Change In Mean Body Temperature Research Articles

The Effect of Upper-Body Positioning on the Aerodynamic-Physiological Economy of Time-Trial Cycling.

Cycling time trials (TTs) are characterized by riders' adopting aerodynamic positions to lessen the impact of aerodynamic drag on velocity. The optimal performance requirements for TTs likely exist on a continuum of rider aerodynamics versus physiological optimization, yet there is little empirical evidence to inform riders and coaches. The aim of the present study was to investigate the relationship between aerodynamic optimization, energy expenditure, heat production, and performance. Eleven trained cyclists completed 5 submaximal exercise tests followed by a TT. Trials were completed at hip angles of 12° (more horizontal), 16°, 20°, 24° (more vertical), and their self-selected control position. The largest decrease in power output at anaerobic threshold compared with control occurred at 12° (-16 [20]W, P = .03; effect size [ES] = 0.8). There was a linear relationship between upper-body position and heat production (R2 = .414, P = .04) but no change in mean body temperature, suggesting that, as upper-body position and hip angle increase, convective and evaporative cooling also rise. The highest aerodynamic-physiological economy occurred at 12° (384 [53]W·CdA-1·L-1·min-1, ES = 0.4), and the lowest occurred at 24° (338 [28]W·CdA-1·L-1·min-1, ES = 0.7), versus control (367 [41]W·CdA-1·L-1·min-1). These data suggest that the physiological cost of reducing hip angle is outweighed by the aerodynamic benefit and that riders should favor aerodynamic optimization for shorter TT events. The impact on thermoregulation and performance in the field requires further investigation.

Heat adaptation in humans: the significance of controlled and regulated variables for experimental design and interpretation

Herein, the principles of homoeostasis are re-visited, but with an emphasis upon repeated homoeostatic disturbances that give rise to physiological adaptation. The central focus is human heat adaptation, and how, for experimental purposes, one might standardise successive adaptation stimuli, and then evaluate and compare the resulting adaptations. To provide sufficient background for that discussion, the principles of physiological control and regulation have been reviewed. The case is presented that, since it is the regulated variables that drive both the effector organs and the processes of physiological adaptation, then it is those variables (e.g., body temperature) that should be used to set and standardise the adaptation stimuli. Alternatively,some have proposed that the same outcome can be achieved through standardising a controlled variable (e.g., heart rate), and sothe merits of that proposition are evaluated. Indeed, it can be an effective approach, although some experimental pitfalls are describedto highlight its limitations with regard to between-group (e.g., able-bodied versus spinal-injured participants) and between-treatment comparisons (e.g., hot-water versus hot-air adaptation stimuli). The concept of setting the adaptation stimulus relative to an anaerobic or lactate threshold is also critically evaluated. Finally, an appraisal is offered concerning the merits of three different strategies for using deep-body and mean body temperature changes for evaluating thermoeffector adaptations.

Improved neural control of body temperature following heat acclimation in humans.

With the advent of more frequent extreme heat events, adaptability to hot environments will be crucial for the survival of many species, including humans. However, the mechanisms that mediate human heat adaptation have remained elusive. We tested the hypothesis that heat acclimation improves the neural control of body temperature. Skin sympathetic nerve activity, comprising the efferent neural signal that activates heat loss thermoeffectors, was measured in healthy adults exposed to passive heat stress before and after a 7day heat acclimation protocol. Heat acclimation reduced the activation threshold for skin sympathetic nerve activity, leading to an earlier activation of cutaneous vasodilatation and sweat production. These findings demonstrate that heat acclimation improves the neural control of body temperature in humans. Heat acclimation improves autonomic temperature regulation in humans. However, the mechanisms that mediate human heat adaptation remain poorly understood. The present study tested the hypothesis that heat acclimation improves the neural control of body temperature. Body temperatures, skin sympathetic nerve activity, cutaneous vasodilatation, and sweat production were measured in 14healthy adults (nine men and five women, aged 27±5 years) during passive heat stress performed before and after a 7day heat acclimation protocol. Heat acclimation increased whole-body sweat rate [+0.54Lh-1 (0.32, 0.75), P<0.01] and reduced resting core temperature [-0.29°C (-0.40, -0.18), P<0.01]. During passive heat stress, the change in mean body temperature required to activate skin sympathetic nerve activity was reduced [-0.21°C (-0.34, -0.08), P<0.01] following heat acclimation. The earlier activation of skin sympathetic nerve activity resulted in lower activation thresholds for cutaneous vasodilatation [-0.18°C (-0.35, -0.01), P=0.04] and local sweat rate [-0.13°C (-0.24, -0.01), P=0.03]. These results demonstrate that heat acclimation leads to an earlier activation of the neural efferent outflow that activates the heat loss thermoeffectors of cutaneous vasodilatation and sweating.

