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In this third installment of our four-part historical series, we evaluate contributions that shaped our understanding of heat and cold stress during occupational and athletic pursuits. Our first topic concerns how we tolerate, and sometimes fail to tolerate, exercise-heat stress. By 1900, physical activity with clothing- and climate-induced evaporative impediments led to an extraordinarily high incidence of heat stroke within the military. Fortunately, deep-body temperatures > 40 °C were not always fatal. Thirty years later, water immersion and patient treatments mimicking sweat evaporation were found to be effective, with the adage of cool first, transport later being adopted. We gradually acquired an understanding of thermoeffector function during heat storage, and learned about challenges to other regulatory mechanisms. In our second topic, we explore cold tolerance and intolerance. By the 1930s, hypothermia was known to reduce cutaneous circulation, particularly at the extremities, conserving body heat. Cold-induced vasodilatation hindered heat conservation, but it was protective. Increased metabolic heat production followed, driven by shivering and non-shivering thermogenesis, even during exercise and work. Physical endurance and shivering could both be compromised by hypoglycaemia. Later, treatments for hypothermia and cold injuries were refined, and the thermal after-drop was explained. In our final topic, we critique the numerous indices developed in attempts to numerically rate hot and cold stresses. The criteria for an effective thermal stress index were established by the 1930s. However, few indices satisfied those requirements, either then or now, and the surviving indices, including the unvalidated Wet-Bulb Globe-Thermometer index, do not fully predict thermal strain., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

This review is the final contribution to a four-part, historical series on human exercise physiology in thermally stressful conditions. The series opened with reminders of the principles governing heat exchange and an overview of our contemporary understanding of thermoregulation (Part 1). We then reviewed the development of physiological measurements (Part 2) used to reveal the autonomic processes at work during heat and cold stresses. Next, we re-examined thermal-stress tolerance and intolerance, and critiqued the indices of thermal stress and strain (Part 3). Herein, we describe the evolutionary steps that endowed humans with a unique potential to tolerate endurance activity in the heat, and we examine how those attributes can be enhanced during thermal adaptation. The first of our ancestors to qualify as an athlete was Homo erectus, who were hairless, sweating specialists with eccrine sweat glands covering almost their entire body surface. Homo sapiens were skilful behavioural thermoregulators, which preserved their resource-wasteful, autonomic thermoeffectors (shivering and sweating) for more stressful encounters. Following emigration, they regularly experienced heat and cold stress, to which they acclimatised and developed less powerful (habituated) effector responses when those stresses were re-encountered. We critique hypotheses that linked thermoregulatory differences to ancestry. By exploring short-term heat and cold acclimation, we reveal sweat hypersecretion and powerful shivering to be protective, transitional stages en route to more complete thermal adaptation (habituation). To conclude this historical series, we examine some of the concepts and hypotheses of thermoregulation during exercise that did not withstand the tests of time., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

In this, the second of four historical reviews on human thermoregulation during exercise, we examine the research techniques developed by our forebears. We emphasise calorimetry and thermometry, and measurements of vasomotor and sudomotor function. Since its first human use (1899), direct calorimetry has provided the foundation for modern respirometric methods for quantifying metabolic rate, and remains the most precise index of whole-body heat exchange and storage. Its alternative, biophysical modelling, relies upon many, often dubious assumptions. Thermometry, used for >300 y to assess deep-body temperatures, provides only an instantaneous snapshot of the thermal status of tissues in contact with any thermometer. Seemingly unbeknownst to some, thermal time delays at some surrogate sites preclude valid measurements during non-steady state conditions. To assess cutaneous blood flow, immersion plethysmography was introduced (1875), followed by strain-gauge plethysmography (1949) and then laser-Doppler velocimetry (1964). Those techniques allow only local flow measurements, which may not reflect whole-body blood flows. Sudomotor function has been estimated from body-mass losses since the 1600s, but using mass losses to assess evaporation rates requires precise measures of non-evaporated sweat, which are rarely obtained. Hygrometric methods provide data for local sweat rates, but not local evaporation rates, and most local sweat rates cannot be extrapolated to reflect whole-body sweating. The objective of these methodological overviews and critiques is to provide a deeper understanding of how modern measurement techniques were developed, their underlying assumptions, and the strengths and weaknesses of the measurements used for humans exercising and working in thermally challenging conditions., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

