A simple and valid method to determine thermoregulatory sweating threshold and sensitivity

Sweating threshold temperature and sweating sensitivity responses are measured to evaluate thermoregulatory control. However, analytic approaches vary, and no standardized methodology has been validated. This study validated a simple and standardized method, segmented linear regression (SReg), for determination of sweating threshold temperature and sensitivity. Archived data were extracted for analysis from studies in which local arm sweat rate (ṁsw; ventilated dew-point temperature sensor) and esophageal temperature (Tes) were measured under a variety of conditions. The relationship ṁsw/Tes from 16 experiments was analyzed by seven experienced raters (Rater), using a variety of empirical methods, and compared against SReg for the determination of sweating threshold temperature and sweating sensitivity values. Individual interrater differences ( n = 324 comparisons) and differences between Rater and SReg ( n = 110 comparisons) were evaluated within the context of biologically important limits of magnitude (LOM) via a modified Bland-Altman approach. The average Rater and SReg outputs for threshold temperature and sensitivity were compared ( n = 16) using inferential statistics. Rater employed a very diverse set of criteria to determine the sweating threshold temperature and sweating sensitivity for the 16 data sets, but interrater differences were within the LOM for 95% (threshold) and 73% (sensitivity) of observations, respectively. Differences between mean Rater and SReg were within the LOM 90% (threshold) and 83% (sensitivity) of the time, respectively. Rater and SReg were not different by conventional t-test ( P > 0.05). SReg provides a simple, valid, and standardized way to determine sweating threshold temperature and sweating sensitivity values for thermoregulatory studies.

Effect of exercise intensity on the postexercise sweating threshold

The hypothesis that the magnitude of the postexercise onset threshold for sweating is increased by the intensity of exercise was tested in eight subjects. Esophageal temperature was monitored as an index of core temperature while sweat rate was measured by using a ventilated capsule placed on the upper back. Subjects remained seated resting for 15 min (no exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption (V̇o2 peak) followed by a 20-min seated recovery. Subjects then donned a liquid-conditioned suit used to regulate mean skin temperature. The suit was first perfused with 20°C water to control and stabilize skin and core temperature before whole body heating. Subsequently, the skin was heated (∼4.0°C/h) until sweating occurred. Exercise resulted in an increase in the onset threshold for sweating of 0.11 ± 0.02, 0.23 ± 0.01, and 0.33 ± 0.02°C above that measured for the no-exercise resting values ( P < 0.05) for the 55, 70, and 85% of V̇o2 peak exercise conditions, respectively. We did note that there was a greater postexercise hypotension as a function of exercise intensity as measured at the end of the 20-min exercise recovery. Thus it is plausible that the increase in postexercise threshold may be related to postexercise hypotension. It is concluded that the sweating response during upright recovery is significantly modified by exercise intensity and may likely be influenced by the nonthermal baroreceptor reflex adjustments postexercise.

Autonomic Nervous System Responses during Sedative Infusions of Dexmedetomidine

Background The purpose of this study was to determine the effects of dexmedetomidine on systemic and cardiac autonomic reflex responses during rest and during thermal stress. Methods Volunteers received either placebo or low- or high-dose dexmedetomidine (target plasma concentrations 0.3 or 0.6 ng/ml, respectively) infusions in a prospectively randomized, double-blinded crossover study design. After 1 h, baroreflex sensitivity was assessed, and then core body temperature was raised to the sweating threshold and then lowered to the shivering threshold. Plasma catecholamines and blood pressure were measured, and cardiac autonomic responses were assessed by analysis of heart rate variability. Results Compared with placebo, plasma norepinephrine concentrations, blood pressure, heart rate, and some heart rate variability measures were lower after 1-h infusion of dexmedetomidine, but baroreflex responses did not differ significantly. Dexmedetomidine blunted the systemic and cardiac sympathetic effects of sweating observed during placebo infusion but had no effect on parasympathetic measures. Increases in blood pressure, and systemic catecholamines due to shivering were observed during placebo and dexmedetomidine, but these responses were less with dexmedetomidine. During shivering, dexmedetomidine infusion was associated with higher low-frequency and high-frequency heart rate variability power but lower heart rate compared with the sweating threshold and with the control period, suggesting nonreciprocal cardiac autonomic responses. Conclusions Infusion of dexmedetomidine results in compensated reductions in systemic sympathetic tone without changes in baroreflex sensitivity. Dexmedetomidine blunts heart rate and the systemic sympathetic activation due to sweating, but it is less effective in blunting cardiac sympathetic responses to shivering. During dexmedetomidine infusion, cardiac sympathetic and parasympathetic tone may have nonreciprocal changes during shivering.

