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This study evaluated if passive controlled hyperthermia heat acclimation modulates cognitive performance during passive heat stress. Eight healthy adults (25 ± 4 years) underwent 7 consecutive days of hot water immersion (core temperature ≥38.6 °C) and a 7-day time-control period. On days 1 and 7 of heat acclimation, participants performed a digital Stroop test at baseline, when core temperature reached 38.6 °C, and after 60 minutes at a core temperature ≥38.6 °C to evaluate reaction time during tasks targeting processing speed (reading and counting) and executive functions (inhibition and switching). On days 1 and 7 of the time-control intervention, participants performed the Stroop test with equivalent amounts of time separating each task as for heat acclimation. During day 1 of heat acclimation, reaction time was quicker during the reading (–44 ms [–71 to –17], P < 0.01) and counting (–39 ms [–76 to –2], P = 0.04) tasks when the rectal temperature reached 38.6 °C, but after a further 60 minutes of heat exposure, reaction time only remained quicker during the reading task (–56 ms [–83 to –29], P < 0.01). Changes in reaction time during heat exposure were unaffected by subsequent heat acclimation (interaction, all P ≥ 0.09). In conclusion, 7 days of heat acclimation does not modulate processing speed and executive functions during passive heat exposure. Novelty: Whether heat acclimation improves cognitive performance during heat exposure remains unclear. We tested the hypothesis that heat acclimation modulates reaction time during cognitive tasks performed at matched levels of thermal strain. Despite the classical signs of heat acclimation, reaction time during heat exposure is unaffected by heat acclimation.

It is generally accepted that older adults display an impaired cardiovascular response to heat stress, and it has been suggested that this impaired response contributes to their increased risk of mortality during extreme heat events. Seminal studies have shown that cutaneous vasodilation, the redistribution of blood flow from visceral organs, and the increase in cardiac output are blunted in older adults during passive heating. The blunted rise of cardiac output was initially attributed to an inability to maintain stroke volume, suggesting that cardiac systolic and/or diastolic function does not adequately respond to the constraints of heat stress in older adults. Recent studies evaluated potential mechanisms underlying these seminal findings and their results challenge some of these initial observations. Notably, stroke volume is maintained during heat exposure in older adults and studies have provided evidence for preserved cardiac systolic and diastolic functions in this population. Nonetheless, a blunted increase in cardiac output during heat exposure remains a consistent observation in older adults, although it is now attributed to a blunted increase in heart rate. Recent studies have also evaluated the possibility that the attenuated capacity of aged skin to vasodilate contributes to a blunted increase in cardiac output during heat stress. The objective of this Mini-Review is to highlight these recent advances and challenge the long-standing view that the control of stroke volume during heat exposure is compromised in older adults. By doing so, our intent is to stimulate future studies to evaluate several unanswered questions in this area of research.

NEW FINDINGS What is the central question of this study? Are fitness-related improvements in thermoregulatory responses during uncompensable heat stress mediated by aerobic capacity VO2max or is it the partial heat acclimation associated with training? What is the main finding and its importance? During uncompensable heat stress, individuals with high and low VO2max displayed similar sweating and core temperature responses whereas exercise training in previously untrained individuals resulted in a greater sweat rate and a smaller rise in core temperature. These observations suggest that it is training, not VO2max per se, that mediates thermoregulatory improvements during uncompensable heat stress. ABSTRACT It remains unclear whether aerobic fitness, as defined by the maximum rate of oxygen consumption VO2max , independently improves heat dissipation in uncompensable environments, or whether the thermoregulatory adaptations associated with heat acclimation are due to repeated bouts of exercise-induced heat stress during regular aerobic training. The present analysis sought to determine if VO2max independently influences thermoregulatory sweating, maximum skin wettedness (ωmax ) and the change in rectal temperature (ΔTre ) during 60 min of exercise in an uncompensable environment (37.0 ± 0.8°C, 4.0 ± 0.2 kPa, 64 ± 3% relative humidity) at a fixed rate of heat production per unit mass (6 W kg-1 ). Retrospective analyses were performed on 22 participants (3 groups), aerobically unfit (UF; n = 7; VO2max : 41.7 ± 9.4 ml kg-1 min-1 ), aerobically fit (F; n = 7; VO2max : 55.6 ± 4.3 ml kg-1 min-1 ; P

We examined if the change in heart rate variability during passive heat exposure is modified by hot water heat acclimation (HA). Sixteen healthy adults (28 ± 5 years, 5 females/11 males) underwent heat exposure in a water-perfused suit, before and after 7 days of HA (60 min at rectal temperature ≥38.6 °C). During passive heat exposure, heart rate, the standard deviation of NN intervals (SDNN), the square root of the mean squared differences of successive NN intervals (RMSSD), and the power in the high-frequency range (HF) were measured. No difference in heart rate (P = 0.22), SDNN (P = 0.87), RMSSD (P = 0.79), and HF (P = 0.23) was observed at baseline. The increase in HR (pre-HA, 43 ± 10; post-HA, 42 ± 9 bpm; P = 0.57) and the decrease of SDNN (pre-HA, −54.1 ± 41.0; post-HA, −52.2 ± 36.8 ms; P = 0.85), RMSSD (pre-HA, −70.8 ± 49.5; post-HA, −72.7 ± 50.4 ms; P = 0.91) and HF (pre-HA, −28.0% ± 14.5; post-HA, −23.2% ± 17.1%; P = 0.27) were not different between experimental visits at fixed increases in esophageal temperature. These results suggest that 7 consecutive days of hot water HA does not modify the change in heart rate variability indices during passive heat exposure. Novelty: It remains unclear if HA alters the change in heart rate variability that occurs during passive heat exposure. At matched levels of thermal strain, 7 consecutive days of hot water immersion did not modulate the change in indices of heart rate variability during passive heat exposure.

A lower heart rate (HR) during heat exposure is a classic marker of heat acclimation (HA), although it remains unclear whether this adaptation occurs secondary to reduced thermal strain and/or improvements in cardiac function. We evaluated the hypothesis that short-term passive HA reduces HR and improves cardiac function during passive heating. Echocardiography was performed under thermoneutral and hyperthermic conditions in 10 healthy adults (9 men/1 woman, 29 ± 6 yr old), pre and post 7 days of controlled hyperthermia. HR (P = 0.61), stroke volume (P = 0.99), and cardiac output (P = 0.99), were similar on days 1 and 7 of HA. Core (pre: 38.17 ± 0.42, post: 38.15 ± 0.27°C, P = 0.95) and mean skin (pre: 38.24 ± 0.41, post: 38.51 ± 0.29°C, P = 0.17) temperatures were similar during hyperthermic echocardiographic assessments. Cardiac systolic function was unaffected by HA (P ≥ 0.10). HA attenuated the decrease in end-diastolic volume (pre: -18 ± 18, post: -12 ± 19 mL, P = 0.05), accentuated the greater atrial contribution to diastolic filling (pre: +11 ± 5, post: +14 ± 5%, P = 0.02), and attenuated the increase in left atrial reservoir strain rate (pre: +1.5 ± 1.2, post: +0.8 ± 0.8 1/s, P = 0.02) during heating. Nonetheless, there were no differences in HR (pre: 106 ± 12, post: 104 ± 12 beats/min, P = 0.50), stroke volume (pre: 65 ± 15, post: 68 ± 13 mL, P = 0.55), or cardiac output (pre: 6.9 ± 2.0, post: 7.1 ± 1.7 L/min, P = 0.70) during passive heating. Short-term controlled hyperthermia HA results in limited adaptations of cardiac function during passive heating.NEW & NOTEWORTHY A lower heart rate during heat exposure is a classic marker of heat acclimation (HA). It remains unknown if improved cardiac function contributes to this response. A 7-day passive HA protocol did not alter cardiac systolic function during passive heating, whereas it improved some indexes of diastolic function in young adults. Nonetheless, heart rate during heating was unaffected by HA. These results suggest that passive HA induces limited adaptations in cardiac function during passive heating.

NEW FINDINGS What is the central question of this study? Does passive heat acclimation alter glomerular filtration rate and urine-concentrating ability in response to passive heat stress? What is the main finding and its importance? Glomerular filtration rate remained unchanged after passive heat stress, and heat acclimation did not alter this response. However, heat acclimation mitigated the reduction in urine-concentrating ability and reduced the incidence of albuminuria in young healthy adults after passive heat stress. Collectively, these results suggest that passive heat acclimation might improve structural integrity and reduce glomerular permeability during passive heat stress. ABSTRACT Little is known about the effect of heat acclimation on kidney function during heat stress. The purpose of this study was to determine the impact of passive heat stress and subsequent passive heat acclimation on markers of kidney function. Twelve healthy adults (seven men and five women; 26 ± 5 years of age; 72.7 ± 8.6 kg; 172.4 ± 7.5 cm) underwent passive heat stress before and after a 7 day controlled hyperthermia heat acclimation protocol. The impact of passive heat exposure on urine and serum markers of kidney function was evaluated before and after heat acclimation. Glomerular filtration rate, determined from creatinine clearance, was unchanged with passive heat stress before (pre, 133 ± 41 ml min-1 ; post, 127 ± 51 ml min-1 ; P = 0.99) and after (pre, 129 ± 46 ml min-1 ; post, 130 ± 36 ml min-1 ; P = 0.99) heat acclimation. The urine-to-serum osmolality ratio was reduced after passive heating (P

KEY POINTS 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 7 day 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. ABSTRACT 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 14 healthy adults (nine men and five women, aged 27 ± 5 years) during passive heat stress performed before and after a 7 day heat acclimation protocol. Heat acclimation increased whole-body sweat rate [+0.54 L h-1 (0.32, 0.75), P

