In a landmark paper that brought together information from echo studies done on more than 1,000 athletes in a wide variety of sports, Maron found that on average the athletes had a 46% increase in "left ventricular mass" when compared with non-conditioned control subjects. (Left ventricular mass includes the thickness of the muscle walls as well as the size of the expanded chamber itself.) This increase was accompanied by an average 33% increase in the volume of the expanded left ventricle, with a complementary increase in stroke volume.
These are impressive numbers, but probably the most dramatic stats of highly conditioned athletes are their remarkably low resting heart rates. Because of their big stroke volume, athletes' hearts don't have to beat as often during periods of inactivity. While the average resting heart rate for a healthy adult is about 72 beats per minute, among athletes rates in the 50's and 40's are common. "Sometimes these heart rates go down as low as 30 in marathon runners when they're just sitting around," Crawford says. "You or I would probably pass out if our heart rate was 30. But it's fine with them, because their hearts are pumping such a large amount of blood."
Another fascinating aspect of athlete's heart is how quickly the condition comes and goes. It can develop within weeks and vanish just as fast. In 1993 Crawford and a few colleagues studied 10 New Mexico varsity endurance athletes—four swimmers, three runners and three skiers—who returned to school with normal-sized hearts after a summer of reduced and unsupervised training. The students were examined in August, before they began their team training programs, and again in December, after more than three months of workouts. Not only had their hearts increased in size, but this gain in size was also the athletes' chief mechanism for getting back to a competitive level of fitness.
"It's the only thing we could find that really changed that much," says Crawford. "The athletes' oxygen consumption didn't change that much, so it doesn't look as if they lose oxygen consumption over the summer, but they do lose heart size. So, at least for somebody who is intermittently athletic, it seems like the main thing that comes and goes when they don't train is the heart size." Crawford says there is no evidence that such fluctuations are dangerous: "It's the same as with your biceps. You work it out, then you don't, then you do, and it doesn't seem to get hurt."
The amount of exercise required to bring about such change in heart size, and the speed with which it can occur, were documented in an earlier study of eight swimmers at St. Louis University. After laying off for two to seven months, the swimmers were followed during a nine-week training program of two-hour sessions six days a week. They swam 5,000 to 7,000 yards per session. In the first week their average left ventricular mass increased by 23%, while average stroke volume increased 33%. Things leveled off after that, save for a gradual thickening of the muscle walls that wasn't apparent until the fifth week.
The results are equally striking when athletes cease training. As part of the study involving the St. Louis swimmers, six crosscountry runners from nearby Washington University, who had been training 60 to 70 miles per week for at least three months, took three weeks off. By the end of their third week of inactivity their average left ventricular mass was down 38%, and their average stroke volume was down 23%.
Probably the most important factor in the development of athlete's heart is the type of exercise the athlete engages in. That determines the type of "load" placed on the heart, which in turn determines the exact nature of changes in the heart. Endurance training, such as running, involves aerobic exercise and puts a "volume load" on the heart: The muscles demand more oxygen for extended periods of time. Strength training, such as weightlifting, involves anaerobic exercise and puts a "pressure load" on the heart: There are brief, very strenuous bursts of activity during which the athlete's blood pressure can go as high as 300. (Normal blood pressure for a 25-year-old male is 120 over 80.)
Volume loading primarily increases the size of the left ventricle and the stroke volume. Pressure loading mainly increases the thickness of the muscle walls, with little or no increase in the heart's internal dimensions. So an Olympic weightlifter's heart should have a normal-sized left ventricle, but the muscle walls should be thick, while an Olympic marathon runner should have an enlarged left ventricle without a significant increase in wall thickness.
A number of sports combine both types of exercise, aerobic and anaerobic. In cycling, for instance, gripping the handlebars involves enough strength (or isometric) exercise to cause some additional thickening of the walls beyond what is caused by the endurance (or isotonic) element of the training. Then there is rowing. "The sport is unique, with the involvement of both the arms and the legs, both isotonic and isometric exercise," says Maron. It's like running and lifting weights at the same time. At the elite level, rowing involves probably the most complete mixture of strength and endurance training in sports, producing some of the most exceptional hearts ever studied: hearts with the enlarged left ventricles of endurance athletes and some of the thickest muscle walls ever identified in healthy individuals.
A related feature of athlete's heart is how specific its adaptations are. Improvements in an athlete's cardiac function apply only to the type of activity involved in his or her training. If, for instance, a runner who developed athlete's heart doing leg exercises were to perform arm exercises, his cardiovascular response would be the same as that of a nonconditioned person. This is due, at least in part, to the fact that the increased cardiac output of a highly conditioned athlete is matched by an increase in the ability of the trained muscles to extract oxygen from the blood. Such "peripheral adaptations" involve an increase in the number of small blood vessels supplying the trained muscles.