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Posts Tagged ‘cardio’

Marathon heart attacks: new data

January 13th, 2012

There’s a big new study out in the New England Journal of Medicine that takes a comprehensive look at every case of cardiac arrest during every marathon or half-marathon in the U.S. with more than 100 participants between 2000 and 2010. It’s being widely covered in the press; you can read a good summary in the New York Times or in the Globe and Mail, among other places. The primary message: these events are rare. There 59 cases of cardiac arrest, of which 42 were fatal. That translates to a 1 in 259,000 chance of dying, which is much lower than previous reports and than many other sports.

I’m actually in Houston right now for the U.S. Olympic Marathon Trials, and it happens that Aaron Baggish of Mass General, the senior author of the study, was giving a talk this morning to the members of the World Road Race Medical Society — so I popped in to hear what he had to say. A couple points he made that I found interesting:

Weather wasn’t a factor. The average starting temperature during events where someone suffered a heart attack was almost identical to the 10-year average (55.9 vs. 55.5 F), and the average deviation was just 0.3 degrees.

For 31 of the cases, they were able to track down either the survivor or the next-of-kin and get full medical records, autopsy results, and running history — so this allowed them to really look at the causes of death in detail. One of the surprises is that none of the runners died from a ruptured plaque producing a blood clot, which is (or at least was) thought to be one of the possible mechanisms of sudden death in athletes. The problem with ruptured plaques is that they’re hard to predict in advance. But if underlying coronary artery disease is the real problem (more on that in a sec), then pre-exercise cardiac screening should be able to pick some of that up, Baggish argues.

The average age of the people who survived cardiac events was 53; the average age of the people who died was 34. There are two distinct groups here. One is young people with thick hearts (“hypertrophic cardiomyopathy”), an underlying genetic conditionl; when they collapse, they’re very hard to revive and tend to die. The other is older men with narrowed arteries (coronary artery disease) due to the usual risk factors; when they collapse, they can often be revived if someone gets to them soon enough.

That brings me to one of Baggish’s key point: the absolute best predictor of whether someone would survive cardiac arrest during a race was simple: did a bystander start CPR immediately, before paramedics got there? The lesson is simple: we should all — runners, family members, spectators, heck, everyone in society — have basic CPR training. It could make all the difference to someone, including you.

Baggish’s overall message: running (and by extension, other aerobic activity) is generally safe — but it doesn’t give you immunity from heart disease. That means that everyone, and particularly older males, should be alert for warning signs and not ignore them. Some key ones:

  • a burning sensation in the chest (could be confused with acid reflux) that comes on when you start running then gradually fades away, and keeps recurring;
  • breathing more heavily than you’d expect given your effort;
  • persistent, unusual fatigue.

None of these risk factors necessarily mean something is wrong, but they can be a signal that it’s worth checking in with your doctor to see is you’ve got coronary artery disease that needs to be addressed before racing a marathon.

Last point. Previous studies have shown that most marathon race deaths occur in the final mile or at the finish; this study confirms that. The implication: if you have reason to worry about your heart’s health and want to minimize that risk, think twice about your final sprint. Here’s the data, broken down by race quartile:

Maternal exercise lowers fetal heart rate

January 7th, 2012

A new study in Medicine & Science in Sports & Exercise, from the same group in Kansas City that previously found lower fetal heart rates when mothers exercised during pregnancy. This time, they were looking for a dose-response effect — the more exercise, the lower the heart rate — which would strengthen the case for causality rather than correlation. Here’s what they found:

“A” is “active” and “Q” is “quiet (as in whether the fetus is moving around or lying still). The Q results weren’t statistically significant, but for the A results, greater intensity did indeed lead to lower heart rates. But perhaps most significant is what they didn’t find:

Interestingly, maternal factors (i.e. maternal age, maternal resting HR, maternal weight gain, pre-pregnant BMI) did not influence the associations between physical activity and fetal parameters. Fetal cardiac autonomic control was enhanced in mothers who participated in physical activity regardless of the amount of weight they gained, their weight status prior to pregnancy, resting HR or age.

In other words, they’re not saying that fit mothers have fit babies; they’re saying that active mothers have fit babies.

“Reduced intensity” HIT: the Flutter of exercise

December 2nd, 2011

Anyone remember this Twitter spoof video from back in 2009, when Twitter was just catching on? It’s all about “Flutter,” which “takes microblogging to the next level” by restricting the length of each message to 26 characters instead of 140 characters. Nanoblogging, they call it.

I couldn’t help thinking of this when I read this new study in the European Journal of Applied Physiology about “reduced-exertion high-intensity interval training” (REHIT). Over the last few years, high-intensity interval training (HIT) has gotten a lot of attention as a time-efficient way of getting many of the health benefits of aerobic exercise. There are various protocols — the classic is four to six 30-second sprints with 4:00 easy jogging or cycling to recover between each one; another common one is alternating bouts of 1:00 hard with 1:00 easy. These workouts seem to be highly effective at improving traits like insulin sensitivity. But there’s a catch, according to the authors of the new study:

However, whilst these observations [about HIT] are interesting from a human physiological perspective, their translation into physical activity recommendations for the general population is uncertain for two reasons. First, the relatively high exertion associated with ‘classic’ HIT sessions requires strong motivation and may be perceived as too strenuous for many sedentary individuals. Second, although a typical HIT session requires only 2–3 min of actual sprint exercise, when considered as a feasible exercise session including a warm-up, recovery intervals and cool-down, the total time commitment is more than 20 min [gasp!], reducing the time efficiency. Thus, there is scope for further research to determine whether the current HIT protocol can be modified to reduce the levels of exertion and time-commitment while maintaining the associated health benefits.

