Science / Medicine : Triathlons Pump Up Heart Research : Cardiology: The races have become unique laboratories to study the effects of physical exertion. Scientists hope to gain valuable insight into the workings of heart disease.
The Hawaii Ironman Triathlon is probably the most grueling premeditated test of human athletic endurance ever designed. Besides the extraordinary distances--2.4 miles swimming, 112 miles biking and then 26.2 miles running--competitors may also face choppy ocean waters, 20-m.p.h. winds and temperatures reaching 120 degrees when the course leads them over scorching black lava beds.
In addition to being a supreme test of athletic performance, Hawaii and other Ironman-length triathlons have become unique laboratories for scientists to study the effects of physical exertion on heart function.
A medical research program dubbed “Labman” has been studying triathletes since 1983. One of Labman’s principal investigators and the leading cardiologist on the team, Dr. Pamela Douglas of Boston’s Beth Israel Hospital and Harvard Medical School, says the group wanted to examine “the upper limits of what conditioning could do, and these are among the most fit people in the world.”
Douglas and other Labman researchers are finding curious changes--both short- and long-term--in the hearts of triathletes. Many of these changes would signal possibly severe problems in average people, but in top athletes they seem to be benign products of super conditioning. As scientists learn more about such phenomena, they hope to gain valuable insight into the workings of heart disease.
Serious triathletes usually train 3 to 5 hours a day, up to seven days a week. A key indicator of aerobic fitness is VO2 max, which measures the maximum amount of oxygen the body’s exercising muscles can use for energy production each minute. Through studies of VO2 max, Labman researchers have documented the very high level of fitness triathletes achieve through exercise. Labman started at the University of Pennsylvania Medical School, but has expanded to a number of different institutions.
“Any VO2 max over 65 is very good,” said Labman’s Dr. Mary O’Toole, an exercise physiologist at the University of Tennessee in Memphis. “Recreational athletes usually have levels in the 40s, and sedentary people range from 25 to 30.”
Although a runner with a high VO2 max usually cannot equal that level in another sport, most championship triathletes average VO2 max readings that are just below record levels, from 65 to 70, in each of their sports. Six years ago, Labman researchers recorded the highest VO2 max known to have been measured in a woman, when triathlete Jody Schmidt reached a level of 80 while running.
Aerobic training, like running, biking, and swimming, not only strengthens skeletal muscles and improves the muscles’ ability to use oxygen in energy production, but also strengthens the heart and lungs. Some of the most interesting Labman studies have looked at heart function. “As cardiologists,” Douglas said, “we learn to look at athletes through eyes that are used to looking at patients with heart disease. But athletes’ hearts really give us an entirely different perspective of heart function.”
Triathletes tend to have hearts with chambers that are bigger than normal, with thicker walls, and nearly all have at least one leaky valve. While these findings often mean seriously diminished heart function in non-athletes, they are considered benign physiological adaptations in top athletes. In fact, triathletes show normal to improved heart function, and most have low resting heart rates and high stroke volumes, which means their hearts can pump more blood with less work.
In non-athletes, thickening of the muscle tissue that makes up the heart wall is often linked to high blood pressure. The condition, pathological hypertrophy, usually disrupts diastolic function--the heart’s filling between beats--and leads to heart disease. In one study, Douglas has shown that in triathletes, heart wall hypertrophy is correlated with blood pressure during exercise, but has a slightly different pattern than found in diseased hearts.
“Nobody knows if hypertrophy in athletes is bad or good,” she said. “But exercise-induced hypertrophy does not usually cause functional abnormalities in athletes’ hearts. This suggests that different causes of hypertrophy can have different effects. The explanation for this may even be something that happens on a cellular or subcellular level.”
Ironman-length and longer competitions can also have a short-term effect on the heart. To see what aspects of heart function were most limited during arduous exercise, Douglas and her colleagues used advanced, non-invasive techniques to compare the dimensions of the left and right ventricles of triathletes’ hearts immediately after the race.
During exercise, blood vessels in the legs dilate, making it easier for the left ventricle to pump blood into them. The right ventricle, however, must work much harder because it delivers blood to the lungs, whose vessels do not dilate during exercise.