Suhu Tubuh Bayi Prematur di Inkubator Dinding Tunggal dengan Inkubator Dinding Tunggal Disertai Sungkup

This study aims to compare the average change in body temperature in a single wall incubator with a single wall incubator with hood in preterm infants with hypothermia. The design of this study uses a comparative descriptive method. The results of the study in the group of preterm infants with hypothermia in a single wall incubator with a lid significantly increased mean body temperature changes with a mean value of 36.09 variance 0.152 while for preterm infants with hypothermia in a single wall incubator a mean value of 35.35 variance values 0.859 and obtained t count from the two study groups namely 2.551 and 1.717 t table. In conclusion, a single wall incubator with a lid increases body temperature in premature infants with hypothermia compared to a single wall incubator.&#x0D; &#x0D; Keywords: Hypothermia, Incubator, Premature

Thermoeffector threshold plasticity: The impact of thermal pre-conditioning on sudomotor, cutaneous vasomotor and thermogenic thresholds.

To better understand the relationships between changes in body temperature and displacements of the thermoeffector thresholds (critical temperatures), the passive cooling (and heating) of pre-heated (and pre-cooled) individuals was investigated. Such experiments are necessary to understand the inter-dependence of those thresholds, and may possibly yield human evidence for the existence of separate central controllers. Eight males participated in four trials; two when normothermic, one following pre-experimental heating and the fourth following pre-cooling. Subjects were exposed to passive, whole-body cooling and heating when normothermic (the control trials), and again following pre-heating and pre-cooling (respectively). Cutaneous vasomotor, thermogenic, as well as precursor and discharged sudomotor thresholds from different body segments were compared across those dynamic thermal states. Following pre-heating, the critical mean body temperatures for vasoconstriction (0.37 °C ± 0.10) and thermogenesis (0.67 °C ± 0.20) were significantly elevated during passive cooling, relative to the corresponding control trial (both P < 0.05). When passive heating followed pre-cooling, the thresholds for vasodilatation were reduced (0.37 °C ± 0.07; P < 0.05). Conversely, but with the exception of forehead precursor sweating, the sudomotor thresholds were elevated (averaging 0.16 °C ± 0.02; P < 0.05). Most thermoeffectors revealed unique and adjustable activation thresholds, with the threshold displacements for thermogenesis and vasomotion appearing to be linked to the change in mean body temperature. Following pre-cooling, the critical temperatures for vasodilatation and sudomotor activation varied independently, with the exception of forehead precursor sweating. Collectively, those observations are consistent with the presence of independent central controllers for thermally dependent vasomotor and sudomotor responses, and perhaps also for shivering thermogenesis.

