Endurance athletes who exercise for three hours or more have an increased chance of dying from a cardiac arrest
Heart attack risks are greater for athletes who compete in endurance sports. I wish someone would have explained this to me before. I have recently learned that I am one of these athletes, now 50, that faces this challenge. This could be my biggest test of resilience yet. Not getting to swim the English Channel last summer due to poor weather may have just saved my life...read on and I implore you to get a full stress test (not a regular EKG) before you jump in the water.
Channelopathies
(A) Two essential elements precipitate a cardiac event in LQTS. First, a cardiac channel defect results in a 'recharging glitch' that often can be seen on the surface ECG by a prolonged QT interval. Second, a trigger is often needed (in this case, swimming) to cause the stable but prolonged recharging system to degenerate into the trademark arrhythmia of LQTS, torsades de pointes (TdP). The outcome (if the heart ever loses control), fainting, seizing or dying, depends on whether or not order is restored to the rhythm, either spontaneously or by a defibrillator. (B) The linear topologies for the three principal cardiac channels that account for two-thirds of LQTS are shown. The gene responsible for LQT1, KCNQ1 (commonly known as KVLQT1) encodes the alpha subunit of the IKs potassium channel. The gene behind LQT2, KCNH2 (commonly known as HERG) encodes the alpha subunit of the IKr potassium channel. SCN5A, responsible for LQT3, encodes the INa sodium channel. Additional heritable arrhythmia syndromes are shown.
© 2004 Nature Publishing Group Ackerman, M. J. Cardiac channelopathies: it's in the genes. Nature Medicine 10, 463-464 (2004) doi:10.1038/nm0504-463. All rights reserved
Article from Peak Performance:
About 1 in 50,000: if you run marathons or participate in other forms of exercise which last for three hours or more, that's your approximate risk of suffering an acute heart attack or sudden cardiac death during - or within 24 hours of - your effort. For every 50,000 athletes, one will be stricken during such prolonged activity(1). Running a marathon or cycling intensely for three hours is riskier than taking a commercial airline flight, even in these troubled times!
You might think we shouldn't make such a claim in a newsletter which appeals to serious competitors, including a large number of marathon runners. But at Peak Performance our job is to provide you with all the facts about your sport, not just the pretty ones.
The truth is that marathon runners, ironman triathletes and long-distance cyclists, swimmers, rowers and cross-country skiers are all in the same boat. In fact, any athlete who participates in a strenuous test of endurance lasting about three hours or more has an increased chance of dying during - and for 24 hours following - the exertion, even when the athlete's chance of a death-door knock is compared with the risk incurred by a cigarette-smoking, sedentary layabout who spends the same 24 hours drinking beer and watching TV. The reasons for this are not entirely clear, but the heightened risks of a visit from the Grim Reaper are unsettling to most athletes, especially those who exercise in the hope of improving cardiovascular and overall health.
To find out why strenuous exercise temporarily increases the risk of death, researchers at the University of Innsbruck in Austria recently studied 38 male participants in the 1999 Tyrolean Otztaler Radmarathon, a cycling race which covers 230k, with an altitude change of 5,500m. The Radmarathon is often said to be comparable in difficulty to the hardest mountain stages of the Tour de France (2).
All 38 subjects were experienced, well-trained amateur cyclists who were free of cardiovascular risk factors and without evidence of heart disease. The Austrian researchers were especially interested in monitoring their blood levels of a specific heart enzyme called cardiac troponin I, which happens to be the most sensitive and specific marker for the detection of heart-muscle death.
Cardiac troponin I values, which were essentially at zero in all athletes before the beginning of the Radmarathon (thankfully, since you don't want your heart to start dying on you just before you begin a 230k bike race!) increased in 13 (34%) of the cyclists immediately after the competition. The risk factors for elevated cardiac troponin I included: age - being young was 'bad'; race time - racing fast increased the risk, and the highest post-race cardiac troponin 1 level was detected in the athlete with the fastest Radmarathon time; pre-race training distance - the higher the overall training volume, the greater the chances of increased cardiac troponin I after the race.
Taken together, these results suggested that younger, fitter athletes, who put more stress on their hearts (via greater training volume and higher racing intensities), were the ones most likely to incur myocardial damage.
