NO is crucial for endothelial function and vascular health. Plasma nitrite (NO2−) is the main oxidation product of NO and has been shown to reflect changes in eNOS activity. We hypothesized that plasma NO2− response to physical exercise stress along with physiological endothelial function would be reduced with increasing severity of vascular disease. Subject groups were: (a) risk factors but no vascular disease (RF); (b) Type 2 diabetes with no vascular disease (DM); (c) diagnosed peripheral arterial disease (PAD); and (d) DM + PAD. Venous blood was drawn at rest and 10 min following maximal exercise. Plasma samples were analyzed by reductive chemiluminescence. Brachial diameters were imaged prior to, during and following 5 min of forearm occlusion (BAFMD). There were no differences in resting plasma NO2− or BA diameters between groups. The PAD groups had lower age adjusted BAFMD responses (p ⩽ 0.05). Within group analysis revealed an increase in NO2− in the RF group (+39.3%), no change in the DM (−15.51%), and a decrease in the PAD (−44.20%) and PAD + DM (−39.95%). This was maintained after adjusting for age and VO2peak (p ⩽ 0.05). ΔNO2− and BAFMD were the strongest independent predictors of VO2peak in multivariate linear regression. These findings suggest ΔNO2− discriminates severity of cardiovascular disease risk, is related to endothelial function and predicts exercise capacity.