Background. Obesity and low cardiorespiratory fitness (CRF) have been shown to independently increase the risk of CVD mortality. The aim of this study was to investigate the relationship between CRF, body fatness and markers of arterial function. Method and Results. Obese (9 male, 18 female; BMI 35.3 ± 0.9 kg·m-2) and lean (8 male, 18 female; BMI 22.5 ± 0.3？kg·m-2) volunteers were assessed for body composition (DXA), cardiorespiratory fitness (predicted max), blood pressure (BP), endothelial vasodilatator function (FMD), and arterial compliance (AC) (via radial artery tonometry). The obese group had more whole body fat and abdominal fat (43.5 ± 1.2% versus 27.2 ± 1.6%; and 48.6 ± 0.9% versus 28.9 ± 1.8%; resp.), and lower FMD (3.2 ± 0.4% versus 5.7 ± 0.7%; ) than the lean subjects, but there was no difference in AC. AC in large arteries was positively associated with CRF ( ; ) but not with fatness. Conclusion. These results indicate distinct influences of obesity and CRF on blood vessel health. FMD was impaired with obesity, which may contribute to arterial and metabolic dysfunction. Low CRF was associated with reduced elasticity in large arteries, which could result in augmentation of aortic afterload. 1. Introduction Obesity and cardiorespiratory fitness (CRF) are independent predictors of cardiovascular (CV) and all-cause mortality [1–5]. Furthermore, it appears that CRF may be protective against the cardiovascular risk associated with obesity [6]. The mechanisms which mediate the relationships between obesity, CRF, and CV mortality risk are not entirely understood [5, 7]. However, given that the protective effects of CRF and the detrimental effects of obesity appear to influence CV mortality independently of other CV risk factors, it is of interest to investigate their influences on established markers of subclinical CV function. This will allow for a better understanding of the potential mechanisms by which obesity and CRF may influence the risk of CV mortality. Increased adiposity, in particular visceral adiposity, is associated with reduced vascular endothelial function [8, 9]. Endothelial function refers to the general functional capacity of vascular endothelial cells, primarily mediated by their capacity to synthesize and release nitric oxide (NO) [10]. Reduced synthesis and/or availability of NO is associated with increased vascular permeability, inflammation, adhesion and thrombosis, and a reduced vasodilatory capacity, and abnormalities of endothelial function have been associated with a number of CV risk factors [11]. The noninvasive
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