Differential thermal behavioral response to heat vs. cold stress in humans

PurposeData from non‐human endotherms indicate that thermal behavioral responses to increases in core temperature (Tcore) are more robust when compared to similar reductions in Tcore. These observations have been interpreted as a protective response, owing to the proximity of the endothermic Tcore to the upper lethal limit compared to the lower lethal limit. In resting humans, thermal behavior is mostly initiated by changes in skin temperature (Tskin). There is some evidence that thermal behavior in humans is more sensitive to increases in Tskin vs. decreases. On the contrary, it is often posited that skin cooling evokes a greater thermoregulatory response compared to equivalent increases in Tskin because of the greater density of cold receptors in the skin. Based on this uncertainty, we tested the hypothesis that thermal behavior is more sensitive during heat vs. cold stress.MethodsWearing a water perfused suit, twelve healthy adults (23 ± 2 y, 6 F) underwent 60 min of heat (HEAT) and cold (COLD) stress that induced gradual changes in mean body temperature (Tbody). Using a custom‐made device, subjects controlled the temperature of their dorsal neck to perceived thermal comfort. Thus, neck temperature provided an index of thermal behavior. Neck temperature, weighted Tskin (6 site), and Tcore (intestinal) were measured continually. Tbody, the integrated stimulus for thermal behavior, was calculated as the unweighted average of Tskin and Tcore. Neck temperature was analyzed using segmental regression analysis, providing an analysis of thermal behavior relative to changes in Tbody. This analysis provided two parameters: a) threshold, which is indicative of the activation of thermal behavior as a function of Tbody, and b) gain, which is the slope of the thermal behavioral response to continued changes in Tbody after the threshold. To permit direct comparisons between HEAT and COLD, data were analyzed as absolute values and the gain was normalized to the maximum change within a trial and subject.ResultsIn HEAT, Tskin increased by 3.7 ± 0.4°C through 36 min (P&lt;0.01) and an increase in Tskin of 4.1 ± 0.2°C was maintained thereafter. Elevations in Tcore occurred at 36 min, with Tcore maximally increasing by 0.9 ± 0.3°C (P&lt;0.01). In HEAT, neck temperature was decreased at 40 min (P=0.03) with a maximal reduction of 7.9 ± 4.6°C. In COLD, Tskin decreased throughout, dropping by 6.0 ± 0.6°C (P&lt;0.01), while Tcore did not change (P=0.10). In COLD, neck temperature was increased at 32 min (P=0.01) with a maximal increase of 4.3 ± 1.9°C. The threshold change in Tbody upon which thermal behavior was initiated was lower in COLD (0.8 ± 0.7 vs. 1.3 ± 0.7°C, P=0.04). However, the relative gain of the response after the threshold was greater in HEAT (3.8 ± 3.1 vs. 1.4 ± 0.9 a.u., P=0.02).ConclusionsCompared to cold stress, thermal behavior during heat stress is initiated following greater changes in Tbody. However, after activation the relative sensitivity of thermal behavior to continued changes in Tbody is greater during heat stress. These findings are consistent with a higher density of cold receptors in the skin, yet also support that thermal behavior more robustly defends increases in Tbody after thermal behavior is initiated.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

An Overt Chemical Protective Garment Reduces Thermal Strain Compared with a Covert Garment in Warm-Wet but Not Hot-Dry Environments.

Objectives: A commercial chemical, biological, radiological and nuclear (CBRN) protective covert garment has recently been developed with the aim of reducing thermal strain. A covert CBRN protective layer can be worn under other clothing, with equipment added for full chemical protection when needed. However, it is unknown whether the covert garment offers any alleviation to thermal strain during work compared with a traditional overt ensemble. Therefore, the aim of this study was to compare thermal strain and work tolerance times during work in an overt and covert ensemble offering the same level of CBRN protection.Methods: Eleven male participants wore an overt (OVERT) or covert (COVERT) CBRN ensemble and walked (4 km·h−1, 1% grade) for a maximum of 120 min in either a wet bulb globe temperature [WBGT] of 21, 30, or 37°C (Neutral, WarmWet and HotDry, respectively). The trials were ceased if the participants' gastrointestinal temperature reached 39°C, heart rate reached 90% of maximum, walking time reached 120 min or due to self-termination.Results: All participants completed 120 min of walking in Neutral. Work tolerance time was greater in OVERT compared with COVERT in WarmWet (P < 0.001, 116.5[9.9] vs. 88.9[12.2] min, respectively), though this order was reversed in HotDry (P = 0.003, 37.3[5.3] vs. 48.4[4.6] min, respectively). The rate of change in mean body temperature and mean skin temperature was greater in COVERT (0.025[0.004] and 0.045[0.010]°C·min−1, respectively) compared with OVERT (0.014[0.004] and 0.027[0.007]°C·min−1, respectively) in WarmWet (P < 0.001 and P = 0.028, respectively). However, the rate of change in mean body temperature and mean skin temperature was greater in OVERT (0.068[0.010] and 0.170[0.026]°C·min−1, respectively) compared with COVERT (0.059[0.004] and 0.120[0.017]°C·min−1, respectively) in HotDry (P = 0.002 and P < 0.001, respectively). Thermal sensation, thermal comfort, and ratings of perceived exertion did not differ between garments at trial cessation (P > 0.05).Conclusion: Those dressed in OVERT experienced lower thermal strain and longer work tolerance times compared with COVERT in a warm-wet environment. However, COVERT may be an optimal choice in a hot-dry environment. These findings have practical implications for those making decisions on the choice of CBRN ensemble to be used during work.

