ALTHOUGH the response of the human heart to exercise has been studied extensively, little information is available on the effects of utterly exhaustive exercise on cardiac performance in man. Marathon running is growing in popularity, however, and thousands of runners, more or less well trained, are taking part in various ultramarathon races (i.e., distances greater than the marathon) all over the world each year. It is well recognized that ultramarathon running is not without risk. In addition to casualties caused by exhaustion, heat stroke, renal failure, and sudden cardiac death," repeated hemoptysis and pulmonary edema due to left ventricular failure has been reported in two welltrained athletes during a 90 km run.5 However, subsequent clinical investigations in these athletes, including cardiac catheterization, revealed no apparent cardiac abnormalities, and it was postulated that some as yet unknown factor (or factors) could lie behind these observations. We had a unique opportunity to make echocardiographic and biochemical measurements on welltrained ultramarathon runners in connection with a competitive 24 hr run. Our results indicate a deleterious effect of such severe prolonged exercise on left ventricular performance. Methods

Digitized M mode echocardiography was used to evaluate the effect of a competitive 24-h run on the left ventricular diastolic function in 12 well-trained marathon runners who completed 146-227 km during the race. Mitral valve opening was delayed, early diastolic filling was decreased and prolonged, and posterior wall thinning was reduced, particularly among those athletes completing close to 200 km or more. Since the alterations were in part the opposite in those running 160 km or less, only the reductions in the peak rate of dimension increase (P less than 0.05) and posterior wall thinning (P less than 0.01) were significant in the group as a whole. The delay in mitral valve opening (r = 0.76), the decrease in the peak rate of dimension increase (r = -0.68), and the prolongation of the early diastolic filling period (r = 0.60) were correlated with the distance completed. The reductions in left ventricular end-diastolic dimension and fractional shortening were not in proportion to the distance run, however (r = 0.23 and 0.46, respectively). Measurements made on six athletes 2-3 days after the race showed reversal of the indices of left ventricular diastolic function. Extremely exhaustive prolonged exercise thus appears to result in a marked reversible impairment in left ventricular relaxation and filling. Since the effect of these abnormalities in cardiac filling during exercise is probably more important due to the shorter diastole, the prevention of hypohydration, which could otherwise further compromise left ventricular filling, becomes crucial.

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