The Mechanisms Underlying the Muscle Metaboreflex Modulation of Sweating and Cutaneous Vascular Conductance in Passively Heated Humans

Previous reports demonstrate that the nonthermal muscle metaboreflex increases sweating and reduces cutaneous perfusion during heat stress. However the mechanisms mediating these responses remain unknown. Given that nitric oxide synthase (NOS) and cyclooxygenase (COX) contribute to the sweating response during heat stress, these enzymes may also play a role in the metaboreflex‐induced increases in sweating during heat stress. Additionally, NOS, COX, and adenosine receptors contribute to cutaneous vascular responses during heat stress. Thus these factors may be involved in reducing cutaneous perfusion in response to metaboreceptor activation during heat stress. Eleven healthy males (31 ± 13 years) donned a water‐perfused suit whereby mean skin temperature was clamped to ~35 °C (pre‐heating; to activate sweating without changes in core temperature) which was followed by a period of whole‐body heating to induce and maintain a 1.0 °C increase in core temperature (post‐heating) above pre‐heating levels. Participants performed the metaboreceptor activation protocol [1 min bout of isometric handgrip (IHG) exercise at 60% of their maximal voluntary contraction followed by 3 min of forearm occlusion (OCC; to stimulate metaboreceptors)] twice at each heating phase (pre‐heating: IHG+OCC‐1 and ‐2; and post‐heating: IHG+OCC‐3 and ‐4), each separated by 10 min. Prior to the start of the trial, participants were instrumented with four intradermal microdialysis fibres in the forearm skin that were continuously perfused with (1) lactated Ringer solution (Control), (2) 10 mM N G ‐nitro‐L‐arginine methylester (L‐NAME; a non‐selective NOS inhibitor), (3) 10 mM ketorolac (KETO; a non‐selective COX inhibitor), or (4) 4 mM theophylline (THEO; a non‐selective adenosine receptor antagonist). Forearm sweat rate (ventilated capsule; n=9) and cutaneous vascular conductance (CVC; perfusion units divided by mean arterial pressure, n=9) were measured at each of the four skin sites. For all sites, sweating increased and remained elevated during IHG and OCC respectively, regardless of the level of hyperthermia (all P < 0.05). The increase in sweat rate from pre‐IHG levels during IHG+OCC‐2 and IHG+OCC‐3 measured at the Control (0.26 ± 0.14 and 0.03 ± 0.01 mg· min −1 · cm −2 , respectively) was partially attenuated by NOS inhibition (23 ± 23 and 22 ± 26%, respectively, P <0.05). During the pre‐heating phase, no influence of IHG+OCC‐1 or ‐2 was observed on CVC (all P >0.05). Moreover, relative to pre‐IHG levels, CVC was reduced during IHG+OCC‐3 at Control (IHG; −9.4 ± 8.2 and OCC; −3.2 ± 3.2 %CVC max , P <0.05). Additionally, at all sites compared to Control, there were no differences in CVC during IHG+OCC at each heating phase (all P >0.05). We show that during heat stress NOS, but not COX and adenosine receptors, contributes to the sweating response to muscle metaboreceptor activation, whereas CVC is not modulated by NOS, COX, and adenosine receptors. Support or Funding Information This study was supported by the Natural Sciences and Engineering Research Council of Canada (Discover grant, RGPIN‐06313‐2014; Discovery Grants Program ‐ Accelerator Supplement, RGPAS‐462252‐2014; funds held by Dr. Glen P. Kenny).

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