Good diet trumps genetic risk of heart disease

THANK YOU FOR VISITING SWEATSCIENCE.COM!

As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

***

I posted last week about “epigenetics” — the idea that, while the genes you’re born with are unchangeable, environmental influences can dictate which of your genes are turned “on” or “off.” A few days later, I saw a mention of this PLoS Medicine study in Amby Burfoot’s Twitter feed. It’s not an epigenetic study, but it again reinforces the idea that the “destiny” imprinted in your genes is highly modifiable by how you live your life.

The study mines the data from two very large heart disease studies, analyzing 8,114 people in the INTERHEART study and 19,129 people in the FINRISK prospective trial. They looked at a particular set of DNA variations that increase your risk of heart attack by around 20%. Then they divided up the subjects based their diet, using a measure that essentially looked at either their raw vegetable consumption, or their fresh veg, fruit and berry consumption. Here’s what the key INTERHEART data looked like:

Breaking it down:

  • The squares on the right represent the “odds ratio,” where the farther you are to the right (i.e. greater than one), the more likely you are to have a heart attack.
  • The top three squares represent the people who ate the least vegetables, and the bottom three squares are those who ate the most vegetables.
  • Within each group of three, GG are the people with the “worst” gene variants for heart attack risk, AG are in the middle, and AA are the people with the least risk.

So if we look at the top group first, we see exactly what we’d expect: the people with the bad genes are about twice as likely to suffer a heart attack as the people with the good genes. But if you look at the middle group (i.e. eat more vegetables), the elevated risk from bad genes is down to about 30%. And in the group eating the most vegetables, there’s essentially no difference between the good and bad genes.

How does this work? The researchers don’t know — partly because no one’s even sure exactly how the bad gene variants cause higher risk. (There are some theories, e.g. that it affects the structure of your veins and arteries.) But the practical message is pretty clear: if you eat your veggies, you don’t have to worry about this particular aspect of your genetic “destiny.”

Brain endurance, mitochondria, and the desire to exercise

THANK YOU FOR VISITING SWEATSCIENCE.COM!

As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

***

Endurance training causes new mitochondria — the “power plants” that use oxygen and glucose to produce ATP — to grow in your muscles. This, in a nutshell, is why your endurance improves, because you’re able to keep your muscles aerobically fuelled for longer. These adaptations take place mainly in the muscles you use during training: legs for runners, arms and legs for swimmers, and so on.

But the muscles aren’t the only place where oxygen and glucose are needed: at rest, your brain sucks up 20 percent of your body’s oxygen supply and 25 percent of its glucose. A neat new study in the American Journal of Physiology (press release here; full text of study freely available here) suggests that aerobic exercise causes new mitochondria to grow in your brain as well as your muscles, which has a couple of interesting implications. The study was done in mice: an eight-week treadmill running program produced the usual changes (increased time to exhaustion, higher mitochondria in muscles), but also produced a series of changes suggesting that new mitochondria had grown in the brain.

One reason this is significant is that figuring out how to boost mitochondria in the brain would be helpful for “various central nervous system diseases and age-related dementia that are often characterized by mitochondrial dysfunction.” That includes, for example, Alzheimer’s disease.

The other is the possible role of brain mitochondria in “central fatigue,” which the researchers define as “the progressive reduction in voluntary drive to motor neurons during exercise” (this is a controversial topic, I should note). The idea is that your body’s absolute top priority is making sure that your brain ALWAYS has enough energy. During intense exercise, your muscles are using oxygen and energy so rapidly that your brain’s oxygen levels start to drop. To prevent disaster, your brain automatically starts to recruit fewer muscle fibres for a given level of effort, so that more resources can be diverted to the brain. You experience this as fatigue: you’re pushing just as hard as before, but you’re getting slower/weaker. But if you have more mitochondria in your brain, you can make use of available energy more efficiently so you won’t have to shut down your muscles quite as soon:

[I]t is reasonable to hypothesize that increased brain mitochondria may play an important role in reducing fatigue through their influence on cerebral energy status.

Another interesting wrinkle in the discussion:

We have also shown a positive association among brain mitochondrial biogenesis [i.e. growing new mitochondria in the brain], voluntary activity and endurance capacity…

What they mean by “voluntary activity” is how much mice, when left to their own devices, decide to run on a wheel in their cage. Researchers have found that the “impulse to exercise” tends to decline with age — so before your body starts to fail, your brain just isn’t as enthusiastic about doing lots of exercise as it used to be. There are some possible hints here that this phenomenon could be linked to declining levels of brain mitochondria. In other words, regular exercise doesn’t just preserve your ability to exercise — it also preserves your desire.

The Talk Test vs. lactate and ventilatory thresholds

THANK YOU FOR VISITING SWEATSCIENCE.COM!

As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

***

Figuring out how hard to push is one of the great challenges in exercise. Personally, I’m a big fan of relying on perceptual methods (“how hard does this feel?”) rather than seemingly objective approaches like heart rate or lactate level. Certainly for competitive athletes, learning to interpret your body’s cues is a crucial step to being able to pace yourself properly in a race. But perceived exertion can be pretty tricky for beginners — which is why simple tricks like the “Talk Test” can be very helpful.