Influence of training on sweating responses during submaximal exercise in horses

Sweating responses were examined in five horses during a standardized exercise test (SET) in hot conditions (32–34°C, 45–55% relative humidity) during 8 wk of exercise training (5 days/wk) in moderate conditions (19–21°C, 45–55% relative humidity). SETs consisting of 7 km at 50% maximal O2 consumption, determined 1 wk before training day (TD) 0, were completed on a treadmill set at a 6° incline on TD0, 14, 28, 42, and 56. Mean maximal O2consumption, measured 2 days before each SET, increased 19% [TD0 to 42: 135 ± 5 (SE) to 161 ± 4 ml · kg−1 · min−1]. Peak sweating rate (SR) during exercise increased on TD14, 28, 42, and 56 compared with TD0, whereas SRs and sweat losses in recovery decreased by TD28. By TD56, end-exercise rectal and pulmonary artery temperature decreased by 0.9 ± 0.1 and 1.2 ± 0.1°C, respectively, and mean change in body mass during the SET decreased by 23% (TD0: 10.1 ± 0.9; TD56: 7.7 ± 0.3 kg). Sweat Na+concentration during exercise decreased, whereas sweat K+concentration increased, and values for Cl− concentration in sweat were unchanged. Moderate-intensity training in cool conditions resulted in a 1.6-fold increase in sweating sensitivity evident by 4 wk and a 0.7 ± 0.1°C decrease in sweating threshold after 8 wk during exercise in hot, dry conditions. Altered sweating responses contributed to improved heat dissipation during exercise and a lower end-exercise core temperature. Despite higher SRs for a given core temperature during exercise, decreases in recovery SRs result in an overall reduction in sweat fluid losses but no change in total sweat ion losses after training.

Equine sweating responses to submaximal exercise during 21 days of heat acclimation

This study examined sweating responses in six exercise-trained horses during 21 consecutive days (4 h/day) of exposure to, and daily exercise in, hot humid conditions (32–34°C, 80–85% relative humidity). On days 0, 3, 7, 14, and 21, horses completed a standardized exercise test on a treadmill (6° incline) at a speed eliciting 50% of maximal O2 uptake until a pulmonary artery temperature of 41.5°C was attained. Sweat was collected at rest, every 5 min during exercise, and during 1 h of standing recovery for measurement of ion composition (Na+, K+, and Cl−) and sweating rate (SR). There was no change in the mean time to reach a pulmonary artery temperature of 41.5°C (range 19.09 ± 1.41 min on day 0 to 20.92 ± 1.98 min on day 3). Peak SR during exercise (ml ⋅ m−2 ⋅ min−1) increased on day 7 (57.5 ± 5.0) but was not different on day 21 (48.0 ± 4.7) compared with day 0 (52.0 ± 3.4). Heat acclimation resulted in a 17% decline in SR during recovery and decreases in body mass and sweat fluid losses during the standardized exercise test of 25 and 22%, respectively, by day 21. By day 21, there was also a 10% decrease in mean sweat Na+ concentration for a given SR during exercise and recovery; this contributed to an ∼26% decrease in calculated total sweat ion losses (3,112 ± 114 mmol on day 0 vs. 2,295 ± 107 mmol on day 21). By day 21, there was a decrease in sweating threshold (∼1°C) but no change in sweat sensitivity. It is concluded that horses responded to 21 days of acclimation to, and exercise in, hot humid conditions with a reduction in sweat ion losses attributed to decreases in sweat Na+concentration and SR during recovery.

Dexmedetomidine Does Not Alter the Sweating Threshold, But Comparably and Linearly Decreases the Vasoconstriction and Shivering Thresholds

Background Clonidine decreases the vasoconstriction and shivering thresholds. It thus seems likely that the alpha2 agonist dexmedetomidine will also impair control of body temperature. Accordingly, the authors evaluated the dose-dependent effects of dexmedetomidine on the sweating, vasoconstriction, and shivering thresholds. They also measured the effects of dexmedetomidine on heart rate, blood pressures, and plasma catecholamine concentrations. Methods Nine male volunteers participated in this randomized, double-blind, cross-over protocol. The study drug was administered by computer-controlled infusion, targeting plasma dexmedetomidine concentrations of 0.0, 0.3, and 0.6 ng/ml. Each day, skin and core temperatures were increased to provoke sweating and then subsequently reduced to elicit vasoconstriction and shivering. Core-temperature thresholds were computed using established linear cutaneous contributions to control of sweating, vasoconstriction, and shivering. The dose-dependent effects of dexmedetomidine on thermoregulatory response thresholds were then determined using linear regression. Heart rate, arterial blood pressures, and plasma catecholamine concentrations were determined at baseline and at each threshold. Results Neither dexmedetomidine concentration increased the sweating threshold from control values. In contrast, dexmedetomidine administration reduced the vasoconstriction threshold by 1.61 +/- 0.80 degrees C x ng(-1) x ml (mean +/- SD) and the shivering threshold by 2.40 +/- 0.90 degrees C x ng(-1) x ml. Hemodynamic responses and catecholamine concentrations were reduced from baseline values, but they did not differ at the two tested dexmedetomidine doses. Conclusions Dexmedetomidine markedly increased the range of temperatures not triggering thermoregulatory defenses. The drug is thus likely to promote hypothermia in a typical hospital environment; it is also likely to prove an effective treatment for shivering.