The effect of exogenous activation of protease-activated receptor 2 on cutaneous vasodilatation and sweating in young males during rest and exercise in the heat

Temperature (Austin). 2018 Sep 6;5(3):257-266. doi: 10.1080/23328940.2018.1506563. eCollection 2018.

Abstract

Protease-activated receptor 2 (PAR2) exists in the endothelial cells of skin vessels and eccrine sweat glands. We evaluated the hypothesis that exogeneous activation of PAR2 augments cutaneous vasodilatation and sweating during rest and exercise in the heat. In 10 young males (23 ± 5 y), cutaneous vascular conductance (CVC) and sweat rate were measured at four forearm skin sites treated with either 1) lactated Ringer (Control), 2) 0.05 mM, 3) 0.5 mM, or 4) 5 mM SLIGKV-NH2 (PAR2 agonist). Participants initially rested in a semi-recumbent posture under a normothermic ambient condition (25°C) for ~60 min. Thereafter, ambient temperature was increased to 35°C while the participants rested for an additional 60 min. Participants then performed a 50-min bout of cycling (~55% of their pre-determined peak oxygen uptake) followed by a 30-min recovery period. Administration of 5 mM SLIGKV-NH2 increased cutaneous vascular conductance relative to the Control site during normothermic resting (P ≤ 0.05). However, we showed that relative to the Control site, no effect on CVC was observed for any administered dose of SLIGKV-NH2 (0.05-5 mM) during rest (33-39%max CVC), end-exercise (68-70%max CVC), and postexercise recovery (49-53%max CVC) in the heat (all P > 0.05). There were no differences in sweat rate between the Control and all SLIGKV-NH2-treated sites throughout the protocol (0.21-0.23, 1.20-1.27, and 0.32-0.33 mg∙min-1∙cm-2 for rest, end-exercise, and postexercise in the heat, respectively, all P > 0.05). We show that while exogeneous PAR2 activation induces cutaneous vasodilatation during normothermic rest, it does not influence the cutaneous blood flow and sweating responses during rest, exercise or recovery in the heat.

Keywords: Trypsin; heat loss responses; inflammation; microcirculation; serine protease.

Grant support

This study was supported by the Natural Sciences and Engineering Research Council of Canada (Discover grant, RGPIN-06313–2014 and Discovery Grants Program - Accelerator Supplement, RGPAS-462252–2014; funds held by Dr. Glen P. Kenny). The study was conducted at the Human and Environmental Physiology of the University of Ottawa. G. P. Kenny is supported by a University of Ottawa Research Chair Award. N. Fujii was supported by the Human and Environmental Physiology Research Unit. The current affiliation of N. Fujii is the University of Tsukuba, Faculty of Health and Sport Sciences, Tsukuba City, Japan.