Impact of moderate- and high-intensity exercise on the endothelial ultrastructure and function in mesenteric arteries from hypertensive rats

Abstract

Oxidative stress (OS) influences vascular function and structure in spontaneously hypertensive rats (SHRs). It is also responsible for the decreased nitric oxide (NO) bioavailability that influences endothelial vasodilation. The effects of high-intensity exercise on endothelial function and ultrastructure in hypertension remain unknown. Thus, this study investigated the effects of moderate-and high-intensity exercise on hypertension-associated endothelial dysfunction and ultrastructural remodeling. Moderate-intensity (SHR-M) and high-intensity (SHR-H) aerobic exercise training groups were compared in age-matched sedentary SHRs (SHR-C) and normotensive Wistar-Kyoto rats (WKY-C). The results showed that the endothelial ultrastructure was impaired in the SHR-H and SHR-C groups. Glutathione peroxidase levels were significantly increased in the SHR-M group compared to the SHR-C group. MDA content was higher in the SHR-H group than in the SHR-C group, but the levels of antioxidant enzymes did not increase accordingly. Apocynin scavenging reactive oxygen species (ROS) ameliorated endotheliumdependent vasodilator function in the SHR-H group. However, the SHR-M and WKY-C groups abolished the increased vasodilation induced by apocynin. L-NAME, a NO synthase inhibitor, was applied to isolated mesenteric arteries (MAs) to evaluate NO contribution. Moderate-intensity exercise reversed the decreased NO contribution to MAs in hypertension, and high-intensity exercise aggravated this change. These data suggest that moderate-intensity exercise ameliorated adverse remodeling of the endothelial ultrastructure and function in hypertension by decreasing oxidative stress and increasing NO contribution. However, high-intensity exercise exacerbated all of these changes by increasing OS and ROS contribution, and decreasing NO contribution.

High‐intensity exercise in hypoxia improves endothelial function via increased nitric oxide bioavailability in C57BL/6 mice

“…In animal models however, the superiority of high‐ versus low‐intensity remains debated. Although several studies showed that higher intensity exercise training improves vasorelaxation, 15,16,29 others reported no benefits, or even a deleterious effect, when compared to low intensity 17‐20 . In the present study, we showed no significant difference in aortic vasorelaxation among different exercise training intensities in normoxia in healthy mice.…”

“… 17 , 18 Some studies even described a deleterious effect of high intensity continuous training compared to low and moderate intensity continuous training. 19 , 20 Thus, there is still controversy regarding the potential beneficial effect of high‐intensity exercise training on endothelial function.…”

Effects of different intensities of continuous training on vascular inflammation and oxidative stress in spontaneously hypertensive rats

“…There is evidence that different training intensities have different effects on the vascular function of hypertensive animal models 32–35 . Appropriate training intensity is increasingly becoming the key to training therapy.…”

High‐intensity interval training attenuates the effects caused by arterial hypertension in the ventral prostate

“…Exercise training moderate influences hypertension and reduces BP. 36 In this study, the HIIT protocol was responsible for a significant decrease in SBP values of the HIIT group in the final of 8 weeks of training, while the SHR group remained close to its initial values. Previous studies indicated that the beneficial effect of physical exercise on the BP is maintained in angiotensin II (Ang-II) induced hypertensive rats, 37 increased myocardial capitalization that reflects in bradycardia by modifying blood flow through capillaries and myocardium.…”