Master of Science / Department of Kinesiology / Brett J. Wong / Beetroot juice (BRJ) has been shown to increase NO-dependent dilation through both NOS-dependent and NOS-independent pathways. We hypothesized BRJ supplementation would augment reflex cutaneous active vasodilation. Subjects were equipped with two microdialysis fibers on the forearm and randomly assigned as control (Ringer’s) or NOS inhibition (20mM L-NAME). Whole-body heating was achieved via water-perfused suits to raise core temperature (Tc; ingestible telemetric pill) 0.8°C. Maximal cutaneous vasodilation was reached by administering 54mM SNP and local heating to 43°C. Skin blood flow was measured via laser-Doppler flowmetry and mean arterial pressure determined; cutaneous vascular conductance (CVC) was calculated and expressed as %CVCmax. Subjects underwent heat stress pre- and post-nitrate supplementation (3 days of BRJ: 5mM, 0.45g nitrates per day). BRJ increased the plateau CVC at control (pre: 57 ± 3 vs. post: 80 ± 5 %CVCmax) and L-NAME (pre: 36 ± 3 vs. post: 52 ± 6 %CVCmax; p<0.05 for all conditions) sites. The %NO contribution increased from pre- to post-BRJ (pre: 44 ± 5 %CVCmax vs. post: 64 ± 6 %CVCmax; p<0.05). These data suggest that BRJ augments the NOS-dependent and NOS-independent component of reflex cutaneous vasodilation.

Na+/K+-ATPase has been shown to regulate the sweating and cutaneous vascular responses during exercise; however, similar studies have not been conducted to assess the roles of the Na-K-2Cl cotransporter (NKCC) and K+ channels. Additionally, it remains to be determined if these mechanisms underpinning the heat loss responses differ with exercise intensity. Eleven young (24±4 years) males performed three 30-min semi-recumbent cycling bouts at low (30% VO2peak), moderate (50% VO2peak), and high (70% VO2peak) intensity exercise, respectively, each separated by 20-min recovery periods. Using intradermal microdialysis, four forearm skin sites were continuously perfused with either: 1) lactated Ringer solution (Control), 2) 6 mᴍ ouabain (Na+/K+-ATPase inhibitor), 3) 10 mᴍ bumetanide (NKCC inhibitor), or 4) 50 mᴍ BaCl2 (non-specific K+ channel inhibitor); sites at which we assessed local sweat rate (LSR) and cutaneous vascular conductance (CVC). Inhibition of Na+/K+-ATPase attenuated LSR compared to Control during the moderate and high intensity exercise bouts (both P˂0.01), whereas attenuations with NKCC and K+ channel inhibition were only apparent during the high intensity exercise bout (both P≤0.05). Na+/K+-ATPase inhibition augmented CVC during all exercise intensities (all P˂0.01), whereas CVC was greater with NKCC inhibition during the low intensity exercise only (P˂0.01) and attenuated with K+ channel inhibition during the moderate and high intensity exercise conditions (both P˂0.01). We show that Na+/K+-ATPase, NKCC and K+ channels all contribute to the regulation of sweating and cutaneous blood flow but their influence is dependent on the intensity of exercise.