Evidence of impaired left ventricular performance after an uninterrupted competitive 24 hour run.

The effect of extremely exhaustive exercise on left ventricular performance was studied echocardiographically in 13 experienced male ultramarathon runners who took part in a competitive 24 hr run, completing distances of 114 to 227 km. Although the left ventricular end-diastolic dimension (EDD) was reduced by 7% (54 +/- 5 to 50 +/- 7 mm; p less than .005), the end-systolic dimension (ESD) increased slightly (33 +/- 5 to 34 +/- 6 mm; NS). As a consequence, the stroke dimension (21 +/- 2 to 16 +/- 2 mm; p less than .005) and fractional shortening (38 +/- 5% to 32 +/- 5%; p less than .005) declined by 24% and 16%, respectively. The reduction in fractional shortening was related to delta ESD (r = -.66; p less than .05) but not to delta EDD (r = .22; NS). In spite of reduced afterload, the mean velocity of circumferential fiber shortening also decreased by an average of 9% (p less than .01) in proportion to the distance completed (r = -.69; p less than .01). The systolic blood pressure/ESD ratio was 21% lower after the race (4.2 +/- 0.9 to 3.3 +/- 0.6; p less than .005). Body weight loss was not related to any alterations in left ventricular dimensions or ejection phase indexes. The stroke dimension and ejection phase indexes continued to decline within the last 6 hr of the race but returned to the prerace level 2 to 3 days after the race. Total serum creatine kinase peaked at 3917 to 64740 U/liter (mean 27427) and its MB percentage peaked at 2% to 6%.(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive evaluation of the athletic heart: sprinters versus endurance runners.

To evaluate possible differences in the cardiac effects of different types of running training, 22 competing male runners--10 sprinters and 12 endurance runners--were studied with a physical examination, electrocardiography, chest X-ray film and echocardiography. Thirteen sedentary men served as control subjects. There were no differences between the athletic groups in physical findings. However, left ventricular hypertrophy in the electrocardiogram was more apparent in the endurance runners (P less than 0.05), whose relative heart size on chest X-ray examination was also greater than in the sprinters (P less than 0.02). On echocardiography the left ventricular end-diastolic volume was equally greater than normal in both groups of athletes (P less than 0.005), but in the endurance runners the percent chance of the minor axis diameter in systole was greater than in the sprinters or control subjects (P less than 0.02). Values for left ventricular wall thickness and mass were greater than normal in both groups of athletes but were higher in the endurance runners than in the sprinters (P less than 0.001). The left atrial diameter was apparently greater in the endurance runners than in the sprinters or control subjects (P less than 0.001), whereas that of the sprinters did not differ from normal. Thus, intensive sprinter training seems to dilate the left ventricle but causes less increase in wall thickness and mass than training for endurance running and no change in left ventricular function or left atrial size. Endurance running causes left ventricular dilatation equal to that of sprinter training, greater wall hypertrophy and improved systolic emptying of the left ventricle, and it also dilates the left atrium perhaps because of decreased left ventricular compliance.