Following exercise, mean arterial pressure (MAP) is reduced ~5–10 mmHg from preexercise baseline. In nonendurance-trained males, postexercise hypotension results from peripheral vasodilation not offset by increased cardiac output (CO). By contrast, postexercise hypotension occurs through a reduction in CO from preexercise baseline in endurance-trained males. The reason(s) explaining these divergent responses remain unknown. Exercise at fixed percentage of peak oxygen consumption (V̇o2peak) is associated with a greater rate of metabolic heat production in trained individuals and therefore elevated sweat rates, both when compared with untrained individuals. We hypothesized that greater fluid loss would explain the postexercise reduction in CO of endurance-trained males. Twelve endurance-trained males (Trained: V̇o2peak, 64 ± 5 ml O2·kg−1·min−1) cycled for 60 min at 60% V̇o2peak (Trained60%). On separate days, 12 nonendurance trained males (Untrained: V̇o2peak, 49 ± 3 ml O2·kg−1·min−1) cycled at 1) 60% V̇o2peak (Untrained60%), and 2) a rate of heat production equivalent to that achieved by the Trained group (UntrainedMatched). Fluid loss was similar between Trained60% (−1.32 ± 0.20 kg) and UntrainedMatched (−1.32 ± 0.23 kg; P = 0.99) but was greater in these conditions relative to Untrained60% (−0.95 ± 0.11 kg; both P < 0.01). During the final 30 min of postexercise supine recovery, MAP was similarly reduced by 5 ± 2 mmHg in all three conditions ( P = 0.91). The reduction in MAP was mediated by a 0.5 ± 0.3 l/min reduction in CO from baseline in Trained60% ( P = 0.01). In contrast, CO returned to baseline following exercise during UntrainedMatched and Untrained60% (both P ≥ 0.30). These data demonstrate that greater fluid loss does not fully explain the divergent postexercise hemodynamic responses observed in trained relative to untrained males. NEW & NOTEWORTHY Even when matched for exercise-induced fluid loss, cardiac output was decreased in trained males but returned to baseline following exercise in their untrained counterparts. However, as per our hypothesis, reductions in stroke volume were similar between groups. This suggests that exercise-induced fluid loss is an important determinant of the stroke volume response during recovery but factors affecting heart rate such as exercise intensity and/or heat stress are also important determinants of postexercise hemodynamics.

Local heating of an extremity increases blood flow and vascular shear stress throughout the arterial tree. Local heating acutely improves macrovascular dilator function in the upper limbs of young healthy adults through a shear stress-dependent mechanism but has no such effect in the lower limbs of this age group. The effect of acute limb heating on dilator function within the atherosclerotic prone vasculature of the lower limbs of aged adults is unknown. Therefore, the purpose of this study was to test the hypothesis that acute lower limb heating improves macro- and microvascular dilator function within the leg vasculature of aged adults. Nine young and nine aged adults immersed their lower limbs at a depth of ~33 cm into a heated (~42°C) circulated water bath for 45 min. Before and 30 min after heating, macro (flow-mediated dilation)- and microvascular (reactive hyperemia) dilator functions were assessed in the lower limb, following 5 min of arterial occlusion, via Doppler ultrasound. Compared with preheat, macrovascular dilator function was unchanged following heating in young adults ( P = 0.6) but was improved in aged adults ( P = 0.04). Similarly, microvascular dilator function, as assessed by peak reactive hyperemia, was unchanged following heating in young adults ( P = 0.1) but was improved in aged adults ( P < 0.01). Taken together, these data suggest that acute lower limb heating improves both macro- and microvascular dilator function in an age dependent manner. NEW & NOTEWORTHY We demonstrate that lower limb heating acutely improves macro- and microvascular dilator function within the atherosclerotic prone vasculature of the leg in aged adults. These findings provide evidence for a potential therapeutic use of chronic lower limb heating to improve vascular health in primary aging and various disease conditions.

New Findings What is the central question of this study? Does attenuated skin blood flow diminish sweating and reduce the critical environmental limit for heat balance, which indicates maximal heat loss potential, during severe heat stress? What is the main finding and its importance? Isosmotic hypovolaemia attenuated skin blood flow by ∼20% but did not result in different sweating rates, mean skin temperatures or critical environmental limits for heat balance compared with control and volume-infusion treatments, suggesting that the lower levels of skin blood flow commonly observed in aged and diseased populations may not diminish maximal whole-body heat dissipation. Attenuated skin blood flow (SkBF) is often assumed to impair core temperature (Tc) regulation. Profound pharmacologically induced reductions in SkBF (∼85%) lead to impaired sweating, but whether the smaller attenuations in SkBF (∼20%) more often associated with ageing and certain diseases lead to decrements in sweating and maximal heat loss potential is unknown. Seven healthy men (28 ± 4 years old) completed a 30 min equilibration period at 41°C and a vapour pressure (Pa) of 2.57 kPa followed by incremental steps in Pa of 0.17 kPa every 6 min to 5.95 kPa. Differences in heat loss potential were assessed by identifying the critical vapour pressure (Pcrit) at which an upward inflection in Tc occurred. The following three separate treatments elicited changes in plasma volume to achieve three distinct levels of SkBF: control (CON); diuretic-induced isosmotic dehydration to lower SkBF (DEH); and continuous saline infusion to maintain SkBF (SAL). The Tc, mean skin temperature (Tsk), heart rate, mean laser-Doppler flux (forearm and thigh; LDFmean), mean local sweat rate (forearm and thigh; LSRmean) and metabolic rate were measured. In DEH, a 14.2 ± 5.7% lower plasma volume resulted in a ∼20% lower LDFmean in perfusion units (PU) (DEH, 139 ± 23 PU; CON, 176 ± 22 PU; and SAL, 186 ± 22 PU; P = 0.034). However, LSRmean and whole-body sweat losses were unaffected by treatment throughout (P > 0.482). The Pcrit for Tc was similar between treatments (CON, 5.05 ± 0.30 kPa; DEH, 4.93 ± 0.16 kPa; and SAL, 5.12 ± 0.10 kPa; P = 0.166). Furthermore, no differences were observed in the skin-air temperature gradient, metabolic rate or changes in Tc (P > 0.197). In conclusion, a ∼20% reduction in SkBF alters neither sweat rate nor the upper limit for heat loss from the skin during non-encapsulated passive heat stress.

During heat stress, stroke volume is maintained in young adults despite reductions in cardiac filling pressures. This is achieved by a general augmentation of cardiac function, highlighted by a left and upward shift of the Frank-Starling relation. In contrast, healthy aged adults are unable to maintain stroke volume during heat stress. We hypothesized that this would be associated with a lack of shift in the Frank-Starling relation. Frank-Starling relations were examined in 11 aged [69 ± 4 (SD) yr, 4 men/7 women] and 12 young (26 ± 5 yr, 6 men/6 women) adults during normothermic and heat stress (1.5°C increase in core temperature) conditions. During heat stress, increases in cardiac output were attenuated in aged adults (+2.5 ± 0.3 (95% CI) vs. young: +4.5 ± 0.5 l/min, P < 0.01) because of an attenuated chronotropic response (+30 ± 4 vs. young: +42 ± 5 beats/min, P < 0.01). In contrast to our hypothesis, a leftward shift of the Frank-Starling relation maintained stroke volume during heat stress in aged adults (76 ± 8 vs. normothermic: 74 ± 8 ml, P = 0.38) despite reductions in cardiac filling pressure (6.6 ± 1.0 vs. normothermic: 8.9 ± 1.1 mmHg, P < 0.01). In a subset of participants, volume loading was used to return cardiac filling pressure during heat stress to normothermic values, which resulted in a greater stroke volume for a given cardiac filling pressure in both groups. These results demonstrate that the Frank-Starling relation shifts during heat stress in healthy young and aged adults, thereby preserving stroke volume despite reductions in cardiac filling pressures.

Cardiovascular diseases (CVD) are highly prevalent in spinal cord injury (SCI), and peripheral vascular dysfunction might be a contributing factor. Recent evidence demonstrates that exposure to heat stress can improve vascular function and reduce the risk of CVD in uninjured populations. We therefore aimed to examine the extent of vascular dysfunction in SCI and the acute effects of passive heating. Fifteen participants with cervical SCI and 15 uninjured control (CON) participants underwent ultrasound assessments of vascular function and venous blood sampling for biomarkers of endothelial activation (i.e., CD62e+) and apoptosis (i.e., CD31+/42b−) before and after a 60-min exposure to lower limb hot water immersion (40°C). In SCI, macrovascular endothelial function was reduced in the brachial artery [SCI: 4.8 (3.2)% vs. CON: 7.6 (3.4)%, P = 0.04] but not the femoral artery [SCI: 3.7 (2.6)% vs. CON: 4.0 (2.1)%, P = 0.70]. Microvascular function, via reactive hyperemia, was ~40% lower in SCI versus CON in both the femoral and brachial arteries ( P < 0.01). Circulating concentrations of CD62e+ were elevated in SCI versus CON [SCI: 152 (106) microparticles/µl vs. CON: 58 (24) microparticles/µl, P < 0.05]. In response to heating, macrovascular and microvascular function remained unchanged, whereas increases (+83%) and decreases (−93%) in antegrade and retrograde shear rates, respectively, were associated with heat-induced reductions of CD62e+ concentrations in SCI to levels similar to CON ( P = 0.05). These data highlight the potential of acute heating to provide a safe and practical strategy to improve vascular function in SCI. The chronic effects of controlled heating warrant long-term testing. NEW & NOTEWORTHY Individuals with cervical level spinal cord injury exhibit selectively lower flow-mediated dilation in the brachial but not femoral artery, whereas peak reactive hyperemia was lower in both arteries compared with uninjured controls. After 60 min of lower limb hot water immersion, femoral artery blood flow and shear patterns were acutely improved in both groups. Elevated biomarkers of endothelial activation in the spinal cord injury group decreased with heating, but these biomarkers remained unchanged in controls.

