Determination of the Maximum Rate of Eccrine Sweat Glands’ Ion Reabsorption Using the Galvanic Skin Conductance to Local Sweat Rate Relationship

Purpose The purpose of the present study was to develop and describe a simple method to evaluate the rate of ion reabsorption of eccrine sweat glands in human using the measurement of galvanic skin conductance (GSC) and local sweating rate (SR). This purpose was investigated by comparing the SR threshold for increasing GSC with following two criteria of sweat ion reabsorption in earlier studies such as 1) the SR threshold for increasing sweat ion was at approximately 0.2 to 0.5 mg/cm2/min and 2) exercise-heat acclimation improved the sweat ion reabsorption ability and would increase the criteria 1. Methods Seven healthy non-heat-acclimated male subjects received passive heat treatment both before and after 7 days of cycling in hot conditions (50% maximum oxygen uptake, 60 min/day, ambient temperature 32°C, and 50% relative humidity). Results Subjects became partially heat-acclimated, as evidenced by the decreased end-exercise heart rate (p<0.01), rate of perceived exhaustion (p<0.01), and oesophageal temperature (p=0.07), without alterations in whole-body sweat loss, from the first to the last day of training. As hypothesised, we confirmed that the SR threshold for increasing GSC was near the predicted SR during passive heating before exercise heat acclimation, and increased significantly after training (0.19 ± 0.09 to 0.32 ± 0.10 mg/cm2/min, p<0.05). Conclusions The reproducibility of sweat ion reabsorption by the eccrine glands in the present study suggests that the relationship between GSC and SR can serve as a new index for assessing the maximum rate of sweat ion reabsorption of eccrine sweat glands in humans

The nitric oxide dependence of cutaneous microvascular function to independent and combined hypoxic cold exposure

Hypoxic modulation of nitric oxide (NO) production pathways in the cutaneous microvasculature and its interaction with cold-induced reflex vasoconstriction, independent of local cooling, have yet to be identified. This study assessed the contribution of NO to nonglabrous microvasculature perfusion during hypoxia and whole body cooling with concomitant inhibition of NO synthase [NOS; via NG-nitro-l-arginine methyl ester (l-NAME)] and the nitrite reductase, xanthine oxidase (via allopurinol), two primary sources of NO production. Thirteen volunteers were exposed to independent and combined cooling via water-perfused suit (5°C) and normobaric hypoxia (FIO2, 0.109 ± 0.002). Cutaneous vascular conductance (CVC) was assessed across four sites with intradermal microdialysis perfusion of 1) lactated Ringers solution (control), 2) 20 mmol l-NAME, 3) 10 µmol allopurinol, or 4) combined l-NAME/allopurinol. Effects and interactions were assessed via four-way repeated measures ANOVA. Independently, l-NAME reduced CVC (43%, P < 0.001), whereas allopurinol did not alter CVC (P = 0.5). Cooling decreased CVC (P = 0.001), and the reduction in CVC was consistent across perfusates (~30%, P = 0.9). Hypoxia increased CVC (16%, P = 0.01), with this effect abolished by l-NAME infusion (P = 0.04). Cold-induced vasoconstriction was blunted by hypoxia, but importantly, hypoxia increased CVC to a similar extent (39% at the Ringer site) irrespective of environmental temperature; thus, no interaction was observed between cold and hypoxia (P = 0.1). l-NAME restored vasoconstriction during combined cold-hypoxia (P = 0.01). This investigation suggests that reflex cold-induced cutaneous vasoconstriction acts independently of NO suppression, whereas hypoxia-induced cutaneous vasodilatation is dependent on NOS-derived NO production

Cardiovascular Function During Supine Rest in Endurance Trained Males with New Zealand Blackcurrant: A Dose-Response Study

Purpose Blackcurrant contains anthocyanins that could alter cardiovascular function and reduce cardiovascular disease risk. We examined dose responses of New Zealand blackcurrant (NZBC) extract on cardiovascular function during supine rest. Methods Fifteen endurance trained male cyclists (age: 38±12 years, height: 178±5 cm, body mass: 76±10 kg, V?O2max: 56±8 mL?kg-1?min-1, mean±SD) were randomly assigned using a counterbalanced Latin square design to complete four conditions, a control of no NZBC, or one of three doses (300, 600 or 900 mg?day-1) of NZBC extract (CurraNZTM) for seven-days with a fourteen-day washout. Cardiovascular function (i.e. blood pressure, heart rate, ejection time, cardiac output, stroke volume and total peripheral resistance) during supine rest was examined (Portapres® Model 2). Results Systolic and diastolic blood pressure, heart rate and ejection time were unchanged by NZBC. A dose effect (P<0.05) was observed for cardiac output, stroke volume and total peripheral resistance. A trend for a dose effect was observed for mean arterial blood pressure. Cardiac output increased by 0.6±0.6 L·min-1 (15%) and 1.0±1.0 L·min-1 (28%) and stroke volume by 5±8 mL (7%) and 6±17 mL (18%) between control and 600, and 900 mg?day-1, respectively. Total peripheral resistance decreased by 4±3 mmHg·L-1·min-1 (20%) and 5±9 mmHg·L-1·min-1 (20%) for 600, and 900 mg?day-1. Conclusion Seven-days intake of New Zealand blackcurrant extract demonstrated dose-dependent changes on some cardiovascular parameters during supine rest in endurance-trained male cyclists

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 &lt; 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. NEW &amp; NOTEWORTHY Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The last may underlie central fatigue. We are the first to demonstrate that hyperthermia-induced hyperventilation is not suppressed by the resultant hypocapnia and that hypocapnia explains only 36% of cerebral hypoperfusion elicited by hyperthermia. These new findings advance our understanding of the mechanisms controlling ventilation and cerebral blood flow during heat stress, which may be useful for developing interventions aimed at preventing central fatigue during hyperthermia

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

This paper was accepted for publication in the journal Journal of Applied Physiology and the definitive published version is available at https://doi.org/10.1152/japplphysiol.00089.2018