This contribution is the first of a four-part, historical series encompassing foundational principles, mechanistic hypotheses and supported facts concerning human thermoregulation during athletic and occupational pursuits, as understood 100 years ago and now. Herein, the emphasis is upon the physical and physiological principles underlying thermoregulation, the goal of which is thermal homeostasis (homeothermy). As one of many homeostatic processes affected by exercise, thermoregulation shares, and competes for, physiological resources. The impact of that sharing is revealed through the physiological measurements that we take (Part 2), in the physiological responses to the thermal stresses to which we are exposed (Part 3) and in the adaptations that increase our tolerance to those stresses (Part 4). Exercising muscles impose our most-powerful heat stress, and the physiological avenues for redistributing heat, and for balancing heat exchange with the environment, must adhere to the laws of physics. The first principles of internal and external heat exchange were established before 1900, yet their full significance is not always recognised. Those physiological processes are governed by a thermoregulatory centre, which employs feedback and feedforward control, and which functions as far more than a thermostat with a set-point, as once was thought. The hypothalamus, today established firmly as the neural seat of thermoregulation, does not regulate deep-body temperature alone, but an integrated temperature to which thermoreceptors from all over the body contribute, including the skin and probably the muscles. No work factor needs to be invoked to explain how body temperature is stabilised during exercise., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Purpose: The first aim of this experiment was to evaluate the appropriateness of linear and non-linear (allometric) models to scale peak aerobic power (oxygen consumption) against body mass. The possibilities that oxygen consumption would scale allometrically across the complete metabolic range, and that the scaling exponents would differ significantly between basal and maximal-exercise states, were then evaluated. It was further hypothesised that the scaling exponent would increase in a stepwise manner with elevations in exercise intensity. Finally, the utility of applying the scaling exponent derived for peak aerobic power to another population sample was evaluated., Methods: Basal, steady-state walking and peak (treadmill) oxygen-consumption data were measured using 60 relatively homogeneous men (18-40 year; 56.0-117.1 kg), recruited across five mass classes. Linear and allometric regressions were applied, with the utility of each scaling method evaluated., Results: Oxygen consumption scaled allometrically with body mass across the complete metabolic range, and was always superior to both ratiometric analysis and linear regression. The scaling exponent increased significantly from rest (mass 0.57 ) to maximal exercise (mass 0.75 ; P < 0.05), but not between steady-state walking (mass 0.87 ) and maximal exercise (P > 0.05). When used with an historical database, the maximal-exercise exponent successfully removed the mass bias., Conclusion: It has been demonstrated that the oxygen consumption of healthy humans scales allometrically with body mass across the entire metabolic range. Moreover, only two scaling exponents (rest and exercise) were required to produce mass-independent outcomes from those data. Accordingly, ratiometric and linear regression analyses are not recommended as scaling methods., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Purpose: In tachymetabolic species, metabolic rate increases disproportionately with body mass, and that inter-specific relationship is typically modelled allometrically. However, intra-specific analyses are less common, particularly for healthy humans, so the possibility that human metabolism would also scale allometrically was investigated., Methods: Basal metabolic rate was determined (respirometry) for 68 males (18-40 years; 56.0-117.1 kg), recruited across five body-mass classes. Data were collected during supine, normothermic rest from well-rested, well-hydrated and post-absorptive participants. Linear and allometric regressions were applied, and three scaling methods were assessed. Data from an historical database were also analysed (2.7-108.9 kg, 4811 males; 2.0-96.4 kg, 2364 females)., Results: Both linear and allometric functions satisfied the statistical requirements, but not the biological pre-requisite of an origin intercept. Mass-independent basal metabolic data beyond the experimental mass range were not achieved using linear regression, which yielded biologically impossible predictions as body mass approached zero. Conversely, allometric regression provided a biologically valid, powerful and statistically significant model: metabolic rate = 0.739 * body mass 0.547 (P < 0.05). Allometric analysis of the historical male data yielded an equivalent, and similarly powerful model: metabolic rate = 0.873 * body mass 0.497 (P < 0.05)., Conclusion: It was established that basal and resting metabolic rates scale allometrically with body mass in humans from 10-117 kg, with an exponent of 0.50-0.55. It was also demonstrated that ratiometric scaling yielded invalid metabolic predictions, even within the relatively narrow experimental mass range. Those outcomes have significant physiological implications, with applications to exercising states, modelling, nutrition and metabolism-dependent pharmacological prescriptions.

