The Effect of Protease‐Activated Receptor 2 on Cutaneous Vasodilation and Sweating in Young Males During Exercise in the Heat

Protease‐activated receptor 2 (PAR‐2) is a G protein‐coupled receptor stimulated by the enzyme trypsin and is responsible for modulating the inflammatory response. It has been localized ‐on both the eccrine sweat glands and cutaneous vascular endothelial cells. In particular, activation of PAR‐2 contributes to the degranulation of secretory cells in the eccrine sweat glands and may therefore play a role in modulating the sweating response in humans. However, it is unknown if activation of PAR‐2 augments cutaneous vasodilation and sweating during exercise in the heat. Therefore, the purpose of the present study was to investigate these heat loss responses in young adults exercising in the heat. Five healthy, habitually active, young males (25 ± 6 years) performed 50‐min of moderate intensity (~55% VO 2peak ) cycling in the heat (35°C, 20% relative humidity) followed by a 30‐min recovery period. Local forearm sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC, laser‐Doppler perfusion units/mean arterial pressure) were recorded at four skin sites, continuously perfused with: 1) Lactated Ringer's (Control), 2) 0.05 mM, 3) 0.5 mM, or 4) 5 mM SLIGKV‐NH2 (PAR‐2 agonist) via intradermal microdialysis. There were two baseline measurements conducted at different ambient temperatures. The first baseline (Baseline 1) was measured at 25°C, 20% relative humidity and the second baseline (Baseline 2) depicted the onset of heat stress and was measured at 35°C, 20% relative humidity. During Baseline 1, there was a tendency for an increase in CVC at both the 0.5 mM (14 ± 3% CVC max , P = 0.078) and 5 mM (21 ± 7% CVC max , P = 0.067) SLIGKV‐NH2 site relative to Control. At the end of the 50‐min exercise bout, there were no significant differences in CVC between all sites (Control: 71 ± 4% CVC max ; 0.05 mM: 69 ± 8% CVC max ; 0.5 mM: 68 ± 5% CVC max ; 5 mM: 74 ± 9% CVC max ; P > 0.05) Further, we also show that activation of PAR‐2 at all concentrations of SLIGKV‐NH2 did not elicit significant changes in sweat rate at the end of exercise (Control: 1.31 ± 0.24; 0.05 mM: 1.52 ± 0.21; 0.5 mM: 1.55 ± 0.12; 5 mM: 1.51 ± 0.13 mg·min −1 ·cm −2 ; P > 0.05). In summary, our preliminary findings demonstrate that PAR‐2 activation exhibits a tendency to increase CVC at higher concentrations (0.5 and 5 mM) of SLIGKV‐NH2 relative to Control during baseline conditions. However, this increase is not present at the onset of and during heat stress, thereby indicating that PAR‐2 does not contribute to the modulation of sweating and cutaneous vasodilation during moderate intensity exercise in the heat. Support or Funding Information This study was supported by the Natural Sciences and Engineering Research Council of Canada (Discovery grant, RGPIN‐06313‐2014; Discovery Grants Program ‐ Accelerator Supplement, RGPAS‐462252‐2014; funds held by Dr. Glen P. Kenny).