The recommended Threshold Limit Values for heat exposure fail to maintain body core temperature within safe limits in older working adults

ABSTRACTPurpose: The American Conference of Governmental and Industrial Hygienists (ACGIH®) Threshold Limit Values (TLV® guidelines) for work in the heat consist of work-rest (WR) allocations designed to ensure a stable core temperature that does not exceed 38°C. However, the TLV® guidelines have not been validated in older workers. This is an important shortcoming given that adults as young as 40 years demonstrate impairments in their ability to dissipate heat. We therefore evaluated body temperature responses in older adults during work performed in accordance to the TLV® recommended guidelines.Methods: On three occasions, 9 healthy older (58 ± 5 years) males performed a 120-min work-simulated protocol in accordance with the TLV® guidelines for moderate-to-heavy intensity work (360 W fixed rate of heat production) in different wet-bulb globe temperatures (WBGT). The first was 120 min of continuous (CON) cycling at 28.0°C WBGT (CON[28°C]). The other two protocols were 15-min intermittent work bouts performed with different WR cycles and WBGT: (i) WR of 3:1 at 29.0°C (WR3:1[29°C]) and (ii) WR of 1:1 at 30.0°C (WR1:1[30°C]). Rectal temperature was measured continuously. The rate of change in mean body temperature was determined via thermometry (weighting coefficients: rectal, 0.9; mean skin temperature, 0.1) and direct calorimetry.Results: Rectal temperature exceeded 38°C in all participants in CON[28°C] and WR3:1[29°C] whereas a statistically similar proportion of workers exceeded 38°C in WR1:1[30°C] (χ2; P = 0.32). The average time for rectal temperature to reach 38°C was: CON[28°C], 53 ± 7; WR3:1[29°C], 79 ± 11; and WR1:1[30°C], 100 ± 29 min. Finally, while a stable mean body temperature was not achieved in any work condition as measured by thermometry (i.e., >0°C·min−1; all P<0.01), heat balance as determined by direct calorimetry was achieved in WR3:1[29°C] and WR1:1[30°C] (both P ≥ 0.08).Conclusion: Our findings indicate that the TLV® guidelines do not prevent body core temperature from exceeding 38°C in older workers. Furthermore, a stable core temperature was not achieved within safe limits (i.e., ≤38°C) indicating that the TLV® guidelines may not adequately protect all individuals during work in hot conditions.

Sustained increases in skin blood flow are not a prerequisite to initiate sweating during passive heat exposure.

Some studies have observed a functional relationship between sweating and skin blood flow. However, the implications of this relationship during physiologically relevant conditions remain unclear. We manipulated sudomotor activity through changes in sweating efficiency to determine if parallel changes in vasomotor activity are observed. Eight young men completed two trials at 36°C and two trials at 42°C. During these trials, air temperature remained constant while ambient vapor pressure increased from 1.6 to 5.6 kPa over 2 h. Forced airflow across the skin was used to create conditions of high (HiSeff) or low (LoSeff) sweating efficiency. Local sweat rate (LSR), local skin blood flow (SkBF), as well as mean skin and esophageal temperatures were measured continuously. It took longer for LSR to increase during HiSeff at 36°C (HiSeff: 99 ± 11 vs. LoSeff: 77 ± 11 min, P < 0.01) and 42°C (HiSeff: 72 ± 16 vs. LoSeff: 51 ± 15 min, P < 0.01). In general, an increase in LSR preceded the increase in SkBF when expressed as ambient vapor pressure and time for all conditions (P < 0.05). However, both responses were activated at a similar change in mean body temperature (average across all trials, LSR: 0.26 ± 0.15 vs. SkBF: 0.30 ± 0.18°C, P = 0.26). These results demonstrate that altering the point at which LSR is initiated during heat exposure is paralleled by similar shifts for the increase in SkBF. However, local sweat production occurs before an increase in SkBF, suggesting that SkBF is not necessarily a prerequisite for sweating.

Variations in body morphology explain sex differences in thermoeffector function during compensable heat stress.

