The influence of local skin temperature on the sweat glands maximum ion reabsorption rate

PURPOSE: Changes in mean skin temperature (Tsk) have been shown to modify the maximum rate of sweat ion reabsorption. This study aims to extend this knowledge by investigating if modifications could also be caused by local Tsk. METHODS: The influence of local Tsk on the sweat gland maximum ion reabsorption rates was investigated in ten healthy volunteers (three female and seven male; 20.8 ± 1.2 years, 60.4 ± 7.7 kg, 169.4 ± 10.4 cm) during passive heating (water-perfused suit and lower leg water immersion). In two separate trials, in a randomized order, one forearm was always manipulated to 33 °C (Neutral), whilst the other was manipulated to either 30 °C (Cool) or 36 °C (Warm) using water-perfused patches. Oesophageal temperature (Tes), forearm Tsk, sweat rate (SR), galvanic skin conductance (GSC) and salivary aldosterone concentrations were measured. The sweat gland maximum ion reabsorption rates were identified using the ∆SR threshold for an increasing ∆GSC. RESULTS: Thermal [Tes and body temperature (Tb)] and non-thermal responses (aldosterone) were similar across all conditions (p > 0.05). A temperature-dependent response for the sweat gland maximum ion reabsorption rates was evident between 30 °C (0.18 ± 0.10 mg/cm2/min) and 36 °C (0.28 ± 0.14 mg/cm2/min, d = 0.88, p  0.05. CONCLUSION: The data indicate that small variations in local Tsk may not affect the sweat gland maximum ion reabsorption rates but when the local Tsk increases by > 6 °C, ion reabsorption rates also increase

The effects of exercise and passive heating on the sweat glands ion reabsorption rates

The sweat glands maximum ion reabsorption rates were investigated (n = 12, 21.7 ± 3.0 years, 59.4 ± 9.8 kg, 166.9 ± 10.4 cm and 47.1 ± 7.5 mL/kg/min) during two separate endogenous protocols; cycling at 30% (LEX) and 60% VO2max(MEX) and one exogenous trial; passive heating (PH) (43°C water lower leg immersion) in 27°C, 50%RH. Oesophageal temperature (Tes), skin temperature (Tsk), and forearm, chest and lower back sweat rate (SR) and galvanic skin conductance (GSC) were measured. Salivary aldosterone was measured pre-and postheating (n = 3). Using the ∆SR threshold for an increasing ∆GSC to identify maximum sweat ion reabsorption rate revealed higher reabsorption rates during MEX compared to PH (mean of all regions: 0.63 ± 0.28 vs. 0.44 ± 0.3 mg/cm2/min, P  0.05). Aldosterone increased more during MEX (72.8 ± 36.6 pg/mL) compared to PH (39.2 ± 17.5 pg/mL) and LEX (1.8 ± 9.7 pg/mL). The back had a higher threshold than the forearm (P  0.05) (mean of all conditions; 0.64 ± 0.33, 0.42 ± 0.25, 0.54 ± 0.3 mg/cm2/min, respectively). Although the differences between conditions may be influenced by thermal or nonthermal mechanism, our results indicate a possibility that the sweat glands maximum ion reabsorption rates may be different between exercise and passive heating without mediating skin regional differences

Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated humans

Elevating core temperature at rest causes increases in minute ventilation (V̇e), which lead to reductions in both arterial CO2 partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (Tes) to reach 39°C. During heating in two separate trials, end-tidal CO2 partial pressure decreased from the level before heating (39.4 ± 2.0 mmHg) to the end of heating (30.5 ± 6.3 mmHg) (P = 0.005) in the Control trial. This decrease was prevented by breathing CO2-enriched air throughout the heating such that end-tidal CO2 partial pressure did not differ between the beginning (39.8 ± 1.5 mmHg) and end (40.9 ± 2.7 mmHg) of heating (P = 1.00). The sensitivity to rising Tes (i.e., slope of the Tes − V̇E relation) did not differ between the Control and CO2-breathing trials (37.1 ± 43.1 vs. 16.5 ± 11.1 l·min−1·°C−1, P = 0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P < 0.01), despite the absence of hyperventilation-induced hypocapnia. CO2 breathing increased MCAV relative to Control at the end of heating (P = 0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia and that most of the decrease in cerebral blood flow occurs independently of hypocapnia

Effects of CO2 on ventilatory and cerebrovascular responses during passive heating in humans

Effects of CO2 on ventilatory and cerebrovascular responses during passive heating in human

The effect of dietary nitrate supplementation on the spatial heterogeneity of quadriceps deoxygenation during heavy-intensity cycling

This study investigated the influence of dietary inorganic nitrate (NO3-) supplementation on pulmonary O2 uptake ( o2) and muscle deoxyhemoglobin/myoglobin (i.e. deoxy[Hb+Mb]) kinetics during submaximal cycling exercise. In a randomized, placebo-controlled, cross-over study, eight healthy and physically active male subjects completed multiple step cycle tests at a work rate equivalent to 50% of the difference between the gas exchange threshold and peak o2 over separate 4-day supplementation periods with NO3--rich (BR; providing 8.4 mmol NO3-∙day-1) and NO3--depleted (placebo; PLA) beetroot juice. Pulmonary o2 was measured breath-by-breath and time-resolved near-infrared spectroscopy was utilized to quantify absolute deoxy[Hb+Mb] and total[Hb+Mb] within the rectus femoris, vastus lateralis, and vastus medialis. There were no significant differences (P > 0.05) in the primary deoxy[Hb+Mb] mean response time or amplitude between the PLA and BR trials at each muscle site. BR significantly increased the mean (three-site) end-exercise deoxy[Hb+Mb] (PLA: 91 ± 9 vs. BR: 95 ± 12 µM, P < 0.05), with a tendency to increase the mean (three-site) area under the curve for total(Hb+Mb) responses (PLA: 3650 ± 1188 vs. BR: 4467 ± 1315 µM·s-1, P = 0.08). The o2 slow component reduction after BR supplementation (PLA: 0.27 ± 0.07 vs. BR: 0.23 ± 0.08 L·min-1, P = 0.07) correlated inversely with the mean increases in deoxy[Hb+Mb] and total[Hb+Mb] across the three muscle regions (r2 = 0.62 and 0.66, P < 0.05). Dietary NO3- supplementation increased O2 diffusive conductance across locomotor muscles in association with improved o2 dynamics during heavy-intensity cycling transitions

Characteristics of human thermoregulation and its regional difference (Japanese)

Characteristics of human thermoregulation and its regional difference (Japanese

Reply to Parkes: Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated humans

Reply to Parkes: Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated human