Figure 1. Divergent dilatory signaling between sedentary individuals and exercisers in response to high pressure.

At rest, arterioles from both sedentary individuals and regular aerobic or resistance exercisers exhibit nitric oxide (NO)-dependent vasodilation (left panel). This is supported by several studies demonstrating that this dilation is nearly abolished by the NO synthase (NOS) inhibitor L-N^G-Nitroarginine methyl ester (L-NAME) (4, 5, 7). Following exposure to high intraluminal pressure or acute resistance exercise, arterioles from sedentary individuals demonstrate reduced vasodilation and reduced sensitivity to L-NAME and the H₂O₂ scavenger catalase. In contrast, arterioles from regular aerobic and resistance exercisers demonstrate preserved vasodilation, and an enhanced response to catalase, suggesting a greater reliance on H₂O₂-dependent dilation (4, 5, 7).