In its most basic form, the Talk Test is pretty simple: if you can talk in complete sentences, you’re below threshold. If you can’t talk, you’re above threshold. If you’re in the middle — you can say a few words at a time — you’re pretty close to threshold. So what is this “threshold” we’re talking about? Ah, that’s where it gets complicated. As exercise gets more intense, your body may or may not pass through several thresholds related to breathing rate, lactate accumulation in the blood, and other physiological parameters. The precise definition of these thresholds — and their very existence, in some cases — is hotly debated. As a crude simplification, threshold pace corresponds to the fastest pace you can sustain aerobically, which usually turns out to be the pace you’d hold in a race lasting about an hour.

All of this is by way of introduction to a new study from researchers at the University of New Hampshire, published in the Journal of Sports Sciences, that compared the exercise intensity at various points in the Talk Test to the exercise intensity at the ventilatory and lactate thresholds. Here’s the data, expressed in terms of heart rate and VO2:

“Negative Talk Test” is when the subjects couldn’t talk comfortably; “positive Talk Test” was when they could talk comfortably; “equivocal Talk Test” was in the middle. It’s clear that this middle zone corresponds pretty closely to lactate threshold. This is a bit surprising, since you’d expect ventilatory threshold — when breathing gets significantly harder — to be more closely tied to talking ability. But it’s convenient, because people care a lot more about lactate threshold than ventilatory threshold.

So how do we use this information? Here’s a basic “training zone pyramid” that I included in a Jockology column on pacing last year, based on research by Carl Foster and others about the typical training patterns of endurance athletes:

So most of your training should be below threshold — a common mistake beginners make, since they’re so unfit, is to be pushing above threshold on every bout of exercise. And some of your training should be at threshold — and I’d bet many competitive runners would badly fail the Talk Test during what they claim are “tempo runs” at threshold! On the other hand, casually spinning the wheels of an exercise bike while reading a magazine is unlikely to do much for you, as the press release from the UNH researchers points out:

“If you are beginning an exercise program and can still talk while you’re exercising, you’re doing OK,” Quinn says. “But if you really want to improve, you’ve got to push a little bit harder.”

 

Exercise intensity is more important than duration

THANK YOU FOR VISITING SWEATSCIENCE.COM!

As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

***

This is a really interesting graph:

It comes from a study called the Copenhagen City Heart Study, which followed a random sample of about 12,000 people in Copenhagen for 21 years. This particular data (which was presented at the European Society of Cardiology conference last week) looked at the cycling habits of the subjects, teasing out the separate effects of how hard they typically cycle and how long they spend cycling on a typical day. What you see is that it’s all about intensity: men who typically cycled “fast” (as subjectively determined by self-report) lived 5.3 years longer than those who cycled “slow,” whereas duration had no significant effect.

Since this is just a conference presentation, I don’t have full details on the data and analysis. Obviously there are likely to be some correlations in action — people who are unhealthy for whatever reason are likely to cycle slower and die earlier. That being said, the results were corrected for “age, gender, number of other sports activities, BMI, systolic blood pressure (including antihypertensive medication), HDL-cholesterol, smoking, income, alcohol-intake and diabetes”. Here’s the comparable data for women:

Heart arrhythmias and endurance sports

THANK YOU FOR VISITING SWEATSCIENCE.COM!

As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

***

I’m starting to really dislike these jerks who keep studying Swedish cross-country skiers and producing findings that conflict with my worldview… First it was arthritis; now, the researchers studied 47,000 people who participated in the 90-km Vasaloppet ski race in Sweden between 1989 and 1998, looking for associations between the number of times they participated in the race and the odds that they were subsequently diagnosed with arrhythmias (a task made possible by Sweden’s comprehensive national health records). The result (according to a press release describing a conference presentation; the findings haven’t yet appeared in a peer-reviewed journal):

Compared to those who had completed one single race, those who had completed 7 or more races had 29% higher risk of a subsequent arrhythmia. Further, elite athletes finishing at 100-160% of the winning time had 37% higher risk of arrhythmias than recreational athletes finishing at more than 241% of the winning time.

Leaving aside the quibble that “elite” is a bit generous for someone finishing at 160% of the winning time, the findings seem to suggest pretty clearly that extensive endurance training increases the chances of arrhythmia. The biggest differences were found in subjects under 45, and were exclusively associated with atrial fibrillation and bradyarrhythmias, which are considered less serious than the “potentially lethal” ventricular arrhythmias, according to the researchers:

Dr. Andersen summarizes: “Basically, this study shows, that even though physical activity is generally healthy, athletes committed to endurance sports at elite level have higher risk of suffering from a heart rhythm disorder… We emphasize that we do not find any increased incidence of potential lethal heart rhythm disorders. However, this study only compares athletes at different levels and a future large scale study comparing athletes against the normal population would be very interesting.”

The last point is interesting. It does seem increasingly clear that training as an elite endurance athlete is more likely to have an impact on the heart than training at a recreational level — but what about compared to sedentary life? Is this a linear relationship, or a “U-curve” where moderate training produces the best results?

Bottom line: although the press release skips some relevant details (like how common were these arrhythmias in absolute terms?!), I don’t think this changes my risk-benefit assessment. It’s like the well-known trade-off for exercise of any sort: your chance of a heart attack rises temporarily during extreme exertion, but your overall odds of heart attack decline with exercise. In this case, it’s worth bearing in mind the findings from previous studies of the same race: the more Vasaloppets you do, the longer you live. So whatever the downsides of arrhythmias, they’re evidently outweighed by other benefits.