A century of exercise physiology: concepts that ignited the study of human thermoregulation. Part 4: evolution, thermal adaptation and unsupported theories of thermoregulation.

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.

A century of exercise physiology: concepts that ignited the study of human thermoregulation. Part 3: Heat and cold tolerance during exercise.

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.

A century of exercise physiology: concepts that ignited the study of human thermoregulation. Part 1: Foundational principles and theories of regulation.

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.

A century of exercise physiology: concepts that ignited the study of human thermoregulation. Part 2: physiological measurements.

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.

The scaling of human basal and resting metabolic rates.

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 mass0.547 (P < 0.05). Allometric analysis of the historical male data yielded an equivalent, and similarly powerful model: metabolic rate = 0.873 * body mass0.497 (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.

Scaling the peak and steady-state aerobic power of running and walking humans.

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 (mass0.57) to maximal exercise (mass0.75; P < 0.05), but not between steady-state walking (mass0.87) 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.

Physiological interactions with personal-protective clothing, physically demanding work and global warming: An Asia-Pacific perspective.

The Asia-Pacific contains over half of the world's population, 21 countries have a Gross Domestic Product <25% of the world's largest economy, many countries have tropical climates and all suffer the impact of global warming. That 'perfect storm' exacerbates the risk of occupational heat illness, yet first responders must perform physically demanding work wearing personal-protective clothing and equipment. Unfortunately, the Eurocentric emphasis of past research has sometimes reduced its applicability to other ethnic groups. To redress that imbalance, relevant contemporary research has been reviewed, to which has been added information applicable to people of Asian, Melanesian and Polynesian ancestry. An epidemiological triad is used to identify the causal agents and host factors of work intolerance within hot-humid climates, commencing with the size dependency of resting metabolism and heat production accompanying load carriage, followed by a progression from the impact of single-layered clothing through to encapsulating ensembles. A morphological hypothesis is presented to account for inter-individual differences in heat production and heat loss, which seems to explain apparent ethnic- and gender-related differences in thermoregulation, at least within thermally compensable states. The mechanisms underlying work intolerance, cardiovascular insufficiency and heat illness are reviewed, along with epidemiological data from the Asia-Pacific. Finally, evidence-based preventative and treatment strategies are presented and updated concerning moisture-management fabrics and barriers, dehydration, pre- and post-exercise cooling, and heat adaptation. An extensive reference list is provided, with >25 recommendations enabling physiologists, occupational health specialists, policy makers, purchasing officers and manufacturers to rapidly extract interpretative outcomes pertinent to the Asia-Pacific.

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 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.

Hyperthermia, but not dehydration, alters the electrical activity of the brain.

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.

Hyperthermia and dehydration: their independent and combined influences on physiological function during rest and exercise.

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 H2O-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.

The origin, significance and plasticity of the thermoeffector thresholds: Extrapolation between humans and laboratory rodents.

In this review, there is an overarching emphasis on the extrapolation of knowledge from one physiological regulator to another, with a particular emphasis on autonomic thermoregulation in humans and rodents. Through mammalian phylogenetics, one finds evidence for the gradual acquisition of an ability to maintain whole-body thermal stability, with discrete autonomic mechanisms arising for the generation, retention and dissipation of thermal energy. The sequential attainment of those thermoeffectors, over aeons, makes it unlikely that they are controlled by a common central processor, so the presence of a single activation switch is perhaps inconceivable. Instead, effector activation is associated with the arrival at lower and upper critical (threshold) body temperatures, with regions between those points defining zones of mammalian thermoneutrality. As thermal energy content deviates from thermoneutrality, there is a progression from purely passive (physical) heat exchanges through to autonomic (thermoeffector) recruitment. That activation is morphologically dependent, with an obligatory greater basal metabolic heat production evident in smaller individuals within both hypo- and normothermic states. Indeed, a first-principles, morphological case is presented for the existence of an effector recruitment cascade, with human observations providing the empirical support. That sequential activation is consistent with the presence of multiple central controllers, and both animal and human experiments supporting that possibility are reviewed. Finally, the case is presented that mammals possess multiple thermoreceptive fields, thermoeffectors with discrete neural pathways and several central, but independent, controllers of thermoeffector function. Those concepts are summarised in updated conceptual and neuronal models for human thermoregulation.

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 ±â€¯0.10) and thermogenesis (0.67 °C ±â€¯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 ±â€¯0.07; P < 0.05). Conversely, but with the exception of forehead precursor sweating, the sudomotor thresholds were elevated (averaging 0.16 °C ±â€¯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.

Thermogenic and psychogenic sweating in humans: Identifying eccrine glandular recruitment patterns from glabrous and non-glabrous skin surfaces.

In this experiment, psychogenic (mental arithmetic), thermogenic (mean body temperature elevation of 0.6 °C) and combined thermo-psychogenic treatments were used to explore eccrine sweat-gland recruitment from glabrous (volar hand and forehead) and non-glabrous skin surfaces (chest). It was hypothesised that each treatment would activate the same glands, and that glandular activity would be intermittent. Nine individuals participated in a single trial with normothermic and mildly hyperthermic phases. When normothermic, a 10-min arithmetical challenge was administered, during which sudomotor activity was recorded. Following passive heating and thermal clamping, sweating responses were again evaluated (10 min). A second arithmetical challenge (10 min) was administered during clamped hyperthermia, with its sudorific impact recorded. The activity of individual sweat glands was recorded at 60-s intervals, using precisely positioned, and uniformly applied, starch-iodide papers. Those imprints were digitised and analysed. Peak activity typically occurred during the thermo-psychogenic treatment, revealing physiologically active densities of 128 (volar hand), 165 (forehead) and 77 glands.cm-2 (chest). Except for the hand (46%), glands uniquely activated by one treatment were consistently <10% of the total glands identified. Glandular activations were most commonly of an intermittent nature, particularly during the thermogenic treatment. Accordingly, we accepted the hypothesis that psychogenic, thermogenic and thermo-psychogenic stimuli activate the same sweat glands in both the glabrous and non-glabrous regions. In addition, this investigation has provided detailed descriptions of the intermittent nature of sweat-gland activity, revealing that a consistent proportion of the physiologically active glands are recruited during these thermal and non-thermal stimuli.