One in 10 deaths worldwide is caused by traumatic injury, and 30% to 40% of those trauma-related deaths are due to hemorrhage. Currently, warming a bleeding victim is the standard of care due to the adverse effects of combined hemorrhage and hypothermia on survival. We tested the hypothesis that heating is detrimental to the maintenance of arterial pressure and cerebral perfusion during hemorrhage, while cooling is beneficial to victims who are otherwise normothermic. Twenty-one men (31 ± 9 y) were examined under two separate protocols designed to produce central hypovolemia similar to hemorrhage. Following 15 min of supine rest, 10 min of 30 mm Hg of lower body negative pressure (LBNP) was applied. On separate randomized days, subjects were then exposed to skin surface cooling (COOL), warming (WARM), or remained thermoneutral (NEUT), while LBNP continued. Subjects remained in these thermal conditions for either 40 min of 30 mm Hg LBNP (N = 9), or underwent a continuous LBNP ramp until hemodynamic decompensation (N = 12). Arterial blood pressure during LBNP was dependent on the thermal perturbation as blood pressure was greater during COOL (P >0.001) relative to NEUT and WARM for both protocols. Middle cerebral artery blood velocity decreased (P

The purpose of this study was to examine if local changes in sweat rate following 14 days of heat acclimation reflect those that occur at the whole-body level. Both prior to and following a 14-day traditional heat acclimation protocol, 10 males exercised in the heat (35 °C, ∼20% relative humidity) at increasing rates of heat production equal to 300 (Ex1), 350 (Ex2), and 400 (Ex3) W·m−2. A 10-min recovery period followed Ex1, while a 20-min recovery period separated Ex2 and Ex3. The exercise protocol was performed in a direct calorimeter to measure whole-body sweat rate and, on a separate day, in a thermal chamber to measure local sweat rate (LSR), sweat gland activation (SGA), and sweat gland output (SGO) on the upper back, chest, and mid-anterior forearm. Post-acclimation, whole-body sweat rate was greater during each exercise bout (Ex1: 14.3 ± 0.9; Ex2: 17.3 ± 1.2; Ex3: 19.4 ± 1.3 g·min−1, all p ≤ 0.05) relative to pre-acclimation (Ex1: 13.1 ± 0.6; Ex2: 15.4 ± 0.8; Ex3: 16.5 ± 1.3 g·min−1). In contrast, only LSR on the forearm increased with acclimation, and this increase was only observed during Ex2 (Post: 1.32 ± 0.33 vs. Pre: 1.06 ± 0.22 mg·min−1·cm−2, p = 0.03) and Ex3 (Post: 1.47 ± 0.41 vs. Pre: 1.17 ± 0.23 mg·min−1·cm−2, p = 0.05). The greater forearm LSR post-acclimation was due to an increase in SGO, as no changes in SGA were observed. Overall, these data demonstrate marked regional variability in the effect of heat acclimation on LSR, such that not all local measurements of sweat rate reflect the improvements observed at the whole-body level.

Grafted skin impairs heat dissipation, but it is unknown to what extent this affects body temperature during exercise in the heat.We examined core body temperature responses during exercise in the heat in a group of individuals with a large range of grafts covering their body surface area (BSA; 0%-75%).Forty-three individuals (19 females) were stratified into groups based on BSA grafted: control (0% grafted, n = 9), 17%-40% (n = 19), and40% (n = 15). Subjects exercised at a fixed rate of metabolic heat production (339 ± 70 W; 4.3 ± 0.8 W·kg) in an environmental chamber set at 40°C, 30% relative humidity for 90 min or until exhaustion (n = 8). Whole-body sweat rate and core temperatures were measured.Whole-body sweat rates were similar between the groups (control: 14.7 ± 3.4 mL·min, 17%-40%: 12.6 ± 4.0 mL·min; and40%: 11.7 ± 4.4 mL·min; P0.05), but the increase in core temperature at the end of exercise in the40% BSA grafted group (1.6°C ± 0.5°C) was greater than the 17%-40% (1.2°C ± 0.3°C) and control (0.9°C ± 0.2°C) groups (P0.05). Absolute BSA of nongrafted skin (expressed in square meters) was the strongest independent predictor of the core temperature increase (r = 0.41). When regrouping all subjects, individuals with the lowest BSA of nongrafted skin (1.0 m) had greater increases in core temperature (1.6°C ± 0.5°C) than those with more than 1.5 m nongrafted skin (1.0°C ± 0.3°C; P0.05).These data imply that individuals with grafted skin have greater increases in core temperature when exercising in the heat and that the magnitude of this increase is best explained by the amount of nongrafted skin available for heat dissipation.

Heat stress followed by an accompanying hemorrhagic challenge may influence hemostasis. We tested the hypothesis that hemostatic responses would be increased by passive heat stress, as well as exercise-induced heat stress, each with accompanying central hypovolemia to simulate a hemorrhagic insult. In aim 1, subjects were exposed to passive heating or normothermic time control, each followed by progressive lower-body negative pressure (LBNP) to presyncope. In aim 2 subjects exercised in hyperthermic environmental conditions, with and without accompanying dehydration, each also followed by progressive LBNP to presyncope. At baseline, pre-LBNP, and post-LBNP (30)] to 5.1% post-LBNP compared with 1.5% (time control) and 2.7% in N-LBNP ( P = 0.05 for main effect). Hyperthermia also potentiated increased platelet counts post-LBNP as follows: 274 K/µl for H-LBNP, 246 K/µl for N-LBNP, and 196 K/µl for time control ( P < 0.05 for the interaction). For aim 2, hydration status associated with exercise in the heat did not affect the hemostatic activity, but fibrinolysis (LY30) was increased to 6–10% when subjects were dehydrated compared with an increase to 2–4% when hydrated ( P = 0.05 for treatment). Central hypovolemia via LBNP is a primary driver of hemostasis compared with hyperthermia and dehydration effects. However, hyperthermia does induce significant thrombocytosis and by itself causes an increase in clot lysis. Dehydration associated with exercise-induced heat stress increases clot lysis but does not affect exercise-activated or subsequent hypovolemia-activated hemostasis in hyperthermic humans. Clinical implications of these findings are that quickly restoring a hemorrhaging hypovolemic trauma patient with cold noncoagulant fluids (crystalloids) can have serious deleterious effects on the body’s innate ability to form essential clots, and several factors can increase clot lysis, which should therefore be closely monitored.

We examined the effect of electric fan use on cardiovascular and thermoregulatory responses of nine young (26 ± 3 yr) and nine aged (68 ± 4 yr) adults exposed to extreme heat and humidity.While resting at a temperature of 42°C, relative humidity increased from 30% to 70% in 2% increments every 5 min. On randomized days, the protocol was repeated without or with fan use. HR, core (Tcore) and mean skin (Tsk) temperatures were measured continuously. Whole-body sweat loss was measured from changes in nude body weight. Other measures of cardiovascular (cardiac output), thermoregulatory (local cutaneous and forearm vascular conductance, local sweat rate), and perceptual (thermal and thirst sensations) responses were also examined.When averaged over the entire protocol, fan use resulted in a small reduction of HR (-2 bpm, 95% confidence interval [CI], -8 to 3), and slightly greater Tcore (+0.05°C; 95% CI, -0.13 to 0.23) and Tsk (+0.03°C; 95% CI, -0.36 to 0.42) in young adults. In contrast, fan use resulted in greater HR (+5 bpm; 95% CI, 0-10), Tcore (+0.20°C; 95% CI, 0.00-0.41), and Tsk (+0.47°C; 95% CI, 0.18-0.76) in aged adults. A greater whole-body sweat loss during fan use was observed in young (+0.2 kg; 95% CI, -0.2 to 0.6) but not aged (0.0 kg; 95% CI, -0.2 to 0.2) adults. Greater local sweat rate and cutaneous vascular conductance were observed with fan use in aged adults. Other measures of cardiovascular, thermoregulatory, and perceptual responses were unaffected by fan use in both groups.During extreme heat and humidity, fan use elevates physiological strain in aged, but not young, adults.

Burn survivors with extensive skin grafts have impaired heat dissipation and thus heat tolerance. This study tested the hypothesis that heat acclimation (HA) improves these factors in this population. Thirty-four burn survivors were stratified into highly [>40% body surface area (BSA) grafted, n = 15] and moderately (17-40% BSA grafted, n = 19) grafted groups. Nine healthy nonburned subjects served as controls. Subjects underwent 7 days of HA involving 90 min of exercise at ∼50% peak oxygen uptake in 40°C, 30% relative humidity. On days 1 and 7, subjects exercised in the heat at a fixed rate of metabolic heat production. Pre-HA, all controls and 18/19 subjects in the 17–40% group completed 90 min of exercise. Conversely, heat exercise tolerance was lower ( P < 0.01) in the >40% group, with 7/15 subjects not completing 90 min of exercise. Post-HA, heat exercise tolerance was similar between groups ( P = 0.39) as all subjects, except one, completed 90 min of exercise. Pre-HA, the magnitude of the increase in internal temperature during exercise occurred sequentially ( P ≤ 0.03) according to BSA grafted (>40%: 1.6 ± 0.5°C; 17–40%: 1.2 ± 0.3°C; control: 0.9 ± 0.2°C). HA attenuated ( P < 0.01) increases in internal temperature in the control (by 0.2 ± 0.3°C), 17–40% (by 0.3 ± 0.3°C), and >40% (by 0.3 ± 0.4°C) groups, the magnitude of which was similar between groups ( P = 0.42). These data indicate that HA improves heat tolerance and dissipation in burn survivors with grafted skin, and the magnitude of these improvements are not influenced by the extent of skin grafting.

This study tested the hypothesis that sweat rate during passive heat stress is limited by baroreceptor unloading associated with heat stress. Two protocols were performed in which healthy subjects underwent passive heat stress that elicited an increase in intestinal temperature of ∼1.8°C. Upon attaining this level of hyperthermia, in protocol 1 ( n = 10, 3 females) a bolus (19 ml/kg) of warm (∼38°C) isotonic saline was rapidly (5–10 min) infused intravenously to elevate central venous pressure (CVP), while in protocol 2 ( n = 11, 5 females) phenylephrine was infused intravenously (60–120 μg/min) to return mean arterial pressure (MAP) to normothermic levels. In protocol 1, heat stress reduced CVP from 3.9 ± 1.9 mmHg (normothermia) to −0.6 ± 1.4 mmHg ( P < 0.001), while saline infusion returned CVP to normothermic levels (5.1 ± 1.7 mmHg; P > 0.999). Sweat rate was elevated by heat stress (1.21 ± 0.44 mg·cm−2·min−1) but remained unchanged during rapid saline infusion (1.26 ± 0.47 mg·cm−2·min−1, P = 0.5), whereas cutaneous vascular conductance increased from 77 ± 10 to 101 ± 20% of local heating max ( P = 0.029). In protocol 2, MAP was reduced with heat stress from 85 ± 7 mmHg to 76 ± 8 mmHg ( P = 0.048). Although phenylephrine infusion returned MAP to normothermic levels (88 ± 7 mmHg; P > 0.999), sweat rate remained unchanged during phenylephrine infusion (1.39 ± 0.22 vs. 1.41 ± 0.24 mg·cm−2·min−1; P > 0.999). These data indicate that both cardiopulmonary and arterial baroreceptor unloading do not limit increases in sweat rate during passive heat stress.

