Acute pulmonary oedema in two athletes during a 90-km running race

Two highly trained Black athletes developed haemoptysis during the 90-km Comrades Marathon in 1978 and completed the race with clinical signs of left ventricular failure. For both athletes this was at least the second occurrence of haemoptysis during races longer than 42 km. Chest radiography showed bilateral pulmonary consolidation, upper lobe venous congestion and cardiomegaly in both athletes, one of whom also had a small pleural effusion. Within 36 hours both athletes were clinically better. In one all the radiological abnormalities had disappeared; in the other, heart size had returned to normal, but some pulmonary shadowing remained. The absence in both athletes of other diseases to account for the radiological findings and the rapidity with which these regressed, despite negligible therapy, strongly suggests pulmonary oedema of cardiac origin. Yet conventional cardiological investigation including electrocardiography, echocardiography, phonocardiography, coronary angiography and ventriculography failed to demonstrate cardiac disease in either athlete. As both athletes compete without symptoms in races of up to 42 km, the authors postulate the presence of a cardiac abnormality as yet unrecognized and susceptible to physiological changes which occur only during very prolonged exercise. One possibility is that myocardial compliance becomes progessively impaired during very prolonged exercise. Experimental evidence for this hypothesis is the finding that the rate of myocardial relaxation is, in part, dependent on the rate at which energy can be produced in the glycolytic pathway (the anaerobic metabolism of glycogen or glucose in the cardiac sarcoplasm). During prolonged exercise, a rise in circulating free fatty acids, together with a fall in cardiac glycogen and in serum insulin, would be expected to reduce the rate of glycolytic energy production, thereby reducing the rate of myocardial relaxation. Reduced left ventricular filling due to impaired myocardial compliance, together with the shortened duration of diastole caused by a high exercising rate, might produce left ventricular failure in a structurally normal heart, thus explaining the clinical presentation in these 2 athletes.