Increasing interest is being directed to the physiological mechanisms controlling the process of fibrinolysis. This interest, in part, stems from the suggestion that impaired fibrinolytic response may play a role in the pathogenesis of atheroma (Astrup, 1959), and possibly in the formation of occlusive vascular thrombi. It has been found that there is considerable variation between individuals in fibrinolytic response to a standardized stress such as exercise. It is postulated, therefore, that there exist, in a subgroup of the "normal" population, individuals who have an impaired or defective mechanism for generating plasminogen activator. Several epidemiologic studies have implicated lack of physical exercise as a possible etiologic factor in the genesis of heart disease. Most theories to account for such an association have dealt with increased fitness, increased collateral circulation, and/or increased vessel diameter. The capacity to generate greater fibrinolytic activity would be another possible beneficial mechanism. In the Evans County Cardiovascular Study it was found that there was a significantly greater risk of developing heart disease in Whites than in Blacks, although standard "risk factors" for coronary heart disease were equal. Only when whites were engaged in physically active occupations was their immunity to heart disease equal to that of the black population. It is proposed that this population would be a good one in which to test the hypothesis that individuals who are habitually physically active will show a greater fibrinolytic response to a standardized stress test than individuals who are sedentary. Such a "response" would be measured by the change in plasminogen activator as measured before and after exercise testing; other known risk factors will be considered as covariables.