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 so the merits of that proposition are evaluated. Indeed, it can be an effective approach, although some experimental pitfalls are described to 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.

Purpose: Whole-body thermal and hydration clamps were used to evaluate their independent and combined impact on the electrical activity of the brain. It was hypothesised that those stresses would independently modify the electroencephalographic (EEG) responses, with those changes being greater when both stresses were superimposed., Methods: Alpha and beta spectral data (eyes closed) were collected from the frontal, central-parietal and occipital cortices of both hemispheres in resting, healthy and habitually active males (N = 8; mean age 25 years). Three dehydration states were investigated (euhydrated and 3% and 5% mass decrements) in each of two thermal states (normothermia [mean body temperature 36.3 °C] and moderate hyperthermia [38.4 °C]). The combination of those passively induced states yielded six levels of physiological strain, with the EEG data from each level separately examined using repeated-measures ANOVA with planned contrasts., Results: When averaged across the frontal cortices, alpha power was elevated relative to the occipital cortices during moderate hyperthermia (P = 0.049). Conversely, beta power was generally reduced during hyperthermia (P = 0.013). Neither the alpha nor beta power spectra responded to dehydration, nor did dehydration elevate the heat-induced responses (P > 0.05)., Conclusion: Moderate hyperthermia, but neither mild nor moderate dehydration, appeared to independently alter brain electrical activity. Moreover, the combination of moderate hyperthermia with 5% dehydration did not further increase those changes. That outcome was interpreted to mean that, when those states were superimposed, the resulting neurophysiological changes could almost exclusively be attributed to the thermal impact per se, rather than to their combined influences.

Purpose: This experiment was designed to quantify the independent and combined influences of hyperthermia and dehydration on effector control during rest and exercise., Methods: To achieve that, whole-body hydration of healthy adults (N = 8) was manipulated into each of three states (euhydrated, 3% and 5% dehydrated), and then clamped within each of two thermal states (normothermia [mean body temperature: 36.1 °C] and moderate hyperthermia [mean body temperature: 38.2 °C]). Those treatment combinations provided six levels of physiological strain, with resting physiological data collected at each level. The effects of isothermal, thermally unclamped and incremental exercise were then investigated in normothermic individuals during each level of hydration., Results: At rest, dehydration alone reduced urine flows by 83% (3% dehydrated) and 93% (5% dehydrated), while the reduction accompanying euhydrated hyperthermia was 86%. The sensitivities of renal water conservation to 3% dehydration (-21% mOsm -1  kg H 2 O -1 ) and moderate hyperthermia (-40% °C -1 ) were independent and powerful. Evidence was found for different renal mechanisms governing water conservation between those treatments. Cutaneous vasomotor and central cardiac responses were unresponsive to dehydration, but highly sensitive to passive thermal stress. Dehydration did not impair either whole-body or regional sweating during rest or exercise, and not even during incremental cycling to volitional exhaustion., Conclusion: In all instances, the physiological impact of these thermal- and hydration-state stresses was independently expressed, with no evidence of interactive influences. Renal water-conservation was independently and powerfully modified, exposing possible between-treatment differences in sodium reabsorption.

