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

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.

The effect of plasma osmolality and baroreceptor loading status on postexercise heat loss responses.

We examined the separate and combined effects of plasma osmolality and baroreceptor loading status on postexercise heat loss responses. Nine young males completed a 45-min treadmill exercise protocol at 58 ± 2% V̇o2 peak, followed by a 60-min recovery. On separate days, participants received 0.9% NaCl (ISO), 3.0% NaCl (HYP), or no infusion (natural recovery) throughout exercise. In two additional sessions (no infusion), lower-body negative (LBNP) or positive (LBPP) pressure was applied throughout the final 45 min of recovery. Local sweat rate (LSR; ventilated capsule: chest, forearm, upper back, forehead) and skin blood flow (SkBF; laser-Doppler flowmetry: forearm, upper back) were continuously measured. During HYP, upper back LSR was attenuated from end-exercise to 10 min of recovery by ∼0.35 ± 0.10 mg·min(-1)·cm(-2) and during the last 20 min of recovery by ∼0.13 ± 0.03 mg·min(-1)·cm(-2), while chest LSR was lower by 0.18 ± 0.06 mg·min(-1)·cm(-2) at 50 min of recovery compared with natural recovery (all P < 0.05). Forearm and forehead LSRs were not affected by plasma hyperosmolality during HYP (all P > 0.28), which suggests regional differences in the osmotic modulation of postexercise LSR. Furthermore, LBPP application attenuated LSR by ∼0.07-0.28 mg·min(-1)·cm(-2) during the last 30 min of recovery at all sites except the forehead compared with natural recovery (all P < 0.05). Relative to natural recovery, forearm and upper back SkBF were elevated during LBPP, ISO, and HYP by ∼6-10% by the end of recovery (all P < 0.05). We conclude that 1) hyperosmolality attenuates postexercise sweating heterogeneously among skin regions, and 2) baroreceptor loading modulates postexercise SkBF independently of changes in plasma osmolality without regional differences.

Muscle metaboreceptors modulate postexercise sweating, but not cutaneous blood flow, independent of baroreceptor loading status.

We examined whether sustained changes in baroreceptor loading status during prolonged postexercise recovery can alter the metaboreceptors' influence on heat loss. Thirteen young males performed a 1-min isometric handgrip exercise (IHG) at 60% maximal voluntary contraction followed by 2 min of forearm ischemia (to activate metaboreceptors) before and 15, 30, 45, and 60 min after a 15-min intense treadmill running exercise (>90% maximal heart rate) in the heat (35°C). This was repeated on three separate days with continuous lower body positive (LBPP, +40 mmHg), negative (LBNP, -20 mmHg), or no pressure (Control) from 13- to 65-min postexercise. Sweat rate (ventilated capsule; forearm, chest, upper back) and cutaneous vascular conductance (CVC; forearm, upper back) were measured. Relative to pre-IHG levels, sweating at all sites increased during IHG and remained elevated during ischemia at baseline and similarly at 30, 45, and 60 min postexercise (site average sweat rate increase during ischemia: Control, 0.13 ± 0.02; LBPP, 0.12 ± 0.02; LBNP, 0.15 ± 0.02 mg·min(-1)·cm(-2); all P < 0.01), but not at 15 min (all P > 0.10). LBPP and LBNP did not modulate the pattern of sweating to IHG and ischemia (all P > 0.05). At 15-min postexercise, forearm CVC was reduced from pre-IHG levels during both IHG and ischemia under LBNP only (ischemia: 3.9 ± 0.8% CVCmax; P < 0.02). Therefore, we show metaboreceptors increase postexercise sweating in the middle to late stages of recovery (30-60 min), independent of baroreceptor loading status and similarly between skin sites. In contrast, metaboreflex modulation of forearm but not upper back CVC occurs only in the early stages of recovery (15 min) and is dependent upon baroreceptor unloading.