“We found that the left side of the heart became smaller after the Ironman, while the right ventricle had dilated,” she said. “This suggests the right ventricle was trying to recruit extra muscle to maintain its pumping efficiency, and that during exercise right heart function may be more limiting than left.”
Research by a number of groups, including Labman, has also shown that prolonged exercise can temporarily disrupt the left ventricle’s ability to fill and empty. To determine what could be causing this effect, Douglas examined heart wall motion in triathletes just after the Ironman.
Some athletes had reduced wall motion in parts of the left ventricle. In a non-athlete, such a patch of paralyzed heart muscle usually means that a major vessel in the heart is fully or partially blocked (clinically described as ischemia), or that there is a serious metabolic problem in that part of the heart. The triathletes’ hearts returned to normal by the day after the race, and they seemed to suffer no ill effects.
Such findings are probably enough to make most heart doctors warn their patients against doing so much exercise, but Douglas is cautious about interpreting the data. “Without doing a more invasive procedure like a biopsy,” she said, “we can’t determine whether their heart tissue has actually been permanently damaged or not.”
Douglas believes triathletes may be experiencing temporary cardiac fatigue--literally a tiring of the heart muscle--and this finding may help explain why people with heart disease tire easily.
“Nobody knows why patients with heart failure have to stop exerting themselves when they do,” she said, “but if we can demonstrate that the concept of cardiac fatigue is valid for healthy people who have exercised a lot, it may shed light on what’s happening in sick people who can’t exercise much at all.”
Because triathletes’ hearts are often so different from those of non-athletes, they may also respond to disease differently, and their care requires a special approach. “Sometimes I will get a call from a physician in another city who’s concerned about a test result from one of my athlete-patients,” Douglas said. “If I’ve explored that particular aspect, and it seems to be just part of his or her heart’s adaptation to exercise, I can tell them that this is a normal finding in that patient.”
She also helps avid triathletes with heart problems train intelligently for their sport. One of Douglas’ patients, 34-year-old Walter Ramos, an investment banker in Philadelphia, was a member of Brazil’s 1976 Olympic swimming team and had been a triathlete since the mid 1980s. In November, 1989, Ramos received an artificial aortic valve to replace his congenitally abnormal one that had been further damaged by infection. “Another guy who had the same operation that day,” Ramos said, “was about 20 pounds overweight, not athletic, and a drinker. He struggled to get out of the intensive care unit in three days, but I walked out of there in 23 hours.”
Douglas followed Ramos’ progress carefully, giving him a training schedule that allowed him to slowly increase the level of intensity of his training by monitoring his heart rate. Six months later, Ramos completed a sprint triathlon (about one-third the distance of the Ironman) in 2 hours, 10 minutes, a time that was one minute under his personal best.
Another of Douglas’ patients, retired Tucson title insurance executive Gary Clark, was the first heart transplant patient to finish a triathlon. Suffering from viral cardiomyopathy, caused by a virus that destroys heart tissue, Clark was hours away from death when he received a transplant in 1985. With the guidance of Douglas and surgeon Jack Copeland of the University of Arizona Heart Center, the previously sedentary Clark accelerated his rehabilitation and eventually competed in triathlons.
“No one who has had a heart problem should undertake this type of training before talking to a lot of people,” Douglas said. Even people who think they are healthy could uncover a heart condition if they engage in such strenuous activity without first having a medical checkup.
The same determination that makes triathletes excellent study subjects for examining the heart’s response to exercise also makes them a danger to themselves sometimes. “The mentality of an endurance athlete is to endure,” said Dr. Douglas Hiller, a member of Labman and an orthopedic surgeon at the University of Hawaii, “so they like to overcome challenges. It’s a standing joke in medical circles that it’s easier to get them to slack off if you tell them it will hurt their performance, than if you tell them it will kill them.”
Measuring Fitness
Researchers use VO2 max, a parameter of aerobic fitness, to measure the maximum amount of oxygen the body’s exercising muscles can use for energy production each minute.
VO2 max levels Sedentary people: 25-30 Recreational athletes: 40-50 Most championship triathletes: 65-70 Highest level recorded: 80 Source: Labman Research