Why heart muscle cells may die during prolonged exercise
Why were cardiac troponin I concentrations up after the Austrian race? According to the researchers, many of the well-trained athletes probably experienced sub-clinical cardiac injury during the event and this was associated with the actual deaths of heart-muscle cells. The mechanism underlying such cardiac cell deaths is unknown, although one popular theory suggests that the heightened adrenaline/noradrenaline levels sometimes observed during prolonged exercise rather perversely lead to the constriction of coronary arteries, which results in localised cell death within the heart. (Adrenaline and noradrenaline - also known as epinephrine and norepinephrine - are hormones released by the adrenal glands in response to stressful situations.)
Heart-cell death during strenuous exercise? Yes, it is a bit like having a small heart attack at the same time that your heart is performing magnificently! In fact, cardiac troponin I is usually undetectable in the blood serum of healthy people but is typically found in those who have suffered a myocardial infarction (heart attack), congestive heart failure, or myocarditis (inflammation of the heart muscle). In fact, the enzyme is used predictively by heart specialists: the higher the level in a particular patient, the poorer his prognosis.
This sounds bad! But has anyone besides the Austrians uncovered evidence of heart-structure damage after strenuous exercise? Actually, yes: one study of finishers in the Hawaii Ironman Triathlon found that 9% displayed elevated cardiac troponin 1 levels and, further, that these individuals also exhibited abnormal heart wall action and function during echocardiographic analyses(3). Another investigation found cardiac-troponin increases in 11% of the finishers of an alpine cross-country marathon (4).
Is the positive post-exercise increase in cardiac troponin I really something to worry about? Were the heart cell deaths merely a small piece of the cardiac pie? Could the lost cells be replaced by regrowth of healthy heart tissue? These key questions are very difficult to answer, especially as no histological analyses of heart tissue were performed as part of these studies, and neither were echocardiograms or electrocardiograms (ECG) carried out to determine whether heart function was impaired. To play it safe, the Austrian researchers suggested that endurance athletes 'should at least undergo serial cardiovascular examinations looking for subtle evidence of myocardial dysfunction'.
The good news for endurance athletes on the cardiac front
Before you get too spooked by these findings, bear in mind that there is also some good news for endurance athletes on the cardiac front. For one thing, it's clear that regular exercise protects you from heart attacks over broad time frames; for example, over the course of a year regular exercisers will have fewer cardiac failures than their sedentary counterparts. Also, some studies have not linked extremely strenuous exercise with cardiac damage: for example, when sports medicine specialists at the University of California studied 23 ultramarathon runners who completed the 100-mile Western States Endurance Run, a rugged race through the Sierra Mountains over steep terrain and through temperature extremes, they were unable to find any race-related cardiac damage (5).
The 23 runners completed the 100-mile race in an average time of 23.5 hours, with a range of 18.9-27.1; their ages ranged from 29 to 62 (with an average of 45) and all but three were men, none with a history of heart disease. Although all of the subjects suffered massive skeletal muscle damage during the competition (as evidenced by huge increases in serum creatine kinase levels after the race), not a single runner exhibited heightened cardiac troponin levels after the extremely prolonged exertion was over.
None the less, an increasing body of evidence indicates that some heart damage can occur during extreme exercise. In the very latest study completed at Massachusetts General Hospital and the Harvard Medical School, researchers tracked 82 runners with an average age of 47 who ran the Boston Athletic Association Marathon for five consecutive years, from 1997 to 2001. These runners had no history of coronary disease, were non-smokers and averaged 25 training miles per week(6). But their cardiac troponin I levels increased roughly 6.5-fold both four and 24 hours post-race.
No one knows how long exertion related heart damage lasts
Again, we must pose the key question - is this exertion-related damage to the heart long-lasting, or does the heart recover promptly without long-term negative effects? Unfortunately, no one knows the answer to this question right now. If you are interested in running marathons, you will have to decide for yourself if the real risk associated with the race is tolerable or not - and whether the long-term perceived risk is serious enough to warrant changing your competitive activities.