What is the central question of this study? Can sex-related differences in cutaneous vascular and sudomotor responses be explained primarily by variations in the ratio between body surface area and mass during compensable exercise that elicits equivalent heat-loss requirements and mean body temperature changes across participants? What is the main finding and its importance? Mass-specific surface area was a significant determinant of vasomotor and sudomotor responses in men and women, explaining 10-48% of the individual thermoeffector variance. Nonetheless, after accounting for changes in mean body temperature and morphological differences, sex explained only 5% of that inter-individual variability. It was concluded that sex differences in thermoeffector function are morphologically dependent, but not sex dependent. Sex is sometimes thought to be an independent modulator of cutaneous vasomotor and sudomotor function during heat exposure. Nevertheless, it was hypothesized that, when assessed during compensable exercise that evoked equal heat-loss requirements across participants, sex differences in those thermoeffectors would be explained by variations in the ratio between body surface area and mass (specific surface area). To evaluate that possibility, vasomotor and sudomotor functions were assessed in 60 individuals (36 men and 24 women) with widely varying (overlapping) specific surface areas (range, 232.3-292.7 and 241.2-303.1cm2 kg-1 , respectively). Subjects completed two trials in compensable conditions (28°C, 36% relative humidity) involving rest (20min) and steady-state cycling (45min) at fixed, area-specific metabolic heat-production rates (light, ∼135Wm-2 ; moderate, ∼200Wm-2 ). Equivalent heat-loss requirements and mean body temperature changes were evoked across participants. Forearm blood flow and vascular conductance were positively related to specific surface area during light work in men (r=0.67 and r=0.66, respectively; both P<0.05) and during both exercise intensities in women (light, r=0.57 and r=0.69; and moderate, r=0.64 and r=0.68; all P<0.05). Whole-body and local sweat rates were negatively related to that ratio (correlation coefficient range, -0.33 to -0.62; all P<0.05) during both work rates in men and women. Those relationships accounted for 10-48% of inter-individual thermoeffector variance (P<0.05). Furthermore, after accounting for morphological differences, sex explained no more than 5% of that variability (P<0.05). It was concluded that, when assessed during compensable exercise, sex differences in thermoeffector function were largely determined morphologically, rather than being sex dependent.

Morphological dependency of cutaneous blood flow and sweating during compensable heat stress when heat-loss requirements are matched across participants.

Human heat loss is thought, in part, to be morphologically related. It was therefore hypothesized that when heat-loss requirements and body temperatures were matched, that the mass-specific surface area alone could significantly explain both cutaneous vascular and sudomotor responses during compensable exercise. These thermoeffector responses were examined in 36 men with widely varying mass-specific surface areas (range, 232.3-292.7 cm(2)/kg), but of similar age, aerobic fitness, and adiposity. Subjects completed two trials under compensable conditions (28.1°C, 36.8% relative humidity), each involving rest (20 min) and steady-state cycling (45 min) at two matched metabolic heat-production rates (light, ∼135 W/m(2); moderate, ∼200 W/m(2)). Following equivalent mean body temperature changes, forearm blood flow and vascular conductance (r = 0.63 and r = 0.65) shared significant, positive associations with the mass-specific surface area during light work (P < 0.05), explaining ∼45% of the vasomotor variation. Conversely, during light and moderate work, whole body sweat rate, as well as local sweat rate and sudomotor sensitivity at three of four measured sites, revealed moderate, negative relationships with the mass-specific surface area (correlation coefficient range -0.37 to -0.73, P < 0.05). Moreover, those relationships could uniquely account for between 10 and 53% of those sweating responses (P < 0.05). Therefore, both thermoeffector responses displayed a significant morphological dependency in the presence of equivalent thermoafferent drive. Indeed, up to half of the interindividual variation in these effector responses could now be explained through morphological differences and the first principles governing heat transfer.

Thermoregulation and pain perception: Evidence for a homoeostatic (interoceptive) dimension of pain.