AB Purpose: The purpose of this study was to quantify how much whole-body heat loss increases during heat acclimation and the decay in these improvements after heat acclimation. Methods: Ten males underwent a 14-d heat acclimation protocol that consisted of 90 min of cycling in the heat (40[degrees]C, 20% relative humidity) at approximately 50% of maximum oxygen consumption. Before (day 0), during (day 7), and at the end (day 14) of the heat acclimation protocol as well as 7 and 14 d after heat acclimation (days 21 and 28), whole-body heat exchange (evaporative and dry) was measured using direct calorimetry during three bouts of 30-min exercise at 300 (Ex1), 350 (Ex2), and 400 W[middle dot]m-2 (Ex3), each separated by 10 and 20 min of recovery, respectively, at 35[degrees]C and 16% relative humidity. Concurrent measurements of metabolic heat production (indirect calorimetry) allowed for the direct calculation of change in body heat content ([DELTA]Hb). Results: After accounting for an increase in net dry heat gain, increases in whole-body evaporative heat loss were evident for Ex2 and Ex3 on day 7 (Ex2, 4.9 +/- 5.6%; Ex3, 9.0 +/- 6.0%; both P

Facial pallor is commonly observed at presyncope in humans, suggestive of reductions in facial skin blood flow (SkBF). Yet, cutaneous vasoconstriction is usually minimal at presyncope when measured at the forearm. We tested the hypothesis that reductions in forehead SkBF at presyncope are greater than in the forearm. Forehead and forearm SkBF (laser-Doppler) and blood pressure (Finometer or radial artery catheterization) were measured during lower body negative pressure (LBNP) to presyncope in 11 normothermic and 13 heat-stressed subjects (intestinal temperature increased ∼1.4°C). LBNP reduced mean arterial pressure from 91 ± 5 to 57 ± 7 mmHg during normothermia ( P ≤ 0.001) and from 82 ± 5 to 57 ± 7 mmHg during heat stress ( P ≤ 0.001). During normothermia, LBNP decreased forehead SkBF 55 ± 14% compared with 24 ± 11% at the forearm ( P = 0.002), while during heat stress LBNP decreased forehead SkBF 39 ± 11% compared with 28 ± 8% in the forearm ( P = 0.007). In both conditions, most (≥68%) of the decreases in SkBF were due to decreases in blood pressure. However, a greater contribution of actively mediated reductions in SkBF was observed at the forehead, relative to the forearm during normothermia (32 ± 13% vs. 11 ± 11%, P = 0.031) and heat stress (30 ± 13% vs. 10 ± 13%, P = 0.004). These data suggest that facial pallor at presyncope is due to a combination of passive decreases in forehead SkBF secondary to reductions in blood pressure and to active decreases in SkBF, the latter of which are relatively greater than in the forearm.

KEY POINTS Age-related changes in cutaneous microvascular and cardiac functions limit the extent of cutaneous vasodilatation and the increase in cardiac output that healthy older adults can achieve during passive heat stress. However, it is unclear if these age-related changes in microvascular and cardiac functions maximally restrain the levels of cutaneous vasodilatation and cardiac output that healthy older adults can achieve during heat stress. We observed that rapid volume loading, performed during passive heat stress, augments both cutaneous vasodilatation and cardiac output in healthy older humans. These findings demonstrate that the microcirculation of healthy aged skin can further dilate during passive heat exposure, despite peripheral limitations to vasodilatation. Furthermore, healthy older humans can augment cardiac output when cardiac pre-load is increased during heat stress. ABSTRACT Primary ageing markedly attenuates cutaneous vasodilatation and the increase in cardiac output during passive heating. However, it remains unclear if these responses are maximally restrained by age-related changes in cutaneous microvascular and cardiac functions. We hypothesized that rapid volume loading performed during heat stress would increase cardiac output in older adults without parallel increases in cutaneous vasodilatation. Twelve young (Y: 26 ± 5 years) and ten older (O: 69 ± 3 years) healthy adults were passively heated until core temperature increased by 1.5°C. Cardiac output (thermodilution), forearm vascular conductance (FVC, venous occlusion plethysmography) and cutaneous vascular conductance (CVC, laser-Doppler) were measured before and after rapid infusion of warmed saline (15 mL kg-1 , ∼7 min). While heat stressed, but prior to saline infusion, cardiac output (O: 6.8 ± 0.4 vs. Y: 9.4 ± 0.6 L min-1 ), FVC (O: 0.08 ± 0.01 vs. Y: 0.17 ± 0.02 mL (100 mL min-1 mmHg-1 )-1 ), and CVC (O: 1.29 ± 0.34 vs. Y: 1.93 ± 0.30 units mmHg-1 ) were lower in older adults (all P

NEW FINDINGS What is the central question of this study? Combined increases in skin and core temperatures reduce tolerance to a simulated haemorrhagic challenge. The aim of this study was to examine the separate and combined influences of increased skin and core temperatures upon tolerance to a simulated haemorrhagic challenge. What is the main finding and its importance? Skin and core temperatures increase during many occupational settings, including military procedures, in hot environments. The study findings demonstrate that both increased skin temperature and increased core temperature can impair tolerance to a simulated haemorrhagic challenge; therefore, a soldier's tolerance to haemorrhagic injury is likely to be impaired during any military activity that results in increased skin and/or core temperatures. Tolerance to a simulated haemorrhagic insult, such as lower-body negative pressure (LBNP), is profoundly reduced when accompanied by whole-body heat stress. The aim of this study was to investigate the separate and combined influence of elevated skin (Tskin ) and core temperatures (Tcore ) on LBNP tolerance. We hypothesized that elevations in Tskin as well as Tcore would both contribute to reductions in LBNP tolerance and that the reduction in LBNP tolerance would be greatest when both Tskin and Tcore were elevated. Nine participants underwent progressive LBNP to presyncope on four occasions, as follows: (i) control, with neutral Tskin (34.3 ± 0.5°C) and Tcore (36.8 ± 0.2°C); (ii) primarily skin hyperthermia, with high Tskin (37.6 ± 0.2°C) and neutral Tcore (37.1 ± 0.2°C); (iii) primarily core hyperthermia, with neutral Tskin (35.0 ± 0.5°C) and high Tcore (38.3 ± 0.2°C); and (iv) combined skin and core hyperthermia, with high Tskin (38.8 ± 0.6°C) and high Tcore (38.1 ± 0.2°C). The LBNP tolerance was quantified via the cumulative stress index (in millimetres of mercury × minutes). The LBNP tolerance was reduced during the skin hyperthermia (569 ± 151 mmHg min) and core hyperthermia trials (563 ± 194 mmHg min) relative to control conditions (1010 ± 246 mmHg min; both P

Heat stress profoundly impairs tolerance to central hypovolemia in humans via a number of mechanisms including heat-induced hypovolemia. However, heat stress also elevates plasma osmolality; the effects of which on tolerance to central hypovolemia remain unknown. This study examined the effect of plasma hyperosmolality on tolerance to central hypovolemia in heat-stressed humans. With the use of a counterbalanced and crossover design, 12 subjects (1 female) received intravenous infusion of either 0.9% iso-osmotic (ISO) or 3.0% hyperosmotic (HYPER) saline. Subjects were subsequently heated until core temperature increased ~1.4°C, after which all subjects underwent progressive lower-body negative pressure (LBNP) to presyncope. Plasma hyperosmolality improved LBNP tolerance (ISO: 288 ± 193 vs. HYPER: 382 ± 145 mmHg × min, P = 0.04). However, no differences in mean arterial pressure ( P = 0.10), heart rate ( P = 0.09), or muscle sympathetic nerve activity ( P = 0.60, n = 6) were observed between conditions. When individual data were assessed, LBNP tolerance improved ≥25% in eight subjects but remained unchanged in the remaining four subjects. In subjects who exhibited improved LBNP tolerance, plasma hyperosmolality resulted in elevated mean arterial pressure (ISO: 62 ± 10 vs. HYPER: 72 ± 9 mmHg, P < 0.01) and a greater increase in heart rate (ISO: +12 ± 24 vs. HYPER: +23 ± 17 beats/min, P = 0.05) before presyncope. No differences in these variables were observed between conditions in subjects that did not improve LBNP tolerance (all P ≥ 0.55). These results suggest that plasma hyperosmolality improves tolerance to central hypovolemia during heat stress in most, but not all, individuals.

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.

When exposed to heat stress, increases in cutaneous blood flow and sweating in well-healed grafted skin are severely attenuated, which could impair whole-body heat loss if skin grafts cover a large portion of total body surface area (TBSA). It is unknown to what extent whole-body heat loss is impaired when skin grafts cover a significant (eg, >50%) proportion of TBSA. The authors examined whole-body heat exchange during and after 60 min of cycling exercise in the heat (35°C; 25% relative humidity), at a fixed rate of metabolic heat production (~400 W) in a woman (age, 36 years; mass, 78.2 kg) with well-healed (17+ years) skin grafts covering 75% of TBSA. Her responses were compared with two noninjured control subjects. Whole-body evaporative and dry heat exchange were measured by direct calorimetry. While exercising in the same ambient conditions and at the same rate of heat production, relative evaporative heat loss of nongrafted skin in the grafted subject (ie, evaporative heat loss per m) was nearly twice that of the control subjects. However, total rate of evaporative heat loss reached only 59% of the amount required for heat balance in the skin-grafted subject compared with 92 ± 3% in controls. Thus, the increase in core temperature was 2-fold greater for the grafted (1.22°C) vs control (0.61 ± 0.19°C) individuals. This case study demonstrates that a large area of grafted skin greatly diminishes maximum evaporative heat loss during exercise in the heat, making a compensable environment for control subjects uncompensable for skin-grafted individuals.

