Effects of a moderate-intensity aerobic program on blood viscosity, platelet aggregation and fibrinolytic balance in young and middle-aged sedentary subjects

Regular physical activity is associated with reduced risk of cardiovascular disease although the mechanisms are unclear. Recent population-based studies suggest that the effect of physical activity may be at least partly a result of action on hemostasis. We tested the hypothesis that moderate-intensity aerobic training improves fibrinolytic activity and reduces platelet aggregation and blood viscosity. In 15 young (111 males and four females; age, 24-32 years) and 15 middle-aged (111 males and four females; age, 45-65 years) healthy, non-smoker, sedentary subjects, the maximum oxygen consumption, adenosine diphosphate-induced platelet aggregation, tissue plasminogen activator and plasminogen activator inhibitor type 1, antigen, hematocrit and blood viscosity were measured at baseline and after 12 weeks of aerobic exercise training (40 min three times a week at a training intensity adjusted to 60% of the individual heart rate reserve). After training, the maximum oxygen consumption was increased by 9% (P < 0.01) in the young group and by 7.3% (P < 0.05) in the middle-aged group. Adenosine diphosphate-platelet aggregation significantly decreased in the young (-30%; P < 0.05). The middle-aged group showed a 10.4% decrease in hernatocrit (P < 0.05), and a 11.6 and 16.6% decrease in blood viscosity at 450/s and at 90/s rates of shear, respectively (P < 0.05), while the plasminogen activator inhibitor type 1 antigen plasma level increased 135% (P < 0.01). These data, some not consistent with others, only partially support the hypothesis that the beneficial effects of physical activity result from action on hemostatic balance. In particular, the changes in the fibrinolytic system in middle-aged subjects might suggest increased thrombotic risk. Thus a simple, straightforward conclusion is not possible at present, and further studies are required. (C) 2004 Lippincott Williams Wilkins.