Marathon runners exhibited significant biventricular enlargement and increased left ventricular mass (212.43 vs 123.48 g, p<0.01) compared to nonathletes, with normal resting myocardial contractility.
Observational (n=32)
Does professional marathon running alter cardiac dimensions and resting function compared to matched nonathletes?
Professional marathon runners exhibit biventricular enlargement and increased left ventricular mass consistent with volume overload, but maintain normal resting myocardial contractility.
Absolute Event Rate: 5.53% vs 4.81%
p-value: p=<0.001
The volume overload type of heart often observed in endurance athletes, was simulate a diseased heart. We used a battery of noninvasive graphic techniques, i.e., echocardiogram, apexcardiogram, carotid pulse, electrocardiogram, vectorcardiogram, phonocardiogram, systolic time intervals, and treadmill stress testing in 12 professional marathon runners, mean age 33.8 +/- 11.1. Twenty nonathletes matched for age, height, sex, and weight served as a control group. Left ventricular (LV) end-diastolic dimension in marathon runners averaged 5.53 +/- 0.5 cm compared to 4.81 +/- 0.04 cm in nonathletes (p less than 0.001), LV end-diastolic volume was 172.69 +/- 43.3 ml compared to 113.57 +/- 30.41 ml in nonathletes (p less than 0.001), stroke volume was 122.27 +/- 32.8 ml compared to 78.42 +/- 20.44 ml in non-athletes (p less than 0.001), the thickness of the posterior LV wall was 1.0 +/- 0.2 cm compared to 0.7 +/- 0.1 cm in nonathletes (p less than 0.001), and LV mass was significantly increased, 212.43 +/- 55.8 g compared to 123.48 +/- 24.54 g in non-athletes (p less than 0.01). Left atrium and aortic root were also relatively larger in athletes (p less than 0.01). Right ventricular end-diastolic dimension was enlarged in marathon runners (2.02 +/- 0.65 cm). No statistically significant differences were noted in ejection fraction, percentage of internal diameter shortening (% delta D) and PEP/LVET. The carotid tracing had a bisferiens pulse in five marathon runners. The apexcardiogram showed a bifid systolic thrust in three and absence of abnormal A wave. These abnormalities were related to the overload type of heart as proven by echocardiogram. "Early repolarization syndrome" (abnormal RS-T segment elevation) and notched T waves in ECG had a counterpart a semilunar configuration in the VCG. Three athletes met ECG criteria and one met VCG criteria of LVH. The treadmill exercise ECG was negative in all 12 athletes. Biventricular enlargement and increased left ventricular mass are present in the marathon runner's heart. Myocardial contractility at rest was, however, not statistically different from nonathletes.
Zoneraich et al. (Sat,) conducted a observational in Endurance athlete heart (n=32). Endurance athletic training (marathon running) vs. Nonathletes was evaluated on Left ventricular end-diastolic dimension (cm) (p=<0.001). Marathon runners exhibited significant biventricular enlargement and increased left ventricular mass (212.43 vs 123.48 g, p<0.01) compared to nonathletes, with normal resting myocardial contractility.
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