Since 2013, this journal has promoted the publication of thematic reviews (Taylor in Eur J Appl Physiol 113:1634, 2013), where leading groups were invited to review the critical literature within each of several sub-topics. The current theme is historically based, and is focussed on estimating the metabolic rate in humans. This review charts the development of our understanding of those methods, from the discovery of oxygen and carbon dioxide, to the introduction of highly sophisticated modern apparatus to examine the composition of expired gas and determine respiratory minute volume. An historical timeline links the six thematic vignettes on this theme. Modern advances have greatly enhanced data collection without significant decrements in measurement accuracy. At the same time, however, conceptual errors, particularly steady-state requirements, are too often ignored. Indeed, it is recognised that we often neglect the past, leading to errors in research design, experimental observations and data interpretation, and this appears to be increasingly prevalent within the open-access literature. Accordingly, the Editorial Board, in recognition of a widening gap between our experimental foundations and contemporary research, embarked on developing a number of thematic review series, of which this series is the first. The intent of each accompanying overview is to introduce and illuminate seminal investigations that led to significant scientific or intellectual breakthroughs, and to thereby whet the appetite of readers to delve more deeply into the historical literature; for it is only when the foundations are understood that we can best understand where we are now, and in which directions we should head.

Purpose: Many researchers have addressed the potential effects of hyperthermia and dehydration on cognition, often revealing contradictory outcomes. A possible reason for this inconsistency is that experiments may have been inadequately designed for such effects. In this study, the impact of hyperthermia, dehydration and their combination on cognition were evaluated in eight young males, after accounting for a range of experimental limitations., Methods: Passive heating and thermal clamping at two mean body temperatures (36.5, 38.5 °C) were performed under three hydration states (euhydrated, 3 and 5% dehydrated) to assess their effects on difficulty-matched working memory and visual perception tasks, and on a difficulty manipulated perceptual task. Data were analysed according to signal detection theory to isolate changes in response sensitivity, bias and speed., Results: Neither moderate hyperthermia (P = 0.141) nor dehydration (P > 0.604) modified response sensitivity, nor did they significantly interact (P > 0.698). Therefore, the ability to distinguish correct from incorrect responses was unaffected. Nevertheless, hyperthermia, but not dehydration (P = 0.301), reduced the response bias (-0.08 versus 2.2 [normothermia]; P = 0.010) and reaction time (mean reduction 49 ms; P < 0.001), eliciting more liberal and faster responses (P = 0.010). Response bias was reduced for the memory relative to the perceptual task (P = 0.037), and this effect was enhanced during hyperthermia (P = 0.031)., Conclusions: These observations imply that, once potentially confounding influences were controlled, moderate hyperthermia, significant dehydration and their combined effects had insufficient impact to impair cognition within the memory and perceptual domains tested. Nonetheless, moderate hyperthermia elicited more liberal and rapid responses.

Purpose: Supra-tolerance head-to-foot directed gravitoinertial load (+Gz) typically induces a sequence of symptoms/signs, including loss of: peripheral vision-central vision-consciousness. The risk of unconsciousness is greater when anti-G-garment failure occurs after prolonged rather than brief exposures, presumably because, in the former condition, mental signs are not consistently preceded by impaired vision. The aims were to investigate if prolonged exposure to moderately elevated +Gz reduces intraocular pressure (IOP; i.e., improves provisions for retinal perfusion), or the cerebral anoxia reserve., Methods: Subjects were exposed to 4-min +Gz plateaux either at 2 and 3 G (n = 10), or at 4 and 5 G (n = 12). Measurements included eye-level mean arterial pressure (MAP), oxygenation of the cerebral frontal cortex, and at 2 and 3 G, IOP., Results: IOP was similar at 1 (14.1 ± 1.6 mmHg), 2 (14.0 ± 1.6 mmHg), and 3 G (14.0 ± 1.6 mmHg). During the G exposures, MAP exhibited an initial prompt drop followed by a partial recovery, end-exposure values being reduced by ≤30 mmHg. Cerebral oxygenation showed a similar initial drop, but without recovery, and was followed by either a plateau or a further slight decrement to a minimum of about -14 μM., Conclusion: Gz loading did not affect IOP. That cerebral oxygenation remained suppressed throughout these G exposures, despite a concomitant partial recovery of MAP, suggests that the increased risk of unconsciousness upon G-garment failure after prolonged +Gz exposure is due to reduced cerebral anoxia reserve., Competing Interests: The authors declare that they have no conflicts of interest.

