Effects of aerobic exercise training upon nitric oxide bioactivity and aorta vasodilatation

Abstract

Aerobic training (AT) is an important way to improve endothelial function. However, it is not completely understood how the blood vessels adapt themselves to the AT. Therefore, the aim of this study was to investigate exercise training-induced adaptations on the nitric oxide (NO) production, antioxidant defense and aorta vasodilatation in normotensive rats. The rats were subjected to an AT protocol (treadmill, ~55% Max Veloc., 5 bouts/week, 60 min/bout, 11 wks). After the AT, it was examined in vitro vasomotor function to acetylcholine (ACh) and sodium nitroprusside (SNP), and biochemical analysis in the aorta. Aerobic training significantly increased (P < 0.05) by 62% the expression of the endothelial nitric oxide synthase (eNOS). However, ET did not modify the relaxation response and sensitivity to ACh. In contrast, AT significantly reduced aortic sensitivity to SNP (-8.26 ± 0.081 vs. -7.79 ± 0.099 Log [M], Sed vs. AT, respectively, P < 0.001). These results demonstrate that aerobic AT was able to modify one important mechanism related to the NO bioactivity, which is the increase of eNOS expression. However, this response did not contribute to improve of the aortic vasodilatation response to acetylcholine and decreased the sensitivity to SNP.