To investigate whether exercise training can modulate endothelium-dependent vasorelaxation, male New Zealand White rabbits were divided into either control or training groups. The training animals were trained on a treadmill with a running speed of 0.88 km/hr on a 0° grade for 10-60 minutes/day, 5 days/week for 8 weeks. After exercise training, the resting heart rate was lowered (p<0.05). At the end of the experiments, three vessel segments, i.e., the thoracic aortas, the pulmonary arteries, and the common carotid arteries, were isolated and precontracted with norepinephrine. Acetylcholine-stimulated endothelium-derived relaxing factor (EDRF) release was assessed by bioassay in the presence of indomethadn (10~s M). Basal release of EDRF was examined by the addition of hemoglobin. In addition, the relaxing responses of the thoracic aortas and pulmonary arteries to A23187, a calcium ionophore, and to sodium nitroprusside, a direct vasodilator of vascular smooth muscle, were compared between control and trained groups to further investigate possible underlying mechanisms. The results indicated that after exercise training 1) both the thoracic aorta and pulmonary artery, but not the carotid artery, became more sensitive to acetylcholine-induced vasorelaxation; 2) no significant differences in basal release of EDRF between control and trained rabbits were observed; and 3) there were no significant differences in the vascular responses to A23187 or sodium nitroprusside between the two groups. Our data suggest that exercise training may enhance endothelium-dependent vasodilation to acetylcholine via the stimulated EDRF release and that this elevated sensitivity to acetylcholine may not be caused by the alteration of the relaxing response in vascular smooth muscle. (Arteriosclerosis and Thrombosis 1993;13:852-856) KEY WORDS • endurance exercise • endothelium • acetylcholine • rabbits • endotheliumderived relaxing factor

Our data suggest that exercise training may decrease NE-induced vasoconstrictive response and may increase NE-stimulated EDRF release.