Purpose: Torso loads restrict chest-wall movement and ventilation, particularly during heavy exercise. Therefore, the differential impact of load carriage and chest-wall restriction was investigated during progressive treadmill exercise. In addition, acceptable work durations were derived across a wide range of submaximal, loaded exercise intensities., Methods: Twelve males participated in two research phases. Phase 1: Three incremental treadmill tests until exhaustion [control (clothing only), load carriage (clothing plus 22-kg vest), and clothing with chest strapping]. Phase 2: Five steady-state exercise trials (clothing plus 22-kg vest) at intensities from 30 to 80 % of peak aerobic power to determine maximal acceptable work durations., Results: Maximal work tolerance [control 17.21 min (±0.93); loaded 13.44 min (±0.68); strapped 17.00 min (±0.83)] and the mass-specific peak aerobic power [control 61.61 mL kg(-1) min(-1) (±2.28); loaded 45.42 mL kg(-1) min(-1) (±1.41); strapped 59.99 mL kg(-1) min(-1) (±1.61)] were reduced only when loaded (P < 0.05). Peak minute ventilation was retained, although loading and chest strapping reduced the breathing reserve. The lower and upper acceptable work duration derivations when working at the 30 % intensity were 133.40 min (±23.77) and 220.10 min (±48.69), but at 80 % intensity, both durations were reduced to <7 min., Conclusion: Thoracic loading significantly reduced exercise tolerance and the breathing reserve, but did not modify peak minute ventilation or the absolute peak aerobic power. Chest strapping, as used herein, exerted minimal impact. However, the projected maximal acceptable work durations were much less than derived using previously published methods.

Aim: The inter-relationships between mean body and local skin temperatures have previously been established for controlling hand and foot blood flows. Since glabrous skin contains many arteriovenous anastomoses, it was important to repeat those experiments on non-glabrous regions using the same sample and experimental conditions., Methods: Mild hypothermia (mean body temperature 31.4 °C), normothermia (control: 36.0 °C) and moderate hyperthermia (38.3 °C) were induced and clamped (climate chamber and water-perfusion garment) in eight males. Within each condition, five localised thermal treatments (5, 15, 25, 33, 40 °C) were applied to the left forearm and right calf. Steady-state forearm and calf blood flows were measured (venous occlusion plethysmography) for each of the resulting 15 combinations of clamped mean body and local skin temperatures., Results: Under the normothermic clamp, cutaneous blood flows averaged 4.2 mL 100 mL(-1) min(-1) (±0.28: forearm) and 5.4 mL 100 mL(-1) min(-1) (±0.27: calf). When mildly hypothermic, these segments were unresponsive to localised thermal stimuli, but tracked those changes when normothermic and moderately hyperthermic. For deep-body (oesophageal) temperature elevations, forearm blood flow increased by 5.1 mL 100 mL(-1) min(-1) °C(-1) (±0.9) relative to normothermia, while the calf was much less responsive: 3.3 mL 100 mL(-1) min(-1) °C(-1) (±1.5). Three-dimensional surfaces revealed a qualitative divergence in the control of calf blood flow, with vasoconstrictor tone apparently being released more gradually., Conclusion: These descriptions reinforce the importance of deep-tissue temperatures in controlling cutaneous perfusion, with this modulation being non-linear at the forearm and appearing linear for the calf.