Experimental and clinical observations of interactions between the nociceptive and thermoceptive systems have suggested that they could be part of the homoeostatic system relating to the condition of the body, described as 'interoception'. Homoeostatic physiological systems are extensively interconnected. Thus, consistent with this hypothesis, we would expect thermoregulatory challenges to be associated with changes in pain perception. The effects of whole-body warming or cooling inducing significant changes in mean body temperature were tested in 15 healthy volunteers (29 ± 6 years old) on: (i) the paradoxical burning pain induced by the application of simultaneous non-noxious thermal stimuli with a 'thermal grill' and (ii) the 'normal' pain evoked by noxious thermal stimuli. Whole-body warming and cooling induced changes in opposite direction of the threshold of the paradoxical pain induced by the thermal grill, consisting of an increase by 1.2 ± 1.7 °C (p = 0.02) during the warming session and a nonsignificant decrease by 0.7 ± 2.7 °C (p = 0.15) during the cooling session. In addition, there was a correlation (r = 0.54; p = 0.002) between the magnitude of the change in mean body temperature and the magnitude of the change in the threshold of the paradoxical pain induced by the thermal grill. By contrast, the thermal challenges induced no significant change in pain evoked by noxious hot or cold stimuli. Our results are consistent with the notion that pain has a homoeostatic (interoceptive) dimension and showed that the thermal grill-induced pain is a unique experimental model to investigate this differentiable pain dimension.

Characteristics of sweating responses and peripheral sweat gland function during passive heating in sprinters

The purpose of this study was to compare sweating function in sprinters who have trained for several years with untrained subjects and trained endurance runners. Two separate experiments were conducted. Nine sprinters, eight untrained men, and nine distance runners (VO2 max 50.9 ± 1.4, 38.2 ± 1.8, and 59.1 ± 1.2 mL/kg/min, respectively; P < 0.05) were passively heated for 50 min (Experiment 1), and ten sprinters, 11 untrained men and nine distance runners (similar VO2 max levels compared with Experiment 1 in each group) had their sweat gland capacity assessed based on acetylcholine-induced sweating rate (SR) (Experiment 2). The slope of the mean non-glabrous SR plotted against change in mean body temperature during passive heating did not differ significantly between sprinters and untrained men (1.21 ± 0.10 and 0.97 ± 0.12 mg cm(-2)/min/°C, respectively); in contrast, compared with untrained men, distance runners exhibited a significantly greater slope (1.42 ± 0.11 mg cm(-2)/min/°C, P < 0.05). The mean body temperature threshold for SR was not significantly different among the groups. Acetylcholine-induced SR did not differ significantly between sprinters and untrained men, whereas distance runners showed a significantly higher induced SR compared with untrained men. The sweating function was not improved in sprinters who have trained 2-3 h/day, 5 days/week, for at least 3 years compared with untrained men, although the VO2 max was markedly greater in sprinters. Thus, there is a case that daily training was not sufficient to improve sweating function in sprinters relative to those in distance runners.

Sex differences in postsynaptic sweating and cutaneous vasodilation

The current study aimed to determine whether a peripheral modulation of sweating contributes to the lower sudomotor thermosensitivity previously observed in females during exercise. We examined dose-response relationships in 12 males and 12 females to incremental doses of acetylcholine (ACh) and methylcholine (MCh) for sweating (ventilated capsule), as well as to ACh and sodium nitroprusside (SNP) for cutaneous vasodilation (laser-Doppler). All drugs were infused using intradermal microdialysis. On a separate day, potential sex differences in the onset threshold and/or thermosensitivity of heat loss responses were assessed during progressive increases in mean body temperature elicited by passive heating. Increases in sweating as a function of increasing concentration of ACh (P = 0.008) and MCh (P = 0.046) significantly differed between males and females. Although the concentration eliciting 50% of the maximal sweating response did not differ between sexes for either agonist (P > 0.1), maximum values were lower in females in response to ACh (0.34 ± 0.12 vs. 0.59 ± 0.19 mg·min(-1)·cm(-2), P = 0.04) and MCh (0.48 ± 0.12 vs. 0.78 ± 0.26 mg·min(-1)·cm(-2), P = 0.05). This observation was paralleled by a lower thermosensitivity of sudomotor activity in females during passive heating (1.29 ± 0.34 vs. 1.83 ± 0.33 mg·min(-1)·cm(-2)·°C(-1), P = 0.03), with no significant differences in the change in mean body temperature at which onset of sweating occurred (0.85 ± 0.19 vs. 0.67 ± 0.13°C, P = 0.10). No sex differences in cutaneous vasodilation were observed in response to ACh and SNP, as well as during passive heating (all P > 0.1). These findings provide direct evidence for a peripheral modulation of sudomotor activity in females. In contrast, sex does not modulate cutaneous vasodilation.