In other words, the “140 character” version of exercise is still too damn long, so we need to shorten it to 26 characters!

So here’s the protocol they used. The subjects (29 sedentary young men and women) did three workouts a week for six weeks. Each of these workouts was exactly 10 minutes long, and consisted almost exclusively of “low intensity” cycling, at 60 W. This is very easy. During each 10-minute workout, the subjects incorporated two 10- to 20-second hard sprints. That’s it. Lo and behold, the men in the REHIT group increased their insulin sensitivity by 28%. Strangely, the women didn’t improve — it’s not clear why there was a gender difference. It may be that the very short sprints are most useful for men, who tend to be more powerful and thus are able to burn through more glycogen in a short time.

Anyway, there you have it: REHIT, the Flutter of exercise. I have to admit, part of me finds this a little funny. Soon we’ll be doing studies to show that, if you’re really and truly unfit, just blinking your eyes will allow you to make “measurable gains” in fitness parameters. On the other hand, the barriers to getting people to exercise really are tough to beat. I’m always encouraging my parents to do a little HIT rather than just stick to low-intensity activity — and they do, but they’re rarely motivated to spend more than 10 minutes in total. So it’s encouraging — and useful — to know that even a very minimal bout of high intensity will help. In the end, though, the message is pretty much what we already knew: every little bit helps — but more is better.

Marathons and the female heart

November 15th, 2011

Is marathon running good or bad for your heart? That question has become a hot topic over the past few years thanks to a few studies showing negative effects like heart scarring and artery hardening in veteran marathon runners. One of those studies was a conference presentation last year that looked at 25 male runners who had each completed the Twin Cities marathon 25 years in a row. Compared to matched controls, the runners had greater plaque volume in their coronary arteries.

Now the same group of researchers has followed up with a similar study of 25 female runners who have run a marathon each year for the past 10 years. In this case, the result (as presented at the American Health Association conference) is exactly the opposite: the runners have fewer coronary plaques than matched controls.

So what to make of this? Neither study has been published in a journal yet, so it’s difficult to analyze the results in detail. It’s possible that the conflicting results are simply a result of the fact that the male marathoners were older, on average, that the female marathoners. Or it may be a physiological gender difference. Or it may have something to do with training history. Or it may be a complete fluke: in the male group, the key difference in the plaque volume was 274±176 vs. 169±170. Those are rather large ranges of uncertainty.

But the real question is none of the above: it’s whether these findings about elevated risk factors translate into compromised health. So far, I’m not aware of any study that links marathon running, or any form of endurance exercise, to elevated risk of death (or any other serious ailment) from any cause. That doesn’t mean such risks don’t exist (they could easily be hidden by the overall positive effect of exercise’s other health benefits). Still, as I wrote in the Globe and Mail a few months ago (and probably reflecting my “wishful thinking” bias), I can’t bring myself to get too worried about these apparent risks in the absence of any direct evidence. As Amby Burfoot wrote, “show me the bodies in the streets.”

Average fitness has (surprise) increased since the 1970s

November 2nd, 2011

Here’s an interesting graph from a new paper from the Cooper Institute, the famous fitness institute founded by Kenneth Cooper, the “inventor” of aerobics:

The paper appears in this month’s issue of Medicine & Science in Sports & Exercise, and it shows the results of 52,785 fitness tests performed on men at the Cooper Institute between 1970 and 2009. Each patient appears only once in the data, so it’s not a longitudinal study of how individuals got more or less fit; it’s a cross-sectional study showing how the initial fitness of patients at the institute has changed over the years. The trend is pretty straightforward: a big jump from the 1970s to the 1980s, then levelling off to the 1990s, then a slight decline into the most recent decade.

So… at first glance, I found this data pretty surprising. My naive guess would have been that fitness (as represented in this graph by VO2max determined in an incremental treadmill test) would have declined steadily from the 1970s to the present. After all, we’re always hearing about how society has never been less fit. Instead, it seems that we’re fitter than we were 30 years ago, and other data in the paper suggests that we’re more active too. So does this mean that our current health woes have nothing to do with physical activity level? After all, the data also shows that average weight in the subjects has increased by 8 kg since 1970, while height has stayed the same. So we’re more active, but fatter — a pretty good indicator that diet, rather than exercise, is driving the rise in obesity.

Of course, there are a few caveats. For one thing:

Cooper Clinic patients are self-referred or referred by their employers and are primarily healthy college educated middle to upper income non- Hispanic whites who have access to medical care.

So there’s really no way of knowing whether the average patient who decides to go to the Cooper Clinic is comparable to the average patient from the 1970s. It could be, for example, that the clinic’s clientele has changed as it became famous, so that it now attracts people who are already a bit more serious about fitness. But that’s just speculation. The data may well be a fair representation of societal trends — and if so, I need to revise some of my assumptions.

Good diet trumps genetic risk of heart disease

October 20th, 2011

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.”

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Brain endurance, mitochondria, and the desire to exercise

September 21st, 2011

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

September 16th, 2011

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

September 4th, 2011

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

September 3rd, 2011

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.