Compensatory reserve represents the proportion of physiological responses engaged to compensate for reductions in central blood volume before the onset of decompensation. We hypothesized that compensatory reserve would be reduced by hyperthermia and exercise-induced dehydration, conditions often encountered on the battlefield. Twenty healthy males volunteered for two separate protocols during which they underwent lower-body negative pressure (LBNP) to hemodynamic decompensation (systolic blood pressure

To assess potential mechanisms responsible for the lower sudomotor thermosensitivity in women during exercise, we examined sex differences in sudomotor function and skin blood flow (SkBF) during exercise performed at progressive increases in the requirement for heat loss. Eight men and eight women cycled at rates of metabolic heat production of 200, 250, and 300 W/m2 of body surface area, with each rate being performed sequentially for 30 min. The protocol was performed in a direct calorimeter to measure evaporative heat loss (EHL) and in a thermal chamber to measure local sweat rate (LSR) (ventilated capsule), SkBF (laser-Doppler), sweat gland activation (modified iodine-paper technique), and sweat gland output (SGO) on the back, chest, and forearm. Despite a similar requirement for heat loss between the sexes, significantly lower increases in EHL and LSR were observed in women ( P ≤ 0.001). Sex differences in EHL and LSR were not consistently observed during the first and second exercise periods, whereas EHL (348 ± 13 vs. 307 ± 9 W/m2) and LSR on the back (1.61 ± 0.07 vs. 1.20 ± 0.09 mg·min−1·cm−2), chest (1.33 ± 0.06 vs. 1.08 ± 0.09 mg·min−1·cm−2), and forearm (1.53 ± 0.07 vs. 1.20 ± 0.06 mg·min−1·cm−2, men vs. women) became significantly greater in men during the last exercise period ( P < 0.05). At each site, differences in LSR were solely due to a greater SGO in men, as opposed to differences in sweat gland activation. In contrast, no sex differences in SkBF were observed throughout the exercise period. The present study demonstrates that sex differences in sudomotor function are only evidenced beyond a certain requirement for heat loss, solely through differences in SGO. In contrast, the lower EHL and LSR in women are not paralleled by a lower SkBF response.

Previous studies have suggested that greater core temperatures during intermittent exercise (Ex) are due to attenuated sweating [upper back sweat rate (SR)] and skin blood flow (SkBF) responses. We evaluated the hypothesis that heat loss is not altered during exercise-rest cycles (ER). Ten male participants randomly performed four 120-min trials: 1) 60-min Ex and 60-min recovery (60ER); 2) 3 × 20-min Ex separated by 20-min recoveries (20ER); 3) 6 × 10-min Ex separated by 10-min recoveries (10ER), or 4) 12 × 5-min Ex separated by 5-min recoveries (5ER). Exercise was performed at a workload of 130 W at 35°C. Whole body heat exchange was determined by direct calorimetry. Core temperature, SR (by ventilated capsule), and SkBF (by laser-doppler) were measured continuously. Evaporative heat loss (EHL) progressively increased with each ER, such that it was significantly greater ( P ≤ 0.05) at the end of the last compared with the first Ex for 5ER (299 ± 39 vs. 440 ± 41 W), 10ER (425 ± 51 vs. 519 ± 45 W), and 20ER (515 ± 63 vs. 575 ± 74 W). The slope of the EHL response against esophageal temperature significantly increased from the first to the last Ex within the 10ER (376 ± 56 vs. 445 ± 89 W/°C, P ≤ 0.05) and 20ER (535 ± 85 vs. 588 ± 28 W/°C, P ≤ 0.05) conditions, but not during 5ER (296 ± 96 W/°C vs. 278 ± 95 W/°C, P = 0.237). In contrast, the slope of the SkBF response against esophageal temperature did not significantly change from the first to the last Ex (5ER: 51 ± 23 vs. 54 ± 19%/°C, P = 0.848; 10ER: 53 ± 8 vs. 56 ± 21%/°C, P = 0.786; 20ER: 44 ± 20 vs. 50 ± 27%/°C, P = 0.432). Overall, no differences in body heat content and core temperature were observed. These results suggest that altered local and whole body heat loss responses do not explain the previously observed greater core temperatures during intermittent exercise.

Purpose: The aim of this study was to investigate heat balance during thermal transients caused by successive exercise bouts. Whole-body heat loss (H[spacing dot above]L) and changes in body heat content ([DELTA]Hb) were measured using simultaneous direct whole-body and indirect calorimetry. Methods: Ten participants performed three successive bouts of 30-min cycling (Ex1, Ex2, and Ex3) at a constant rate of heat production of ~500 W, each separated by 15-min rest (R1, R2, and R3) at 30[degrees]C. Results: Despite identical rates of heat production during exercise, the time constant ([tau]) of the exponential increase in H[spacing dot above]L was greater in Ex1 ([tau] = 12.3 +/- 2.3 min) relative to both Ex2 ([tau] = 7.2 +/- 1.6 min) and Ex3 ([tau] = 7.1 +/- 1.6 min) (P < 0.05). [DELTA]Hb during Ex1 (256 +/- 76 kJ) was greater than during Ex2 (135 +/- 60 kJ) and Ex3 (124 +/- 78 kJ) (P < 0.05). During recovery bouts, heat production was the same, and the [tau] of the exponential decrease in H[spacing dot above]L was the same during R1 ([tau] = 6.5 +/- 1.1 min), R2 ([tau] = 5.9 +/- 1.3 min), and R3 ([tau] = 6.0 +/- 1.2 min). [DELTA]Hb during R1 (-82 +/- 48 kJ), R2 (-91 +/- 48 kJ), and R3 (-88 +/- 54 kJ) were the same. The cumulative [DELTA]Hb was consequently greater at the end of Ex2 and Ex3 relative to the end of Ex1 (P < 0.05). Likewise, cumulative [DELTA]Hb was greater at the end of R2 and R3 relative to R1 (P < 0.05). Conclusion: The proportional decrease in the amount of heat stored in the successive exercise bouts is the result of an enhanced rate of heat dissipation during exercise and not due to a higher rate of heat loss in the recovery period. Despite a greater thermal drive with repeated exercise, the decline in the rate of total heat loss during successive recovery bouts was the same.

We tested the hypothesis that attention, memory, and executive function are impaired to a greater extent in passively heat-stressed older adults than in passively heat-stressed younger adults. In a randomized, crossover design, 15 older (age: 69 ± 5 yr) and 14 younger (age: 30 ± 4 yr) healthy subjects underwent passive heat stress and time control trials. Cognitive tests (outcomes: accuracy and reaction time) from the CANTAB battery evaluated attention [rapid visual processing (RVP), choice reaction time (CRT)], memory [spatial span (SSP), pattern recognition memory (PRM)], and executive function [one touch stockings of Cambridge (OTS)]. Testing was undertaken on two occasions during each trial, at baseline and after internal temperature had increased by 1.0 ± 0.2°C or after a time control period. For tests that measured attention, reaction time during RVP and CRT was slower ( P ≤ 0.01) in the older group. During heat stress, RVP reaction time improved ( P < 0.01) in both groups. Heat stress had no effect ( P ≥ 0.09) on RVP or CRT accuracy in either group. For tests that measured memory, accuracy on SSP and PRM was lower ( P < 0.01) in the older group, but there was no effect of heat stress ( P ≥ 0.14). For tests that measured executive function, overall, accuracy on OTS was lower, and reaction time was slower in the older group ( P ≤ 0.05). Reaction time generally improved during heat stress, but there was no effect of heat stress on accuracy in either group. These data indicate that moderate increases in body temperature during passive heat stress do not differentially compromise cognitive function in younger and older adults.

Passive heat stress increases core and skin temperatures and reduces tolerance to simulated hemorrhage (lower body negative pressure; LBNP). We tested whether exercise-induced heat stress reduces LBNP tolerance to a greater extent relative to passive heat stress, when skin and core temperatures are similar. Eight participants (6 males, 32 ± 7 yr, 176 ± 8 cm, 77.0 ± 9.8 kg) underwent LBNP to presyncope on three separate and randomized occasions: 1) passive heat stress, 2) exercise in a hot environment (40°C) where skin temperature was moderate (36°C, active 36), and 3) exercise in a hot environment (40°C) where skin temperature was matched relative to that achieved during passive heat stress (∼38°C, active 38). LBNP tolerance was quantified using the cumulative stress index (CSI). Before LBNP, increases in core temperature from baseline were not different between trials (1.18 ± 0.20°C; P > 0.05). Also before LBNP, mean skin temperature was similar between passive heat stress (38.2 ± 0.5°C) and active 38 (38.2 ± 0.8°C; P = 0.90) trials, whereas it was reduced in the active 36 trial (36.6 ± 0.5°C; P ≤ 0.05 compared with passive heat stress and active 38). LBNP tolerance was not different between passive heat stress and active 38 trials (383 ± 223 and 322 ± 178 CSI, respectively; P = 0.12), but both were similarly reduced relative to active 36 (516 ± 147 CSI, both P ≤ 0.05). LBNP tolerance is not different between heat stresses induced either passively or by exercise in a hot environment when skin temperatures are similarly elevated. However, LBNP tolerance is influenced by the magnitude of the elevation in skin temperature following exercise induced heat stress.

