During exercise, cutaneous vasodilation and sweating responses occur, whereas these responses rapidly decrease during postexercise recovery. We hypothesized that the activation of endothelin A (ETA) receptors, but not endothelin B (ETB) receptors, attenuate cutaneous vasodilation during high-intensity exercise and contribute to the subsequent postexercise suppression of cutaneous vasodilation. We also hypothesized that both receptors increase sweating during and following high-intensity exercise. Eleven males (24 ± 4 years) performed an intermittent cycling protocol consisting of two 30-min bouts of moderate- (40% VO2peak) and high- (75% VO2peak) intensity exercise in the heat (35°C), each separated by a 20- and 40-min recovery period, respectively. Cutaneous vascular conductance (CVC) and sweat rate were evaluated at four intradermal microdialysis skin sites: 1) lactated Ringer (Control), 2) 500 nM BQ123 (a selective ETA receptor blocker), 3) 300 nM BQ788 (a selective ETB receptor blocker), or 4) a combination of BQ123+BQ788. There were no between-site differences in CVC during each exercise bout (all P > 0.05), however, CVC following high-intensity exercise was greater at BQ123 (56 ± 9 %max) and BQ123+BQ788 (55 ± 14 %max) sites relative to the Control site (43 ± 12 %max) (all P ≤ 0.05). Sweat rate did not differ between sites throughout the protocol (all P > 0.05). We show that neither ETA nor ETB receptors modulate cutaneous vasodilation and sweating responses during and following moderate- and high-intensity exercise in the heat, with the exception that ETA receptors may partly contribute to the suppression of cutaneous vasodilation following high-intensity exercise.
- endothelial cell
- endothelium-derived contracting factors
- Copyright © 2016, Journal of Applied Physiology