Divergent roles of plasma osmolality and the baroreflex on sweating and skin blood flow

Plasma hyperosmolality and baroreceptor unloading have been shown to independently influence the heat loss responses of sweating and cutaneous vasodilation. However, their combined effects remain unresolved. On four separate occasions, eight males were passively heated with a liquid-conditioned suit to 1.0°C above baseline core temperature during a resting isosmotic state (infusion of 0.9% NaCl saline) with (LBNP) and without (CON) application of lower-body negative pressure (-40 cmH2O) and during a hyperosmotic state (infusion of 3.0% NaCl saline) with (LBNP + HYP) and without (HYP) application of lower-body negative pressure. Forearm sweat rate (ventilated capsule) and skin blood flow (laser-Doppler), as well as core (esophageal) and mean skin temperatures, were measured continuously. Plasma osmolality increased by ∼10 mosmol/kgH2O during HYP and HYP + LBNP conditions, whereas it remained unchanged during CON and LBNP (P ≤ 0.05). The change in mean body temperature (0.8 × core temperature + 0.2 × mean skin temperature) at the onset threshold for increases in cutaneous vascular conductance (CVC) was significantly greater during LBNP (0.56 ± 0.24°C) and HYP (0.69 ± 0.36°C) conditions compared with CON (0.28 ± 0.23°C, P ≤ 0.05). Additionally, the onset threshold for CVC during LBNP + HYP (0.88 ± 0.33°C) was significantly greater than CON and LBNP conditions (P ≤ 0.05). In contrast, onset thresholds for sweating were not different during LBNP (0.50 ± 0.18°C) compared with CON (0.46 ± 0.26°C, P = 0.950) but were elevated (P ≤ 0.05) similarly during HYP (0.91 ± 0.37°C) and LBNP + HYP (0.94 ± 0.40°C). Our findings show an additive effect of hyperosmolality and baroreceptor unloading on the onset threshold for increases in CVC during whole body heat stress. In contrast, the onset threshold for sweating during heat stress was only elevated by hyperosmolality with no effect of the baroreflex.

Thermal Basis of Finger Blood Flow Adaptations During Abrupt Perturbations in Thermal Homeostasis

The objective of this experiment was to assess whether reflex alterations in finger blood flow during repetitive hot and cold water immersion are associated with changes in rectal, tympanic, mean body temperature or heat storage. Fifteen healthy adults (eight males) volunteered. Following a 15-minute baseline period, participants were immersed in 42°C water and passively rested until their rectal temperature was raised by 0.5°C above baseline. Thereafter, they were immersed in a different water tank maintained at 12°C water temperature until their rectal temperature was decreased by 0.5°C below baseline. This procedure was conducted twice. Auto-Regressive Integrated Moving Average analysis showed that fluctuations in finger blood flow were associated with changes in mean body temperature (Ljung-Box statistic >0.05; R² = 0.67) and body heat storage (Ljung-Box statistic >0.05; R² = 0.70), but not with rectal (Ljung-Box statistic <0.05; R² = 0.54) or tympanic (Ljung-Box statistic <0.05; R² = 0.49) temperatures. It is concluded that reflex alterations in finger blood flow during repetitive hot and cold water immersions are associated with mean body temperature and the rate of body heat storage, but not with rectal and tympanic temperatures.

Post-exercise cooling techniques in hot, humid conditions

Major sporting events are often held in hot and humid environmental conditions. Cooling techniques have been used to reduce the risk of heat illness following exercise. This study compared the efficacy of five cooling techniques, hand immersion (HI), whole body fanning (WBF), an air cooled garment (ACG), a liquid cooled garment (LCG) and a phase change garment (PCG), against a natural cooling control condition (CON) over two periods between and following exercise bouts in 31 degrees C, 70%RH air. Nine males [age 22 (3) years; height 1.80 (0.04) m; mass 69.80 (7.10) kg] exercised on a treadmill at a maximal sustainable work intensity until rectal temperature (T (re)) reached 38.5 degrees C following which they underwent a resting recovery (0-15 min; COOL 1). They then recommenced exercise until T (re) again reached 38.5 degrees C and then undertook 30 min of cooling with (0-15 min; COOL 2A), and without face fanning (15-30 min; COOL 2B). Based on mean body temperature changes (COOL 1), WBF was most effective in extracting heat: CON 99 W; WBF: 235 W; PCG: 141 W; HI: 162 W; ACG: 101 W; LCG: 49 W) as a consequence of evaporating more sweat. Therefore, WBF represents a cheap and practical means of post-exercise cooling in hot, humid conditions in a sporting setting.

