Acute exertion elicits a H2O2-dependent vasodilator mechanism in the microvasculature of exercise-trained but not sedentary adults

Abstract

Brachial artery flow-mediated vasodilation in exercise-trained (ET) individuals is maintained after a single bout of heavy resistance exercise compared with sedentary individuals. The purpose of this study was to determine whether vasodilation is also maintained in the microcirculation of ET individuals. A total of 51 sedentary and ET individuals underwent gluteal subcutaneous fat biopsy before and after performing a single bout of leg press exercise. Adipose arterioles were cannulated in an organ bath, and vasodilation to acetylcholine was assessed±the endothelial nitric oxide inhibitorl-NG-nitroarginine methyl ester, the cyclooxygenase inhibitor indomethacin, or the hydrogen peroxide scavenger polyethylene glycol catalase. Separate vessels (isolated from the same groups) were exposed to an intraluminal pressure of 150 mm Hg for 30 minutes to mimic the pressor response, which occurs with isometric exercise. Vasodilation to acetylcholine was reduced in microvessels from sedentary subjects after either a single weight lifting session or exposure to increased intraluminal pressure, whereas microvessels from ET individuals maintained acetylcholine-mediated vasodilation. Before weight lifting, vasodilation of microvessels from ET individuals was reduced in the presence of l-NG-nitroarginine methyl ester and indomethacin. After weight lifting or exposure to increased intraluminal pressure, polyethylene glycol catalase significantly reduced vasodilation, whereas l-NG-nitroarginine methyl ester and indomethacin had no effect. These results indicate that (1) endothelium-dependent vasodilation in the microvasculature is maintained after heavy resistance exercise in ET individuals but not in sedentary subjects and that (2) high pressure alone or during weight lifting may induce a mechanistic switch in the microvasculature to favor hydrogen peroxide as the vasoactive mediator of dilation.

Keywords: hydrogen peroxide; hypertension; nitric oxide; reactive oxygen species; vasodilation.

Figure 1

(A) Acetylcholine-mediated vasodilation was significantly reduced in isolated human arterioles from SED subjects after a single weight lifting session (n=10) compared to arterioles obtained prior to weight lifting (n=11). Transiently exposing arterioles from SED subjects to an intraluminal pressure of 150 mmHg for 30 minutes also significantly reduced vasodilation to acetylcholine (n=4). (B) Compared to arterioles obtained prior to weight lifting (n=17), acetylcholine-mediated vasodilation was maintained in arterioles obtained from ET individuals after a single weight lifting session (n=10) or exposure to a 30 minute increase in intraluminal pressure to 150 mmHg (n=5). (C-D) Prior to weight lifting, L-NAME and indomethacin significantly reduced the vasodilator response to acetylcholine in arterioles from both SED (n=8) and ET (n=13) subjects while PEG-Catalase had no effect on the response in either group (n=6 SED; n=10 ET). (E) Acetylcholine-mediated vasodilation was similar in arterioles obtained from SED (n=11) and ET subjects (n=17) prior to weight lifting. All values are plotted as mean ±SEM. *Significant difference (P<0.05) vs. Pre Weight Lifting. n, number of vessels.

Figure 2

Acetylcholine-mediated vasodilation was significantly reduced in isolated arterioles from ET subjects in the presence of L-NAME and indomethacin (n=13) compared to untreated vessels (n=17). L-NAME and indomethacin treatment had no effect on acetylcholine-mediated vasodilation in isolated arterioles obtained after a weight lifting session (n=7) or in isolated arterioles exposed to a 30 minute increase in intraluminal pressure to 150 mmHg (n=5). All values are plotted as mean ±SEM. *Significant difference (P<0.05) L-NAME + Indomethacin vs. Pre Weight Lifting. n, number of vessels. Pre Weight Lifting responses are re-plotted from Figure 1.

Figure 3

The H₂O₂ scavenger PEG-catalase had no effect on acetylcholine-mediated vasodilation in isolated arterioles obtained from ET subjects prior to weight lifting (n=10) compared to untreated control arterioles (n=17). PEG-catalase significantly reduced acetylcholine-mediated vasodilation in isolated arterioles obtained after a weight lifting session (n=6) and in arterioles transiently exposed to an intraluminal pressure of 150 mmHg for 30 minutes (n=5). All values are plotted as mean ±SEM. *Significant difference (P<0.05) Post Weight Lifting – PEG Catalase and Post Increased Intraluminal Pressure – PEG Catalase vs. Pre Weight Lifting. n, number of vessels. Pre Weight Lifting responses are re-plotted from Figure 1.