Augmented reflex cutaneous vasodilatation following short-term dietary nitrate supplementation in humans

What is the central question of this study? Nitrate supplementation via beetroot juice has been shown to have several benefits in healthy humans, including reduced blood pressure and increased blood flow to exercising muscle. Whether nitrate supplementation can improve blood flow to the skin in heat-stressed humans has not been investigated. What is the main finding and its importance? Similar to previous studies, we found that nitrate supplementation reduces blood pressure. Nitrate supplementation increased vasodilatation in the skin of heat-stressed humans but did not directly increase skin blood flow. Nitrate supplementation has been shown to increase NO-dependent vasodilatation through both NO synthase (NOS)-dependent and NOS-independent pathways. We hypothesized that nitrate supplementation would augment reflex cutaneous active vasodilatation. Subjects were equipped with two microdialysis fibres on the forearm randomly assigned as control (Ringer solution) or NOS inhibition (20 mm l-NAME). Whole-body heating was performed to raise core temperature by 0.8°C above baseline core temperature. Maximal cutaneous vasodilatation was achieved via 54 mm sodium nitroprusside and local heating to 43°C. Skin blood flow (measured by laser-Doppler flowmetry) and blood pressure were measured. Cutaneous vascular conductance (CVC) was calculated as skin blood flow divided by mean arterial pressure (MAP) and expressed as a percentage of maximal CVC (%CVCmax ). Subjects underwent heat stress before and after nitrate supplementation (3 days of beetroot juice; 5 mm, 0.45 g nitrates per day). During heat stress, MAP was reduced following nitrate supplementation compared with the control conditions (before 88 ± 3 mmHg versus after 78 ± 2 mmHg; P < 0.05); however, resting MAP was not different between conditions (before 88 ± 3 mmHg versus after 83 ± 2 mmHg; P = 0.117). Nitrate supplementation increased plateau CVC at control sites (before 67 ± 2%CVCmax  versus after 80 ± 5%CVCmax ; P = 0.01) but not at l-NAME-treated sites (before 45 ± 4%CVCmax  versus after 40 ± 5%CVCmax ; P = 0.617). There was no change in the calculated percentage of NOS-dependent vasodilatation before and after supplementation (before 59 ± 4% versus after 64 ± 6%; P = 0.577). These data suggest that nitrate supplementation augments CVC and reduces MAP during heat stress.