The purpose of this review is to describe the unique anatomical and physiological features of the hands and feet that support heat conservation and dissipation, and in so doing, highlight the importance of these appendages in human thermoregulation. For instance, the surface area to mass ratio of each hand is 4-5 times greater than that of the body, whilst for each foot, it is ~3 times larger. This characteristic is supported by vascular responses that permit a theoretical maximal mass flow of thermal energy of 6.0 W (136 W m(2)) to each hand for a 1 °C thermal gradient. For each foot, this is 8.5 W (119 W m(2)). In an air temperature of 27 °C, the hands and feet of resting individuals can each dissipate 150-220 W m(2) (male-female) of heat through radiation and convection. During hypothermia, the extremities are physiologically isolated, restricting heat flow to <0.1 W. When the core temperature increases ~0.5 °C above thermoneutral (rest), each hand and foot can sweat at 22-33 mL h(-1), with complete evaporation dissipating 15-22 W (respectively). During heated exercise, sweat flows increase (one hand: 99 mL h(-1); one foot: 68 mL h(-1)), with evaporative heat losses of 67-46 W (respectively). It is concluded that these attributes allow the hands and feet to behave as excellent radiators, insulators and evaporators.

Purpose: Much is known about the control of blood flow, yet gaps remain concerning the interactions of deep-body and peripheral thermal feedback. In this experiment, changes in the vascular tone of the hands and feet were mapped to demonstrate the separate and combined influences of mean body and local skin temperature changes., Methods: Eight males participated in three trials. Three pre-experimental conditions were established via water immersion (oesophageal temperatures: 36.1, 37.0, 38.5 °C), with core and mean skin temperatures then clamped (water-perfusion garment) whilst five thermal treatments were applied to the right hand and left foot (5, 15, 25, 33, 40 °C). This yielded 15 thermal combinations under which hand and foot blood flows were measured (displacement plethysmography)., Results: Lower volume-specific blood flows were observed at the foot for almost all temperature combinations. When thermoneutral and moderately hyperthermic, the cutaneous thermosensitivity of the hand was significantly greater: thermoneutral: 0.2 vs. 0.1 (foot) mL 100 mL(-1) min(-1) °C(-1) (P < 0.05); moderate hyperthermia: 0.4 vs. 0.2 (foot) mL 100 mL(-1) min(-1) °C(-1) (P < 0.05). The hand was 13 times more responsive to core temperature elevations than an equivalent local skin temperature change. For the foot, this thermosensitivity differed by a factor of 26., Conclusion: These observations identified the hands as heat radiators, with the feet resisting heat loss, and reinforce the dominance of central thermal feedback, particularly in controlling foot blood flow. However, thermosensitivity to local skin temperature changes was highly plastic, site-specific and dictated by thermal and regional variations in vaso- and venoconstrictor tone.

The importance of the head in dissipating body heat under hot conditions is well recognised, although very little is known about local differences in sweat secretion across the surface of the head. In this study, we focused on the intra-segmental distribution of head sweating. Ten healthy males were exposed to passive heating and exercise-induced hyperthermia (36 degrees C, 60% relative humidity, water-perfusion suit: 46 degrees C), with ventilated sweat capsules (3.16 cm(2)) used to measure sweat rates from the forehead and nine sites inside the hairline. Sweat secretion from both non-hairy (glabrous) and hairy areas of the head increased linearly with increments in work rate and core temperature, with heart rate and core temperature peaking at 175 b min(-1) (+/-6) b min(-1) and 39.2 degrees C (+/-0.1). The mean sweat rate during exercise for sites within the hairline was 1.95 mg cm(-2) min(-1). However, the evolution of this secretion pattern was not uniformly distributed within the head, with the average sweat rate for the top of the head being significantly lower than at the anterior lateral aspect of the head (P < 0.05), and representing only 30% of the forehead sweat rate (P < 0.05). It is hypothesised that these intra-segmental observations may reflect variations in the local adaptation of eccrine glands to differences in local evaporation associated either with bipedal locomotion, which will influence forehead sweating, or the hidromeiotic suppression of sweating, which impacts upon sweat glands within the hairline.