Brachial artery flow mediated vasodilation in exercise trained (ET) individuals is maintained after a single bout of heavy resistance exercise compared to sedentary (SED) individuals. The purpose of this study was to determine if vasodilation is also maintained in the microcirculation of ET individuals. A total of 51 SED 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 inhibitor L-NAME, the cyclooxygenase inhibitor indomethacin, or the hydrogen peroxide scavenger PEG-catalase. Separate vessels (isolated from the same groups) were exposed to an intraluminal pressure of 150 mmHg for 30 minutes to mimic the pressor response which occurs with isometric exercise. Vasodilation to acetylcholine was reduced in microvessels from SED subjects after either a single weight lifting session or exposure to increased intraluminal pressure whereas microvessels from ET individuals maintained acetylcholine-mediated vasodilation. Prior to weight lifting, vasodilation of microvessels from ET individuals was reduced in the presence of L-NAME and indomethacin. After weight lifting or exposure to increased intraluminal pressure, PEG-catalase significantly reduced vasodilation while L-NAME and indomethacin had no effect. These results indicate that 1) endothelium-dependent vasodilation in the microvasculature is maintained following heavy resistance exercise in ET individuals but not in SED 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.

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