Our traditional argument that prolonged endurance activity is not bad for the heart is based on evidence that marathon runners have fairly low death rates from cardiovascular disease (when you look at them away from the race itself and the 24-hour 'window' that follows it). Essentially, research indicates that well-trained endurance athletes have about 40% of their sedentary counterpart's risk of dying from a cardiac problem on a typical day (7). If strenuous exercise is really so bad for the heart, why aren't endurance athletes keeling over at higher rates?
Note, though, that this latter argument is not entirely compelling. It is possible that marathoners might have even lower frequencies of heart attacks if they gave up marathoning and focused on shorter events which are less taxing for the heart. In support of this theory, former marathon runner Dr Arthur J Siegel of McLean Hospital in Belmont, Massachusetts (one of the investigators in the study cited above) recently told Reuters Health that running a marathon is, in effect, like overdosing on a good thing. With a more moderate approach, cardiovascular risk would still be lowered, while the elevated risks associated with marathon-like events would be avoided. Add marathon efforts to the brew, and you get the general reduction in risk but with an added risk associated with the race itself (and perhaps its long preparatory runs).
If you are having second thoughts about running marathons, you should know that the previously quoted rate of one death per 50,000 marathon runners might be a bit high. For example, there is evidence that in male runners aged 30-64 who have not been diagnosed with heart disease, there is approximately one death for each 800,000 'person-hours' of running or jogging (8). This implies that if 800,000 healthy middle-aged males began running the New York City Marathon, one of them would probably die during the first hour of the event, another during the second hour and another during the third. This kind of death rate would create some bad publicity, so it is a good thing that the New York Marathon limits the number of entrants to less than 30,000 (thus trimming the incidence of death to about one every seven years). If one assumes an average finishing time of four hours, the 800,000 figure projects a death rate of one per 200,000 marathon entrants, considerably lower than the earlier estimate of one in 50,000. Incidentally, it is known that females have a much lower risk, although the relative mortality rate has not been quantified.
Expressing the 800,000 statistic in a different way, we can say that healthy, middle-aged males who run for one hour each day can expect to die while running once every 2,192 years (800,000 hours divided by 365 hours of running per year = 2,192 years). By the same token, individuals who run two hours per day should die while running about once every 1,096 years. When the risks are seen in this light, many endurance athletes will consider them acceptably low, especially as the general risk of heart disease is reduced by strenuous training.
Heart deaths are not random events
In addition, when deaths do occur, they are certainly not random providential events. Post-mortem analyses usually reveal that something was wrong with a dead athlete's heart prior to the race (no surprise there). For example, in the study which led to the death estimate of one per 50,000 marathon entrants, a total of 215,413 runners who competed in either the Marine Corps Marathon from 1976 to 1994 or the Twin Cities Marathon from 1982 to 1994 were monitored. Three of these 215,413 runners died during their races (always after the 15-mile point) and one succumbed shortly after completion of the event. Autopsies revealed that three of the runners actually had atherosclerotic coronary artery disease (narrowing of two or three key coronary vessels), even though they were symptom-free before the races. The fourth victim (also symptom-free before death) had an anatomical defect related to the left main coronary. Thus, marathon racing didn't destroy these athletes' hearts as they paced along the streets of Washington or Minneapolis but rather uncovered 'weak links' in their cardiac systems which could not stand up to several hours of strenuous, continuous exercise.
This brings us to the issue of screening: could you take a test which might reveal that your heart was vulnerable to trouble during strenuous exercise? The relevant test in this case would, of course, be an exercise stress test, during which an ECG reading is taken as you run at increasing intensities on a treadmill. These 'exams' can frequently unmask fat-filled coronary arteries.
Unfortunately, the tests do not have a very high predictive value since as many as 63% of those who 'fail' a stress test actually have completely normal cardiovascular systems(9). Furthermore, the rate of such 'false positives' among endurance athletes can be 100% (ibid), because the natural thickening of the heart in response to endurance training changes ECG readings!
This high frequency of 'wrong calls' is troubling, not only because of the inaccuracies associated with stress testing it reveals but because many of those with false positive results are then subjected to more rigorous and invasive medical procedures, including thallium stress testing (in which a dye is placed in the bloodstream during exercise) or coronary catheterisation (in which a long tube is snaked through blood vessels into the heart). These tests are expensive and not without risk; in fact, coronary catheterisations may be riskier than marathons!