Adenosine has both vasodilatory and vasoconstrictive properties, yet its influence on cutaneous vascular conductance (CVC) during whole-body cooling remains unknown. The present study evaluated the influence of adenosine on reflex cutaneous vasoconstriction. Four microdialysis probes were inserted into the dorsal forearm skin of eight subjects and infused with the following solutions: (i) lactated Ringer solution (CON); (ii) 4 mm theophylline (Theo), a non-selective adenosine receptor antagonist; (iii) 10 mm l-NAME, an inhibitor of nitric oxide synthase; and (iv) combined 4 mm theophylline and 10 mm l-NAME (Theo + l-NAME). Subjects subsequently donned a water-perfusion garment. Following a thermoneutral baseline period, the suit was perfused with water at 10°C for 20 min (Cooling 1). The suit was then perfused with water at 49°C for 45 min (Heating), followed by a second cooling period of 20 min using 10°C water (Cooling 2). Cutaneous blood flow (laser-Doppler) was measured over each microdialysis probe and used to calculate CVC as a percentage of the maximum determined by sodium nitroprusside infusion and local heating. Cutaneous vascular conductance was significantly elevated at the Theo site relative to CON following Cooling 1 (18 ± 6 versus 8 ± 2%; P = 0.01) and Cooling 2 (27 ± 11 versus 14 ± 5%; P = 0.022). Likewise, CVC at the Theo + l-NAME site remained greater compared with l-NAME after Cooling 1 (13 ± 4 versus 7 ± 3%; P = 0.030) and Cooling 2 (15 ± 3 versus 9 ± 2%; P = 0.009). The present findings demonstrate that non-selective antagonism of adenosine receptors attenuates the decrease in cutaneous vascular conductance during whole-body cooling from hyperthermia.

Although the requirements for heat dissipation during exercise are determined by the necessity for heat balance, few studies have considered them when examining sweat production and its potential modulators. Rather, the majority of studies have used an experimental protocol based on a fixed percentage of maximum oxygen uptake (% ). Using multiple regression analysis, we examined the independent contribution of the evaporative requirement for heat balance (Ereq) and % to whole-body sweat rate (WBSR) during exercise. We hypothesised that WBSR would be determined by Ereq and not by % . A total of 23 males performed two separate experiments during which they exercised for 90 min at different rates of metabolic heat production (200, 350, 500 W) at a fixed air temperature (30°C, n = 8), or at a fixed rate of metabolic heat production (290 W) at different air temperatures (30, 35, 40°C, n = 15 and 45°C, n = 7). Whole-body evaporative heat loss was measured by direct calorimetry and used to calculate absolute WBSR in grams per minute. The conditions employed resulted in a wide range of Ereq (131-487 W) and % (15-55%). The individual variation in non-steady-state (0-30 min) and steady-state (30-90 min) WBSR correlated significantly with Ereq (P0.001). In contrast, % correlated negatively with the residual variation in WBSR not explained by Ereq, and marginally increased (∼2%) the amount of total variability in WBSR described by Ereq alone (non-steady state: R(2) = 0.885; steady state: R(2) = 0.930). These data provide clear evidence that absolute WBSR during exercise is determined by Ereq, not by % . Future studies should therefore use an experimental protocol which ensures a fixed Ereq when examining absolute WBSR between individuals, irrespective of potential differences in relative exercise intensity.

Quantifying sweat gland activation provides important information when explaining differences in sweat rate between populations and physiological conditions. However, no standard technique has been proposed to measure sweat gland activation, while the reliability of sweat gland activation measurements is unknown. We examined the interrater and internal reliability of the modified-iodine paper technique, as well as compared computer-aided analysis to manual counts of sweat gland activation. Iodine-impregnated paper was pressed against the skin of 35 participants in whom sweating was elicited by exercise in the heat or infusion of methylcholine. The number of active glands was subsequently determined by computer-aided analysis. In total, 382 measurements were used to evaluate: 1) agreement between computer analysis and manual counts; 2) the interrater reliability of computer analysis between independent investigators; and 3) the internal reliability of sweat gland activation measurements between duplicate samples. The number of glands identified with computer analysis did not differ from manual counts (68 ± 29 vs. 72 ± 24 glands/cm2; P = 0.27). These measures were highly correlated ( r = 0.77) with a mean bias ± limits of agreement of −4 ± 38 glands/cm2. When comparing computer analysis measures between investigators, values were highly correlated ( r = 0.95; P < 0.001) and the mean bias ± limits of agreement was 4 ± 18 glands/cm2. Finally, duplicate measures of sweat gland activation were highly correlated ( r = 0.88; P < 0.001) with a mean bias ± limits of agreement of 3 ± 29 glands/cm2. These results favor the use of the modified-iodine paper technique with computer-aided analysis as a standard technique to reliably evaluate the number of active sweat glands.

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.

The relative influence of muscle metabo- and baroreflex activity on heat loss responses during post-isometric handgrip (IHG) exercise ischemia remains unknown, particularly under heat stress. Therefore, we examined the separate and integrated influences of metabo- and baroreceptor-mediated reflex activity on sweat rate and cutaneous vascular conductance (CVC) under increasing levels of hyperthermia. Twelve men performed 1 min of IHG exercise at 60% of maximal voluntary contraction followed by 2 min of ischemia with simultaneous application of lower body positive pressure (LBPP, +40 mmHg), lower body negative pressure (LBNP, −20 mmHg), or no pressure (control) under no heat stress. On separate days, trials were repeated under heat stress conditions of 0.6°C (moderate heat stress) and 1.4°C (high heat stress) increase in esophageal temperature. For all conditions, mean arterial pressure was greater with LBPP and lower with LBNP than control during ischemia (all P ≤ 0.05). No differences in sweat rate were observed between pressure conditions, regardless of the level of hyperthermia ( P > 0.05). Under moderate heat stress, no differences in CVC were observed between pressure conditions. However, under high heat stress, LBNP significantly reduced CVC by 21 ± 4% ( P ≤ 0.05) and LBPP significantly elevated CVC by 14 ± 5% ( P ≤ 0.05) relative to control. These results show that sweating during post-IHG exercise ischemia is activated by metaboreflex stimulation, and not by baroreflexes. In contrast, our results suggest that baroreflexes can influence the metaboreflex modulation of CVC, but only at greater levels of hyperthermia.

The purpose of this study was to examine arterial blood pressure responses during isometric handgrip (IHG) exercise performed at increasing levels of heat stress. Ten male subjects performed 1 min of IHG exercise at 60 % of maximal voluntary contraction under no heat stress (NHS), moderate heat stress [MHS, 0.6 °C increase in esophageal temperature (T (es))] and high heat stress (HHS, 1.4 °C increase in T (es)). For all conditions, IHG exercise significantly elevated mean arterial pressure (MAP) (NHS: 124 ± 6 vs. 90 ± 4 mmHg, MHS: 112 ± 6 vs. 89 ± 6 mmHg, HHS: 107 ± 7 vs. 91 ± 5 mmHg, P ≤ 0.05) and cardiac output (CO) (NHS: 9.0 ± 1.5 vs. 6.1 ± 0.6 L/min, MHS: 9.8 ± 1.8 vs. 7.6 ± 1.3 L/min, HHS: 10.0 ± 2.0 vs. 8.5 ± 1.9 L/min, P ≤ 0.05) relative to baseline, whereas no differences in total peripheral resistance (TPR) were observed (P > 0.05). However, the relative increases in MAP and CO were significantly reduced during MHS (MAP: 23 ± 6 mmHg, CO: 2.1 ± 0.9 L/min) and HHS (MAP: 16 ± 7 mmHg, CO: 1.5 ± 0.8 L/min) compared to NHS (34 ± 5 mmHg, CO: 2.9 ± 1.1 L/min, P ≤ 0.05). Furthermore, these elevations were significantly attenuated during HHS compared to MHS (P ≤ 0.05). Our findings show that heat stress attenuates the increase in arterial blood pressure during isometric handgrip exercise and this attenuation is cardiac output dependent, since TPR did not change during exercise for all heat stress conditions.

Context:Cold-water immersion is recommended for the immediate field treatment of exertional heat stroke. However, concerns exist over potential overcooling of hyperthermic individuals during cold-water immersion.Objective:To evaluate the recommendation that removing previously hyperthermic individuals from a cold-water bath at a rectal temperature (Tre) of 38.6°C would attenuate overcooling.Design:Controlled laboratory study.Setting:University research laboratory.Patients or Other Participants:Participants included 6 men and 4 women (age = 22 ± 3 years, height = 172 ± 10 cm, mass = 67.8 ± 10.7 kg, body fat percentage = 17.1% ± 4.5%, maximum oxygen consumption = 59.3 ± 8.7 mL·kg−1·min−1).Intervention(s):After exercising at an ambient temperature of 40.0°C for 38.5 ± 9.4 minutes, until Tre reached 39.5°C, participants were immersed in a 2.0°C circulated water bath until Tre decreased to either 37.5°C or 38.6°C. Subsequently, participants were removed from the water bath and recovered for 20 minutes at an ambient temperature of 25°C.Main Outcome Measure(s):Rectal and esophageal temperatures were measured continuously during the immersion and recovery periods.Results:Because of the experimental design, the overall time of immersion was greater during the 37.5°C trial (16.6 ± 5.7 minutes) than the 38.6°C trial (8.8 ± 2.6 minutes) (t9 = −4.740, P = .001). During the recovery period after cold-water immersion, both rectal (F1,9 = 50.540, P < .001) and esophageal (F1,6 = 20.365, P = .007) temperatures remained greater in the 38.6°C trial than in the 37.5°C trial. This was evidenced by low points of 36.47°C ± 0.70°C and 37.19°C ± 0.71°C for rectal temperature (t9 = 2.975, P = .016) and of 35.67°C ± 1.27°C and 36.72°C ± 0.95°C for esophageal temperature (t6 = 3.963, P = .007) during the recovery period of the 37.5°C and 38.6°C trials, respectively.Conclusions:Immersion for approximately 9 minutes to a rectal temperature cooling limit of 38.6°C negated any risk associated with overcooling hyperthermic individuals when they were immersed in 2°C water.

