Hypertension, which is attenuated by regular aerobic exercise, is associated with an increase in cytosolic platelet calcium [Ca+2](i). How aerobic exercise might lower blood pressure is unknown. We tested the hypothesis that exercise would influence the agonist-induced effect on platelet cytosolic calcium [Ca+2](i). Twenty, healthy normotensive men between 20 and 60 years of age (five per decade) were studied while resting supine for 30 min and after bicycle ergometry at a work load sufficient to achieve a heart rate of 200 beats per min minus age in years. On the next day, the protocol was repeated with the subjects exercising at 75% their maximum heart rare for 6 min. Venous blood was obtained from an indwelling cannula. Exercise had no effect on total or ionised serum calcium values. Adrenaline values increased from 0.2+/-0.03 to 0.55+/-0.1 (s.e.m.) nmol/l (P < 0.05), while noradrenaline increased from 1.46+/-0.18 to 4.72+/-0.44 nmol/l (P < 0.05). Resting platelet [Ca+2](i) concentrations were 95.4+/-3.9 and 94.4+/-3.0 nmol/l on the two study days. The values were not correlated with age or level of fitness. The platelet [Ca+2](i) was 99.2+/-4.2 nmol/l after exercise, not different from the resting values. Platelet activation with adrenaline and thrombin across a wide range of doses resulted in prompt increases in [Ca+2](i), which were 50% less in platelets after exercise than at rest (P < 0.05). Activation with angiotensin (Ang) II, on the other hand, was less pronounced and less clearly influenced by exercise. We conclude that exercise influences the platelet activation state and reactivity. The decreased [Ca+2](i) responses to adrenaline and thrombin suggest that [Ca+2](i) stores were in part depleted at exercise compared to rest, an effect not observed with Ang II perhaps because of the smaller number of Ang II-operative receptors on platelets.