None the less, about 34% of physicians who run the Boston Marathon believe that people should undergo an exercise stress test before beginning a strenuous exercise programme(10). Interestingly enough, though, only about half of these doctors actually permitted stress tests to be performed on themselves before they began training for Boston!
Stress tests carry their own risks
One reason for this 'do as I say, not as I do' attitude may be that stress tests themselves are not without risk. The risk of dying during a stress test is a matter for debate, but has been estimated at anything between 1-in-20,000(11) and 1-in-500,000 tests(12). As you can quickly calculate for yourself, if the true stress test death rate happened to be 1-in-25,000 and the true marathon death rate stayed at 1-in-50,000, and if stress testing was used to 'screen' marathon entrants, two people would be killed during stress testing for every one athlete potentially saved!
There's more! The vast majority of individuals who die during or shortly after exercise would have had completely normal stress tests, even if the tests were given the day before they died (13). Some experts believe that stress testing can only detect about 20-25% of the likely victims of sudden, exercise-related death. None the less, if you have one or more of the known risk factors for coronary disease (obesity, diabetes, cigarette smoking, high total cholesterol, low HDL-cholesterol, high blood pressure, high stress levels, or a family history of heart disease) you may want to talk to your doctor about stress testing. If you happened to be in that 20-25% group, it would be helpful to have your cardiovascular problem detected.
Distance eventers should look for signs of heart trouble
Whether or not you have risk factors for heart disease, if you compete in distance events you should monitor yourself closely for premonitory symptoms of heart trouble. The warning signs we all know about include chest discomfort or squeezing, throat tightness, and pain that radiates into the jaw or left arm. There are other signs of trouble which are less well-known, including unusual fatigue. If you are uncharacteristically tired and are confident that this is not due to an increased training load or a recent infection, don't ignore it; mention the problem to your doctor and see if you can arrange for a routine physical examination.
In addition, a sudden, unexplained drop-off in performance which is not associated with overtraining could also indicate that something is amiss with your ticker, as could the sudden onset of heart palpitations. Finally, be particularly wary of chest discomfort of any kind which appears during exercise and then disappears afterwards. Angina often does not express itself as sharp pain; typical symptoms include squeezing sensations in the chest, and feelings of pressure or chest tightness. It is possible that up to 50% of people who have heart attacks while exercising experience a fair number of small warning signals during the days or weeks leading up to the attack - so watch out! As noted US cardiologist Paul Thompson points out, 'If you think there is something wrong, there usually is, and a physician should be consulted'.
Pheidippides, one of the first endurance athletes in recorded history, dropped dead shortly after his 21-mile, 1,470-yard run from the plain of Marathon to the agora of Athens in 490 BC. True, no autopsy was performed on the Greek messenger, and his death could have been caused by dehydration or an unsettling encounter with the god Pan in the mountains north of Athens (described in some early accounts of this first 'marathon'). In addition, we don't know how fit Pheidippides was before his fateful run, which certainly would have delivered a great shock to an untrained cardiovascular system. None the less, it is certain that exertion-related deaths do occur at a low frequency, even in well-trained athletes. The paradox of exercise is that it increases your risk of dying at the same time that it reduces it.
Re Print from Peak Performance Owen Anderson
References
1. Journal of the American College of Cardiology, vol 28, pp 428-431, 1996
2. American Journal of Cardiology, vol 87, pp 369-371, 2000
3. American Journal of Cardiology, vol 83, pp 1085-1089, 1999
4. Journal of the American Medical Association, vol 282, p19, 1999
5. American Journal of Cardiology, vol 80, pp 379-380, 1997
6. American Journal of Cardiology, vol 88, pp 920-923, 2001
7. New England Journal of Medicine, vol 311, pp 874-877, 1984
8. Journal of the American Medical Association, vol 247(18), pp 2535-2538, 1982
9. New England Journal of Medicine, vol 293, pp 367-371, 1975
10. The New England Journal of Medicine, vol 301, pp 792-793, 1979
11. Chest, vol 77, pp 94-97, 1980
12. Running Research News, vol 5(6), pp 1, 6-10, November-December 1989
13. The New England Journal of Medicine, vol 321, pp 320-324, 1989