On separate days, eight physically active younger (22 +/- 2 years) and eight highly trained middle-aged (45 +/- 4 years) men matched for physical fitness and body composition performed 90 min of semi-recumbent cycling at a constant rate of heat production (290 W) followed by 60 min of seated recovery in either a temperate (T, 30 degrees C), warm (W, 35 degrees C) or hot (H, 40 degrees C) ambient condition. Rectal temperature (T (re)) was measured continuously, while the rate of whole-body heat loss (H (L)), as well as changes in body heat content (H (b)) was measured simultaneously using direct whole-body and indirect calorimetry. No difference in H (L) was observed between age groups for all ambient conditions. Accordingly, the average H (b) during the 90-min exercise was similar for the younger (+193 +/- 52, 212 +/- 82 and +211 +/- 44 kJ for T, W and H, respectively) and middle-aged men (+192 +/- 119, +225 +/- 76 and +217 +/- 130 kJ for T, W and H, respectively). This was paralleled by a similar increase in T (re) of 0.40 +/- 0.20, 0.36 +/- 0.14 and 0.34 +/- 0.23 degrees C for T, W and H, respectively in the younger men and 0.37 +/- 0.23, 0.32 +/- 0.19 and 0.28 +/- 0.14 degrees C for T, W and H, respectively in the middle-aged men. After 60 min of recovery, H (b) was similar for the younger and the middle-aged men, respectively (-45 +/- 52 and -38 +/- 31 kJ for T; -57 +/- 78 and -40 +/- 25 kJ for W; and -32 +/- 71 and 11 +/- 96 kJ for H). End recovery T (re) remained elevated to similar levels in both the younger and middle-aged men, respectively, for each of the ambient conditions (0.24 +/- 019 and 0.18 +/- 0.18 degrees C for T; 0.25 +/- 0.11 and 0.24 +/- 0.14 degrees C for W and 0.33 +/- 0.21 and 0.33 +/- 0.13 degrees C for H). We conclude that highly trained middle-aged men demonstrate a similar capacity for heat dissipation when compared with physically active younger men.

We evaluated the hypothesis that with increasing levels of hyperthermia, thermal influences would predominate over nonthermal baroreceptor control of cutaneous vascular conductance (CVC) and local sweat rate (LSR). On separate days, eight male participants were positioned in either an upright seated posture (URS) or a 15° head-down tilt (HDT) posture in a thermoneutral condition and during passive heating, until mean body temperature (T body) increased by 1.5°C. Hemodynamic [heart rate (HR), cardiac output, mean arterial pressure (MAP)] and thermal responses [T re, CVC, LSR] were measured continuously. MAP showed a gradual decrease in the early- to mid-stages of heating for both HDT and URS. At a T body > 0.6°C, MAP achieved a stable, albeit reduced level from baseline resting for the duration of the heating, whereas MAP decreased significantly throughout the heating period in the URS position (p

The Frank–Starling mechanism, by which changes in end-diastolic volume alter stroke volume, is one of the more fundamental concepts of human physiology. In humans, this concept is represented by a hyperbolic pulmonary capillary wedge pressure (index of left-ventricular filling pressure) to stroke volume curve. In a recent issue of the Journal of Physiology, Wilson et al. (2009) have provided an elegant example of how such fundamental concepts can be applied to elucidate underlying mechanisms of altered physiological responses, in this case, during combined orthostatic and thermal stresses. Thermal stress brings about significant cardiovascular adjustments that ultimately affect cardiac filling pressure and therefore the Frank–Starling mechanism. During passive heat stress, increases in core and skin temperatures require a redistribution of blood flow from non-cutaneous vascular beds and an increase in skin blood flow so that heat can be transferred from the body core to the skin. In such situations, central venous pressure and central blood volume decrease (Crandall et al. 2008). Despite these reductions in cardiac filling pressure, stoke volume is well maintained due to increased cardiac contractility (Brothers et al. 2009). As such, cardiac output can increase to upwards of ∼13 l min−1 which, along with splanchnic and renal vasoconstriction, allows skin blood flow to reach levels as high as ∼8 l min−1 (Rowell, 1974). Although mean arterial pressure is well maintained in the supine position, a competition develops between the maintenance of blood pressure and the need to maintain adequate skin perfusion for heat exchange when gravitational stress (e.g. lower body negative pressure, LBNP) is superimposed on whole-body heat stress. As such, many studies have shown that orthostatic tolerance is greatly reduced in the heat stressed human. On the other hand, during passive cold stress, peripheral vasoconstriction attenuates the rate of heat dissipation from the body by reducing the temperature gradient between the skin and the environment. Contrary to heat stress, decreases in skin blood flow parallel increases in total peripheral resistance and mean arterial pressure (Cui et al. 2005). As such, cold stress greatly improves orthostatic tolerance not only relative to hyperthermia but also to normothermia. While studies have established clear differences in orthostatic tolerance between heat and cold stresses, the underlying mechanisms for these differences have not been entirely elucidated. Cold stress has been shown to maintain greater levels of central blood volume, central venous pressure and consequently stroke volume for a given level of LBNP compared to both normothermia and hyperthermia (Cui et al. 2005). The maintained stroke volume during cold stress suggests a plasticity in the operating point of the Frank–Starling mechanism according to an individual's thermal status, thereby eliciting a different change in stroke volume for a given decrease in left-ventricular filling pressure. To test the hypothesis that such a mechanism might contribute to the observed differences in orthostatic tolerances between heat and cold stresses, Wilson et al. (2009) examined changes in stroke volume as a function of changes in pulmonary capillary wedge pressure in 11 healthy volunteers under the following conditions: (1) normothermia, (2) cold stress, and (3) heat stress. Capillary wedge pressure, an index of left-ventricular filling pressure, was determined by balloon inflation of a pulmonary artery catheter. Cardiac output was determined by thermodilution, and subsequently used to calculate stroke volume. Participants were fitted with a water-perfused suit and were placed in the supine position in a LBNP chamber. During the normothermic trial, water at 34°C perfused the suit. Subsequently, the water temperature was reduced to 20°C for a 20 min period of skin surface cooling (cold stress) while it was increased to 46°C until core temperature increased by 1°C for the heat stress trial. At each thermal condition, baseline measurements were followed by 15 mmHg of LBNP for 15 min which was immediately followed by 30 mmHg of LBNP for an additional 15 min. The two different levels of LBNP were used to induce changes in pulmonary capillary wedge pressure, to which changes in stroke volume were subsequently related. The results revealed that the thermal status of the individual clearly influenced the operating point of the Frank–Starling curve. Specifically, the pre-LBNP values for the operating point in normothermia were located midway between the flatter and steeper portion of the curve, whereas cold stress shifted the operating point to the right (i.e. further towards the flatter portion of the curve). In contrast, heat stress shifted the operating point to the left (i.e. closer to the steep portion of the curve) (see Fig. 1). As such, large reductions in stroke volume during heat stress were brought about by relatively small changes in pulmonary capillary wedge pressure, while stroke volume remained on or near the flat portion of the curve even at the highest level of LBNP during skin surface cooling. The plasticity in the operating point of the Frank–Starling mechanism as a function of an individuals’ thermal status represents a novel mechanism for the observed differences in orthostatic tolerance between cold and heat stress conditions. Although orthostatic tolerance was not directly assessed in the study of Wilson et al. (2009), three participants experienced syncopal symptoms while heat stressed at 30 mmHg LBNP. In contrast, all participants completed the 30 mmHg LBNP without any signs of syncope during the normothermic and cold stress conditions. Figure 1 Schematic illustration of the Frank–Starling relationship and how the operating point (i.e. prior to any perturbation in cardiac filling pressure) is shifted during cold (triangle) and heat (square) stress relative to normothermia (circle) Note ... While multi-mechanistic in nature, orthostatic intolerance during heat stress will ultimately develop due to substantial reductions in cardiac output which cannot be compensated by increases in systemic vascular resistance. As evidenced by the data of Wilson et al. (2009), the shift in the operating point of the Frank–Starling mechanism towards the flatter portion of the curve during skin surface cooling creates a ‘reserve’ such that cardiac filling pressure can decrease to a greater extent relative to heat stress before stroke volume, and therefore cardiac output, is significantly reduced. In fact, skin surface cooling in the study of Wilson et al. (2009) significantly attenuated the reductions in stroke volume, cardiac output and pulse pressure at both levels of LBNP compared to the heat stress condition. Thus, attenuated decreases in cardiac output due to skin surface cooling are a likely mechanism by which orthostatic tolerance is preserved. The data of Wilson et al. (2009) therefore provide a good example of how a fundamental concept of human physiology can be applied to determine the mechanisms of altered physiological responses.

We evaluated differences between sexes in core cooling rates during cold water immersion after exercise-induced hyperthermia.Ten male (M) and nine female (F) participants, matched for body surface area-to-mass ratio (AD/M) (F: 268 +/- 19 vs M: 261 +/- 16 cm2 x kg(-1)), were recruited for the study. Participants exercised until rectal temperature reached 39.5 degrees C and were subsequently immersed in a 2.0 degrees C circulated water bath until rectal temperature decreased to 37.5 degrees C. Rectal and mean skin temperatures and the relative rate of nonevaporative heat loss (W x m(-2)) were measured continuously during the immersion period.Males were heavier, had a lower body fat percentage, and had a greater amount of lean body mass compared with females (Por = 0.05). Significant differences were found in the overall cooling rate for rectal temperature (F: 0.22 +/- 0.07 vs M: 0.12 +/- 0.03 degrees C x min(-1), P = 0.001) and in the overall immersion times (F: 10.89 +/- 4.49 vs M: 18.13 +/- 4.47 min, P = 0.003). Mean skin temperature was lower in females compared with that in males during the immersion period (P0.001), although there were no differences between sexes in the rate of nonevaporative heat loss (P = 0.180).Although females had a similar AD/M and greater body adiposity, they had approximately 1.7-fold greater rectal cooling rate. Because AD/M and body adiposity do not seem to influence rectal cooling rates in previously hyperthermic individuals, the greater cooling rates in females may be attributed to physical differences in lean body mass.

