Key result
Extracellular hyperosmolality via 3.0% saline infusion augmented metaboreflex-induced increases in global sweat rate compared with 0.9% saline.
Why the study?
Recent work indicates extracellular hyperosmolality may augment metaboreflex-mediated elevations in sympathetic nervous activity, but its effect on metaboreflex-mediated increases in sweat rate was unconfirmed.
Does extracellular hyperosmolality increase metaboreflex-mediated increases in sweat rate in passively heated young men?
Does extracellular hyperosmolality increase metaboreflex-mediated increases in sweat rate in passively heated young men?
Extracellular hyperosmolality augments metaboreflex-induced increases in global sweat rate in passively heated young men.
Answers are grounded in this paper and cite their sources.
Hyperosmolality may augment metaboreflex sweat responses in heated individuals; hypothesis-generating in small cohorts and should not yet change practice.
Metaboreflex activation augments sweating during mild-to-moderate hyperthermia in euhydrated (isosmotic isovolemic) individuals. Recent work indicates that extracellular hyperosmolality may augment metaboreflex-mediated elevations in sympathetic nervous activity. Our primary objective was, therefore, to test the hypothesis that extracellular hyperosmolality would exacerbate metaboreflex-mediated increases in sweat rate. On two separate occasions, 12 young men [means (SD): 25 (5) yr] received a 90-min intravenous infusion of either 0.9% saline (isosmotic condition, ISO) or 3.0% saline (hyperosmotic condition, HYP), resulting in a postinfusion serum osmolality of 290 (3) and 301 (7) mosmol/kgH 2 O, respectively. A whole body water perfusion suit was then used to increase esophageal temperature by 0.8°C above resting. Participants then performed a metaboreflex activation protocol consisting of 90-s isometric handgrip exercise (40% of their predetermined maximum voluntary contraction), followed by 150 s of brachial occlusion (trapping produced metabolites within the limb). Metaboreflex-induced sweating was quantified as the change in global sweat rate (from preisometric handgrip exercise to brachial occlusion), estimated as the surface area-weighted average of local sweat rate on the abdomen, axilla, chest, bicep, quadriceps, and calf, measured using ventilated capsules (3.8 cm 2 ). We also explored whether this response differed between body regions. The change in global sweat rate due to metaboreflex activation was significantly greater in HYP compared with ISO (0.03 mg/min/cm 2 [95% confidence interval: 0.00, 0.06]; P = 0.047), but was not modulated by body region (site × condition interaction: P = 0.679). These findings indicate that extracellular hyperosmolality augments metaboreflex-induced increases in global sweat rate, with no evidence for region-specific differences.
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Rutherford et al. (2021) studied this question. 3.0% saline (hyperosmotic condition) vs. 0.9% saline (isosmotic condition) was evaluated on change in global sweat rate due to metaboreflex activation (MD 0.03 mg/min/cm2, 95% CI 0.00, 0.06, p=0.047). Extracellular hyperosmolality via 3.0% saline infusion augmented metaboreflex-induced increases in global sweat rate compared with 0.9% saline.
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