The mechanisms underlying the muscle metaboreflex modulation of sweating and cutaneous blood flow in passively heated humans.

Abstract

Metaboreceptors can modulate cutaneous blood flow and sweating during heat stress but the mechanisms remain unknown. Fourteen participants (31 ± 13 years) performed 1‐min bout of isometric handgrip (IHG) exercise at 60% of their maximal voluntary contraction followed by a 3‐min occlusion (OCC), each separated by 10 min, initially under low (LHS, to activate sweating without changes in core temperature) and high (HHS, whole‐body heating to a core temperature increase of 1.0°C) heat stress conditions. Cutaneous vascular conductance (CVC) and sweat rate were measured continuously at four forearm skin sites perfused with 1) lactated Ringer's solution (Control), 2) 10 mmol L‐NAME [inhibits nitric oxide synthase (NOS)], 3) 10 mmol Ketorolac [inhibits cyclooxygenase (COX)], or 4) 4 mmol theophylline (THEO; inhibits adenosine receptors). Relative to pre‐IHG levels with Control, NOS inhibition attenuated the metaboreceptor‐mediated increase in sweating under LHS and HHS (P ≤ 0.05), albeit the attenuation was greater under LHS (P ≤ 0.05). In addition, a reduction from baseline was observed with THEO under LHS during OCC (P ≤ 0.05), but not HHS (both P > 0.05). In contrast, CVC was lower than Control with L‐NAME during OCC in HHS (P ≤ 0.05), but not LHS (P > 0.05). We show that metaboreceptor activation modulates CVC via the stimulation of NOS and adenosine receptors, whereas NOS, but not COX or adenosine receptors, contributes to sweating at all levels of heating.