Role of overweight and obesity on vascular responses to the cold pressor test and hypoxia in women.

Sympathetic-mediated vasoconstriction is attenuated during hypoxia in young women with normal weight (NW) (i.e., hypoxic sympatholysis). Obesity is associated with exaggerated sympathetic nervous system activity that may augment sympathetic vasoconstriction and impair hypoxic sympatholysis. We hypothesized that hypoxic sympatholysis would be attenuated in women with overweight (OW) and obesity compared with women with normal weight. Forearm blood flow (FBF, venous occlusion plethysmography), muscle sympathetic nerve activity (MSNA, peroneal microneurography), blood pressure (finger plethysmography), and arterial oxygen saturation ([Formula: see text], pulse oximetry) were measured in women with normal weight (NW; = 15; 24 ± 7 yr; 22 ± 2 kg/m) and women with overweight/obesity (OW; = 9; 27 ± 7 yr; 33 ± 5 kg/m). Participants completed a cold pressor test (CPT) during normoxia (98 ± 1% [Formula: see text]) and hypoxia (82 ± 2% [Formula: see text]). Hypoxia increased MSNA burst frequency in NW but not in OW ( = 0.030). Sympathetic vasoconstriction ( = 0.909) and hypoxic vasodilation ( = 0.295) did not differ between groups. In contrast, hypoxic sympatholysis was lower in OW than NW ( = 0.029). Measures of adiposity were negatively associated with hypoxic sympatholysis: percent body fat ( = -0.406, = 0.049), android fat ( = -0.443, = 0.030), gynoid fat ( = -0.447, = 0.029), and waist circumference ( = -0.458, = 0.024). Hypoxic sympatholysis is attenuated in women with increased adiposity, despite preserved sympathetic vasoconstriction and hypoxic vasodilation compared with women with normal weight. These findings have implications for vascular control of blood flow in conditions associated with obesity and hypoxia (e.g., sleep apnea). Sympathetic-mediated vasoconstriction is attenuated during hypoxia in young women with normal weight, demonstrating the expected hypoxic sympatholysis. Conversely, hypoxic sympatholysis is attenuated in women with increased adiposity, despite preserved sympathetic vasoconstriction and hypoxic vasodilation compared with women with normal weight. These data advance our understanding of the impact of obesity on neurovascular control of blood flow and have implications for individuals with obesity and conditions associated with hypoxia (e.g., sleep apnea).