Human conscious response to thermal input is adjusted to changes in mean body temperature

Objective and Design:To detect the dependable criteria of behavioural thermoregulation through modelling temperature fluctuations of individuals allowed to freely manipulate inlet water temperature of a liquid conditioning garment (LCG) during...

Estimating changes in mean body temperature for humans during exercise using core and skin temperatures is inaccurate even with a correction factor

Changes in mean body temperature (DeltaT(b)) estimated by the traditional two-compartment model of "core" and "shell" temperatures and an adjusted two-compartment model incorporating a correction factor were compared with values derived by whole body calorimetry. Sixty participants (31 men, 29 women) cycled at 40% of peak O(2) consumption for 60 or 90 min in the Snellen calorimeter at 24 or 30 degrees C. The core compartment was represented by esophageal, rectal (T(re)), and aural canal temperature, and the shell compartment was represented by a 12-point mean skin temperature (T(sk)). Using T(re) and conventional core-to-shell weightings (X) of 0.66, 0.79, and 0.90, mean DeltaT(b) estimation error (with 95% confidence interval limits in parentheses) for the traditional model was -95.2% (-83.0, -107.3) to -76.6% (-72.8, -80.5) after 10 min and -47.2% (-40.9, -53.5) to -22.6% (-14.5, -30.7) after 90 min. Using T(re), X = 0.80, and a correction factor (X(0)) of 0.40, mean DeltaT(b) estimation error for the adjusted model was +9.5% (+16.9, +2.1) to -0.3% (+11.9, -12.5) after 10 min and +15.0% (+27.2, +2.8) to -13.7% (-4.2, -23.3) after 90 min. Quadratic analyses of calorimetry DeltaT(b) data was subsequently used to derive best-fitting values of X for both models and X(0) for the adjusted model for each measure of core temperature. The most accurate model at any time point or condition only accounted for 20% of the variation observed in DeltaT(b) for the traditional model and 56% for the adjusted model. In conclusion, throughout exercise the estimation of DeltaT(b) using any measure of core temperature together with mean skin temperature irrespective of weighting is inaccurate even with a correction factor customized for the specific conditions.

Thermal Insulation and Body Temperature Wearing a Thermal Swimsuit during Water Immersion

This study evaluated the effects of a thermal swimsuit on body temperatures, thermoregulatory responses and thermal insulation during 60 min water immersion at rest. Ten healthy male subjects wearing either thermal swimsuits or normal swimsuits were immersed in water (26 degrees C or 29 degrees C). Esophageal temperature, skin temperatures and oxygen consumption were measured during the experiments. Metabolic heat production was calculated from oxygen consumption. Heat loss from skin to the water was calculated from the metabolic heat production and the change in mean body temperature during water immersion. Total insulation and tissue insulation were estimated by dividing the temperature difference between the esophagus and the water or the esophagus and the skin with heat loss from the skin. Esophageal temperature with a thermal swimsuit was higher than that with a normal swimsuit at the end of immersion in both water temperature conditions (p<0.05). Oxygen consumption, metabolic heat production and heat loss from the skin were less with the thermal swimsuit than with a normal swimsuit in both water temperatures (p<0.05). Total insulation with the thermal swimsuit was higher than that with a normal swimsuit due to insulation of the suit at both water temperatures (p<0.05). Tissue insulation was similar in all four conditions, but significantly higher with the thermal swimsuit in both water temperature conditions (p<0.05), perhaps due to of the attenuation of shivering during immersion with a thermal swimsuit. A thermal swimsuit can increase total insulation and reduce heat loss from the skin. Therefore, subjects with thermal swimsuits can maintain higher body temperatures than with a normal swimsuit and reduce shivering thermo-genesis.