Objectives: 

Exercise training improves impaired endothelial function in cardiovascular disease but its effects are less studied in healthy subjects. Therefore the present work was designed to examine the participation of endothelial factors in healthy rabbits subjected to exercise training.

Materials: 

Materials and methods: Eleven male New Zealand white rabbits were exercised during 6 weeks following a chronic exercise protocol on treadmill (trained group) and another twelve rabbits (control group) were stabulated during the same period. When the chronic exercise program was finished, rabbits were anaesthetized, killed and common carotid arteries were dissected. Arterial segments (3 mm long) were mounted for isometric recording of tension in organ baths containing Krebs-Henseleit solution.

Results: 

Acetylcholine (Ach) produced concentration-dependent relaxation responses. Maximal response was higher in control group (93.8±2.1%) than trained group (83.5±3.2%). Indomethacin did not change the relaxation to Ach. L-NAME reduced acetylcholine-induced relaxation. Maximal reduction was greater in arteries from control rabbits (44.0±1.7% vs 34.4±1.2% in training rabbits, P<0.05). The remaining endothelium-dependent relaxation after exposure to L-NAME and indomethacin was further reduced by the combination of charybdotoxin and apamin. This inhibition was similar in both groups (54.8±2.1% in control vs 51.9±1.8% in training rabbits). L-NAME (10-6-3x10-4M) had a contractile effect on arterial rings under resting conditions. The pD2 value for the concentration-response curve was minor in control group (4.64±0.11) vs (5.07±0.09) for trained group, P<0.05.

Conclusions: 

Physical training decreases the relaxation induced by Ach and increases the contraction induced by L-NAME. Together, these results indicate that physical training increases basal NO release but decreases Ach-induced NO without affecting the participation of potassium channels sensitive to charybdotoxin and apamin.