Revisiting the dermatomal recruitment of, and pressure-dependent influences on, human eccrine sweating.

Herein we describe two experiments in which the recruitment and pressure-induced modifications of human eccrine sweating were investigated. In one experiment, the longstanding belief that glandular recruitment follows a gradual, caudal-to-rostral (dermatomal) recruitment pattern was re-evaluated. The onset of sweating was simultaneously determined (ventilated capsules) from four spinal (dermatomal) segments (forehead, dorsal hand, lower chest and dorsal foot) during the passive heating of supine participants (N = 8). No evidence was found to support either dermatomal or simultaneous glandular recruitment patterns. Instead, the results were more consistent with individualised (random) patterns of regional activation (P > 0.05), with significant time delays among sites. Such delays in the appearance of discharged sweat may reflect differences in neurotransmitter sensitivity, precursor sweat production or ductal reabsorption. In the second experiment, the pressure-induced hemihidrotic reflex (contralateral sudomotor enhancement) was revisited, using pressures applied over 10 cm2 areas of the chest (left side: 6 N cm-2) and left heel (3 N cm-2) during both supine and seated postures (N = 12). Participants were passively heated and thermally clamped before pressure application. Hemihidrosis was not observed from the contralateral surfaces within the same (chest) or lower spinal segments (abdomen; both P > 0.05) during chest pressure, but a generalised enhancement followed heel pressure when supine. We suggest that previous observations of hemihidrosis possibly resulted from elevated heat storage, rather than a neural reflex. Chest pressure significantly inhibited ipsilateral sweating (forehead, hand, chest; all P < 0.05), and that influence is hypothesised to result from interactions between ascending mechanoreceptor afferents and the descending sudomotor pathways.

A vascular mechanism to explain thermally mediated variations in deep-body cooling rates during the immersion of profoundly hyperthermic individuals.

NEW FINDINGS: What is the central question of this study? Does the cold-water immersion (14°C) of profoundly hyperthermic individuals induce reductions in cutaneous and limb blood flow of sufficient magnitude to impair heat loss relative to the size of the thermal gradient? What is the main finding and its importance? The temperate-water cooling (26°C) of profoundly hyperthermic individuals was found to be rapid and reproducible. A vascular mechanism accounted for that outcome, with temperature-dependent differences in cutaneous and limb blood flows observed during cooling. Decisions relating to cooling strategies must be based upon deep-body temperature measurements that have response dynamics consistent with the urgency for cooling. ABSTRACT: Physiologically trivial time differences for cooling the intrathoracic viscera of hyperthermic individuals have been reported between cold- and temperate-water immersion treatments. One explanation for that observation is reduced convective heat delivery to the skin during cold immersion, and this study was designed to test both the validity of that observation, and its underlying hypothesis. Eight healthy men participated in four head-out water immersions: two when normothermic, and two after exercise-induced, moderate-to-profound hyperthermia. Two water temperatures were used within each thermal state: temperate (26°C) and cold (14°C). Tissue temperatures were measured at three deep-body sites (oesophagus, auditory canal and rectum) and eight skin surfaces, with cutaneous vascular responses simultaneously evaluated from both forearms (laser-Doppler flowmetry and venous-occlusion plethysmography). During the cold immersion of normothermic individuals, oesophageal temperature decreased relative to baseline (-0.31°C over 20 min; P < 0.05), whilst rectal temperature increased (0.20°C; P < 0.05). When rendered hyperthermic, oesophageal (-0.75°C) and rectal temperatures decreased (-0.05°C) during the transition period (<8.5 min, mostly in air at 22°C), with the former dropping to 37.5°C only 54 s faster when immersed in cold rather than in temperate water (P < 0.05). Minimal cutaneous vasoconstriction occurred during either normothermic immersion, whereas pronounced constriction was evident during both immersions when subjects were hyperthermic, with the colder water eliciting a greater vascular response (P < 0.05). It was concluded that the rapid intrathoracic cooling of asymptomatic, hyperthermic individuals in temperate water was a reproducible phenomenon, with slower than expected cooling in cold water brought about by stronger cutaneous vasoconstriction that reduced convective heat delivery to the periphery.

Foundational insights into the estimation of whole-body metabolic rate.

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.

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

NEW FINDINGS: 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 241.2-303.1 cm2  kg-1 , respectively). Subjects completed two trials in compensable conditions (28°C, 36% relative humidity) involving rest (20 min) and steady-state cycling (45 min) at fixed, area-specific metabolic heat-production rates (light, ∼135 W m-2 ; moderate, ∼200 W m-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.

Intraocular pressure and cerebral oxygenation during prolonged headward acceleration.

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.

The independent influences of heat strain and dehydration upon cognition.

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.