activity and all-cause mortality: systematic review and dose-response meta-analysis of cohort studies. International Journal of Epidemiology, 2011.

2.           Berry, J.D., et al., Lifetime Risks for Cardiovascular Disease Mortality by Cardiorespiratory Fitness Levels Measured at Ages 45, 55, and 65 Years in Men: The Cooper Center Longitudinal Study.J Am Coll Cardiol, 2011. 57(15): p. 1604-1610.

3.           Laukkanen, J.A., et al., Cardiovascular Fitness as a Predictor of Mortality in Men. Archives of Internal Medicine, 2001. 161(6): p. 825-831.

4.           SAWADA, S.S., et al., Cardiorespiratory Fitness and Cancer Mortality in Japanese Men: A Prospective Study. Medicine and Science in Sports and Exercise, 2003. 35(9): p. 1546-1550.

5.           Buchman, A.S., et al., Total daily physical activity and the risk of AD and cognitive decline in older adults.Neurology, 2012.

Samitz G, Egger M, & Zwahlen M (2011). Domains of physical activity and all-cause mortality: systematic review and dose-response meta-analysis of cohort studies. International journal of epidemiology, 40 (5), 1382-400 PMID: 22039197

Berry JD, Willis B, Gupta S, Barlow CE, Lakoski SG, Khera A, Rohatgi A, de Lemos JA, Haskell W, & Lloyd-Jones DM (2011). Lifetime risks for cardiovascular disease mortality by cardiorespiratory fitness levels measured at ages 45, 55, and 65 years in men. The Cooper Center Longitudinal Study. Journal of the American College of Cardiology, 57 (15), 1604-10 PMID: 21474041

Laukkanen, J. (2001). Cardiovascular Fitness as a Predictor of Mortality in Men Archives of Internal Medicine, 161 (6), 825-831 DOI: 10.1001/archinte.161.6.825

SAWADA, S., MUTO, T., TANAKA, H., LEE, I., PAFFENBARGER, R., SHINDO, M., & BLAIR, S. (2003). Cardiorespiratory Fitness and Cancer Mortality in Japanese Men: A Prospective Study Medicine & Science in Sports & Exercise, 35 (9), 1546-1550 DOI: 10.1249/01.MSS.0000084525.06473.8E

Buchman AS, Boyle PA, Yu L, Shah RC, Wilson RS, & Bennett DA (2012). Total daily physical activity and the risk of AD and cognitive decline in older adults. Neurology, 78 (17), 1323-9 PMID: 22517108

Your shortcut to longevity.

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. 

 You may have thought about your arteries as elastic tubes, which transport blood to where its oxygen and nutrient load is needed. But there is more to it. For example, there is this very thin lining which separates the muscular elastic wall of the arteries from the blood stream. This lining is called the endothelium, and it is where the difference is made between lifestyle and death style.

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.   

1.           Braunwald, E., Shattuck lecture--cardiovascular medicine at the turn of the millennium: triumphs, concerns, and opportunities.N Engl J Med, 1997. 337(19): p. 1360-9.

2.           Schnohr, P., et al., Intensity versus duration of cycling, impact on all-cause and coronary heart disease mortality: the Copenhagen City Heart Study. European Journal of Cardiovascular Prevention & Rehabilitation, 2011.

3.           Ciolac, E.G., et al., Effects of high-intensity aerobic interval training vs. moderate exercise on hemodynamic, metabolic and neuro-humoral abnormalities of young normotensive women at high familial risk for hypertension. Hypertension Research, 2010. 33(8): p. 836-843.

4.           Kent, W., The effects of sprint interval training on aerobic fitness in untrained individuals: a systematic review.British Journal of Sports Medicine, 2011. 45(15): p. A8.

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 European Journal of Cardiovascular Prevention & Rehabilitation, 19 (1), 73-80 DOI: 10.1177/1741826710393196