For the first time, researchers are beginning to understand exactly how various forms of exercise impact the heart. Massachusetts General Hospital (MGH) investigators have found that 90 days of vigorous athletic training produces significant changes in cardiac structure and function and that the type of change varies with the type of exercise performed. Their study appears in the April Journal of Applied Physiology.

“Most of what we know about cardiac changes in athletes and other physically active people comes from ‘snapshots,’ taken at one specific point in time. What we did in this first-of-a-kind study was to follow athletes over several months to determine how the training process actually causes change to occur,” said lead author Aaron Baggish, MD, a fellow in the MGH cardiology division.

To investigate how exercise affects the heart over time, researchers enrolled two groups of Harvard University student athletes. One group was comprised of endurance athletes — 20 male and 20 female rowers — and the other, strength athletes — 35 male football players.

Student athletes were studied while participating in their normal team training, with emphasis on how the heart adapts to a typical season of competitive athletics. Echocardiography studies were taken at the beginning and end of the 90-day study period.

Endurance training included one- to three-hour sessions of on-water practice or use of indoor rowing equipment. The strength athletes took part in skill-focused drills — exercises designed to improve muscle strength and reaction time, and supervised weight training.

At the end of the 90-day study period, researchers observed a significant increase in left ventricular (LV) mass in both types of athletes. Although this increase in LV mass was of similar magnitude in both groups, it was associated with distinct training-specific structural and function profiles. Endurance athletes, performing daily sustained aerobic exercise, experienced LV dilation, enhanced LV diastolic function, biatrial enlargement, and right ventricular (RV) dilation with increased systolic and diastolic function.

In contrast, strength athletes, performing repetitive short burst-type power exercises, experienced concentric LV hypertrophy, a reduction in LV diastolic function, and demonstrated no changes in atrial dimensions or RV parameters.

“We were quite surprised by both the magnitude of changes over a relatively short period and by how great the differences were between the two groups of athletes,” Baggish said. “The functional differences raise questions about the potential impact of long-term training, which should be followed up in future studies.”

Researchers suggested some mechanistic explanations for the observed changes, but cautioned that they remain speculative. They said that endurance athletes must maintain sustained elevation in cardiac output that must be handled by both sides of the heart.

“It is plausible that this repetitive volume challenge accounts for the biatrial enlargement and the biventricular structural and functional changes we observed in endurance athletes,” they wrote.

In contrast, strength training-induced change appeared to be confined to the LV. Based on this and other studies, researchers suggested that there is strong evidence that repetitive power activity has the capacity to alter structure and function of the heart and proximal arteries.

“We propose that daily sessions of strength training, accompanied both by transient increases in LV afterload and by small but significant increases in resting systolic blood pressure, are responsible for the isolated concentric LV hypertrophy and reduced diastolic LV function observed in strength athletes,” they wrote.

Baggish and colleagues said their results refute the notion that individuals with “athlete’s heart” morphology are simply more likely to rise to the competitive ranks of sport and that their training endeavors are at least in part directly responsible for their cardiac morphology.

While this study looks at young athletes with healthy hearts, the information it provides may someday benefit heart disease patients.

They also suggested that their findings may ultimately prove relevant to the many individuals with intrinsic heart disease who engage in exercise for recreation or rehabilitation and should be considered during the design of future therapeutic exercise trials.

“The take-home message is that, just as not all heart disease is equal, not all exercise prescriptions are equal,” Baggish said. “This should start us thinking about whether we should tailor the type of exercise patients should do to their specific type of heart disease. The concept will need to be studied in heart disease patients before we can make any definitive recommendations.”

Comparison of Pre- and Post-training LV Parameters
Left Ventricular Internal Diastolic Diameter/Body Surface Area, mm/m2
Endurance Athletes	Pretraining: 24.9	Posttraining: 26.3	P Value: <0.001
Strength Athletes	Pretraining: 23.0	Posttraining: 23.4	P Value: NS
Relative Left Ventricular Wall Thickness
Endurance Athletes	Pretraining: 0.39	Posttraining: 0.40	P Value: NS
Strength Athletes	Pretraining: 0.38	Posttraining: 0.44	P Value: 0.001
Right Ventricular Basal Diastolic Diameter/Body Surface Area, mm/m
Endurance Athletes	Pretraining: 24.9	Posttraining: 26.3	P Value: <0.001
Strength Athletes	Pretraining: 23.0	Posttraining: 23.4	P Value: NS
Right Ventricular area change, %
Endurance Athletes	Pretraining: 34	Posttraining: 46	P Value: <0.001
Strength Athletes	Pretraining: 37	Posttraining: 36	P Value: NS