The role of shear stress on cutaneous microvascular endothelial function in humans

Previous studies suggest that exercise and heat stress improve cutaneous endothelial function, caused by increases in shear stress. However, as vasodilatation in the skin is primarily a thermogenic phenomenon, we investigated if shear stress alone without increases in skin temperature that occur with exercise and heat stress increases endothelial function. We examined the hypothesis that repeated bouts of brief occlusion would improve cutaneous endothelial function via shear stress-dependent mechanisms. Eleven males underwent a shear stress intervention (forearm occlusion 5 s rest 10 s) for 30 min, five times center dot week(-1) for 6 weeks on one arm, the other was an untreated control. Skin blood flow was measured using laser-Doppler flowmetry, and endothelial function was assessed with and without NOS-inhibition with L-NAME in response to three levels of local heating (39, 42, and 44 A degrees C), ACh administration, and reactive hyperaemia. Data are cutaneous vascular conductance (CVC, laser-Doppler/blood pressure). There were no changes in the control arm (all d 0.2, p > 0.05). In the experimental arm, CVC to 39 A degrees C was increased after 3 and 6 weeks (d = 0.6; p 0.01). Nitric oxide contribution was increased after 6 weeks compared to baseline (d = 0.85, p < 0.001). Following skin heating to 42 A degrees C and 44 A degrees C, CVC was not different at weeks 3 or 6 (d 0.8, p > 0.05). For both 42 and 44 A degrees C, nitric oxide contribution was increased after weeks 3 and 6 (d < 0.4, p < 0.03). Peak and area-under-the-curve responses to ACh increased following 6 weeks (p < 0.001). Episodic increases in shear stress, without changes in skin or core temperature, elicit an increase in cutaneous microvascular reactivity and endothelial function.