Upright posture and maximal exercise increase platelet aggregability and prostacyclin production in healthy male subjects.

Abstract

It is well accepted that heavy physical exertion can trigger the onset of myocardial infarction, but the mechanism is uncertain. As platelet and endothelial function play an important role in thrombotic events, platelet and prostacyclin responses to maximal treadmill exercise were studied. The study subjects were 40 healthy men, mean (SEM) age 29 (5) years. Platelet aggregation was measured on a four channel aggregometer. Plasma 6-keto-prostaglandin F1alpha was analysed using an enzyme immunoassay technique. Upright posture and exercise produced an increase in platelet aggregability, as indicated by a fall in the threshold concentration of adrenaline (epinephrine) from 7.6 (1.5) microM at rest to 4.3 (1.0) microM after exercise (p = 0.002). The collagen lag time became significantly shorter with exercise (from 79.1 (3.1) seconds at rest to 71.9 (2.6) seconds after exercise, p = 0.003). Exercise was also associated with a 55% increase in plasma 6-keto-prostaglandin F1alpha (from 38.1 (75%CI 29.0 to 46.5) pg/ml at rest to 59.2 (47.3 to 66.8) pg/ml after exercise, p<0.001). In healthy male subjects, upright posture and maximal exercise increased platelet aggregability but this increase was counteracted by an increase in prostacyclin production. In patients with endothelial dysfunction, a reduced prostacyclin response to exercise may promote a transient prothrombotic imbalance that may trigger cardiovascular disease onset.