Contribution of nitric oxide synthase to cutaneous vasodilatation and sweating in men of black‐African and Caucasian descent during exercise in the heat

Abstract

What is the central question of this study? Nitric oxide modulates cutaneous vasodilatation and sweating during exercise-induced heat stress in young men. However, it remains uncertain whether these effects are reduced in black-African descendants, who commonly demonstrate reduced nitric oxide bioavailability. Therefore, we assessed whether black-African descendants display reduced nitric oxide-dependent cutaneous vasodilatation and sweating compared with Caucasians in these conditions. What is the main finding and its importance? Nitric oxide-dependent cutaneous vasodilatation and sweating were similar between groups, indicating that reduced nitric oxide bioavailability in black-African descendants does not attenuate these heat-loss responses during an exercise-induced heat stress. Men of black-African descent are at an increased risk of heat-related illness relative to their Caucasian counterparts. This might be attributable, in part, to reduced cutaneous nitric oxide (NO) bioavailability in this population, which might alter local cutaneous vasodilatation and sweating. To evaluate this, we compared these heat-loss responses in young men (18-30years of age) of black-African (n=10) and Caucasian (n=10) descent during rest, exercise and recovery in the heat. Participants were matched for physical characteristics and fitness, and they were all born and raised in the same temperate environment (i.e. Canada; second generation and higher). Both groups rested for 10min and then performed 50min of moderate-intensity exercise at 200Wm-2 , followed by 30min of recovery in hot, dry heat (35°C, 20% relative humidity). Local cutaneous vascular conductance (CVC%max ) and sweat rate (SR) were measured at two forearm skin sites treated with either lactated Ringer solution (control) or 10mm NG -nitro-l-arginine methyl ester (l-NAME, a nitric oxide (NO) synthase inhibitor). l-NAME significantly reduced CVC%max throughout rest, exercise and recovery in both groups (both P<0.001). However, there were no significant main effects for the contribution of NO to CVC%max between groups (all P>0.500). l-NAME significantly reduced local SR in both groups (both P<0.050). The contribution of NO to SR was similar between groups such that l-NAME reduced SR relative to control at 40 and 50min into exercise (both P<0.05). We demonstrate that ethnicity per se does not influence NO-dependent cutaneous vasodilatation and sweating in healthy young men of black-African and Caucasian descent during exercise in dry heat.