The sensitivity and specificity of technetium-99m hexakis-2-methoxy-2-isobutyl-isonitrile (sestamibi) single-photon emission computed tomographic (SPECT) imaging for the diagnosis of coronary artery disease were studied in 45 patients admitted to the hospital for clinical suspicion of unstable angina. Only patients without prior myocardial infarction were included and all patients had technetium-99m sestamibi injection and a 12-lead electrocardiogram (ECG) during and ≤4 h after an episode of chest pain. Coronary angiography performed in all patients during hospitalization showed significant coronary artery disease (≥250% luminal diameter reduction) in 26 of the 45 patients.The SPECT studies obtained after injection of technetium-99m sestamibi during an episode of spontaneous chest pain showed a sensitivity of 96% for the detection of coronary artery disease; the 12-lead ECG obtained at the time of the injection had a sensitivity of 35%. With the patient in the pain-free state, respective sensitivity values were 65% and 38%. Specificity for the radionuclide study was 79% during pain and 84% in the pain-free state; for the ECG, it was 74% both during and between episodes of pain.The site of the perfusion defect corresponded to the most severe coronary artery lesion in 88% of patients. The severity of the perfusion defect correlated with the extent of coronary artery disease: the defect score was 5.3 ± 3.3 with one-vessel disease, 4.9 ± 2.8 with two-vessel disease and 10.5 ± 5.0 with three-vessel disease (p < 0.01). Persistence of the perfusion defect in the pain-free state was associated with a larger initial defect (p < 0.05) and with involvement of the left anterior descending coronary artery (p < 0.05).This study demonstrates a high accuracy of technetium-99m sestamibi SPECT studies for the detection of coronary disease and the identification of the involved coronary arteries in patients with spontaneous chest pain.

Cutaneous vascular conductance (CVC) and sweat rate are subject to non-thermal baroreflex-mediated attenuation post-exercise. Various recovery modalities have been effective in attenuating these decreases in CVC and sweat rate post-exercise. However, the interaction of recovery posture and preceding exercise intensity on post-exercise thermoregulation remains unresolved. We evaluated the combined effect of supine recovery and exercise intensity on post-exercise cardiovascular and thermal responses relative to an upright seated posture. Seven females performed 15 min of cycling ergometry at low- (LIE, 55% maximal oxygen consumption) or high-(HIE, 85% maximal oxygen consumption) intensity followed by 60 min of recovery in either an upright seated or supine posture. Esophageal temperature, CVC, sweat rate, cardiac output, stroke volume, heart rate, total peripheral resistance, and mean arterial pressure (MAP) were measured at baseline, at end-exercise, and at 2, 5, 12, 20, and every 10 min thereafter until the end of recovery. MAP and stroke volume were maintained during supine recovery to a greater extent relative to an upright seated recovery following HIE (p ≤ 0.05) and were paralleled by an elevated CVC and sweat rate response (p ≤ 0.05). A significantly lower esophageal temperature was subsequently observed when supine throughout recovery (p ≤ 0.05). Although we observed a reflex bradycardia and increased stoke volume with supine recovery following LIE, no differences were observed for MAP, CVC, sweat rate or esophageal temperature. Supine recovery attenuates the post-exercise reductions in MAP, CVC, and sweat rate in a manner dependent directly on exercise intensity. This effect is likely attributable to a non-thermal baroreceptor mechanism.

We evaluated the hypothesis that different rates of metabolic heat production between sexes, during exercise at the same percentage of maximum oxygen consumption $$ \left( {\dot{V}{\text{O}}_{2\max } } \right), $$ give proportional differences in evaporative heat loss. Seven males and seven females, exercised at 41.3 ± 2.7% $$ \dot{V}{\text{O}}_{2\max } $$ for 60-min at 40°C and 30% relative humidity. Whole-body direct air calorimetry measured rate of whole-body evaporative heat loss $$ \left( {\dot{H}_{\text{E}} } \right), $$ while metabolic heat production $$ \left( {\dot{M} - \dot{W}} \right) $$ was measured by indirect calorimetry. $$ \dot{M} - \dot{W} $$ was greater in males (243 ± 18 W m−2) relative to females (201 ± 4 W m−2) (P ≤ 0.05) throughout exercise. This was paralleled by a greater $$ \dot{H}_{\text{E}} $$ at end-exercise in males (207 ± 51 W m−2) relative to females (180 ± 3 W m−2) (P ≤ 0.05). Differences in metabolic heat production between sexes during exercise at a fixed percentage of $$ \dot{V}{\text{O}}_{2\max } $$ give differences in evaporative heat loss. To compare thermoregulatory function between sexes, differences in metabolic heat production must therefore be accounted for.

This study evaluated the effect of body adiposity on core cooling rates, as measured by decreases in rectal (T (re)), esophageal (T (es)) and aural canal (T (ac)) temperatures, of individuals rendered hyperthermic by dynamic exercise in the heat. Seventeen male participants were divided into two groups; low body fat (LF, 12.9 +/- 1.9%) and high body fat (HF, 22.3 +/- 4.3%). Participants exercised at 65% of their maximal oxygen uptake at an ambient air temperature of 40 degrees C until T (re) increased to 40 degrees C or until volitional fatigue. Following exercise, participants were immersed up to the clavicles in an 8 degrees C circulated water bath until T (re) returned to 37.5 degrees C. No significant differences were found between the LF and HF in the time to reach a T (re) of 39.5 degrees C (P = 0.205), 38.5 degrees C (P = 0.343) and 37.5 degrees C (P = 0.923) during the immersion. Overall cooling rate for T (re) was also similar between groups (0.23 +/- 0.09 degrees C/min (LF) vs. 0.20 +/- 0.09 degrees C/min (HF), P = 0.647) as well as those for T (es) (P = 0.502) and T (ac) (P = 0.940). Furthermore, mean rate of non-evaporative heat loss (702 +/- 217 W/m(2) (LF) vs. 612 +/- 141 W/m(2) (HF), P = 0.239) was not different between groups. These results suggest that a difference of approximately 10% of body adiposity does not affect core cooling rates in active individuals under 25% body fat rendered hyperthermic by exercise.

Purpose: This study investigated the nonthermoregulatory control of cutaneous vascular conductance (CVC) and sweating during recovery from exercise-induced hyperthermia as well as possible sex-related differences in these responses. Two hypotheses were tested in this study: 1) active and passive recovery would be more effective in attenuating the fall in mean arterial pressure (MAP) than inactive recovery, but CVC and sweat rate responses would be similar between all recovery modes; and 2) the magnitude of the change in postexercise heat loss and hemodynamic responses between recovery modes would be similar between sexes. Methods: Nine males and nine females were rendered hyperthermic (esophageal temperature = 39.5[degrees]C) by exercise, followed by 60 min of 1) active, 2) inactive, and 3) passive recovery. CVC, sweat rate, and MAP were recorded at baseline, after 2, 5, 12, and 20 min, and at every 10 min until the end of recovery. Results: MAP was elevated above inactive recovery by 6 +/- 2 and 4 +/- 1 mm Hg for active and passive recovery, respectively (P < 0.001). No differences were observed between modes during the initial 10 min of recovery for CVC and 50 min of recovery for sweat rate. However, relative to inactive recovery CVC and sweat rate were subsequently greater by 16.2 +/- 5.8% of CVCpeak and 0.28 +/- 0.04 mg[middle dot]min-1[middle dot]cm-2, respectively, during active recovery, and by 11.6 +/- 2.9% of CVCpeak and 0.23 +/- 0.03 mg[middle dot]min-1[middle dot]cm-2, respectively, during passive recovery. Conclusion: We conclude that in the presence of a greater thermal drive associated with hyperthermia, the influence of nonthermal input on postexercise heat loss responses is still observed. However, thermal control predominates over nonthermal factors in the first 10 min of recovery for CVC and for up to 50 min postexercise for sweating. Sex did not influence the effect of recovery mode on any variable

Previous studies report greater postexercise heat loss responses during active recovery relative to inactive recovery despite similar core temperatures between conditions. Differences have been ascribed to nonthermal factors influencing heat loss response control since elevations in metabolism during active recovery are assumed to be insufficient to change core temperature and modify heat loss responses. However, from a heat balance perspective, different rates of total heat loss with corresponding rates of metabolism are possible at any core temperature. Seven male volunteers cycled at 75% of V̇o2peak in the Snellen whole body air calorimeter regulated at 25.0°C, 30% relative humidity (RH), for 15 min followed by 30 min of active (AR) or inactive (IR) recovery. Relative to IR, a greater rate of metabolic heat production (Ṁ − Ẇ) during AR was paralleled by a greater rate of total heat loss (ḢL) and a greater local sweat rate, despite similar esophageal temperatures between conditions. At end-recovery, rate of body heat storage, that is, [(Ṁ − Ẇ) − ḢL] approached zero similarly in both conditions, with Ṁ − Ẇ and ḢL elevated during AR by 91 ± 26 W and 93 ± 25 W, respectively. Despite a higher Ṁ − Ẇ during AR, change in body heat content from calorimetry was similar between conditions due to a slower relative decrease in ḢL during AR, suggesting an influence of nonthermal factors. In conclusion, different levels of heat loss are possible at similar core temperatures during recovery modes of different metabolic rates. Evidence for nonthermal influences upon heat loss responses must therefore be sought after accounting for differences in heat production.

Occupational workers and military personnel who perform their activities in hot environmental conditions are not only at risk of hyperthermia, but the cardiovascular adjustments that occur in such settings can also place them at risk for cardiovascular instability, particularly should they suffer from a haemorrhagic injury. The typical cardiovascular adjustments that occur during heat stress are an increase in heart rate resulting in an augmented cardiac output and peripheral vasodilatation, which reduces systemic vascular resistance. The net result is a displacement of blood from the central to the peripheral (skin) circulation to accommodate the skin blood flow requirements for effective heat transfer. While these adjustments generally do not have a negative impact on arterial pressure in the supine posture, the superimposition of central hypovolaemia as incurred during haemorrhage can quickly lead to a precipitous fall in arterial pressure, potentially leading to loss of consciousness and/or cardiovascular collapse. As such, understanding the cardiovascular physiology of haemorrhage in the heat stressed human has obvious clinical implications for the proper management of such scenarios. Recent advances point towards a shift in the operating point of the Frank–Starling mechanism (Wilson et al. 2009), reduced central blood volume (Crandall et al. 2008) and an altered capacity of the cutaneous vasculature to vasoconstrict (Wilson et al. 2002; Crandall et al. 2010), as a multifactorial mechanism for the compromised regulation of arterial pressure during (simulated) haemorrhage in the heat stressed human. In this issue of The Journal of Physiology, Crandall et al. (2012) reveal an intriguing component of the cardiovascular physiology of haemorrhage under heat stress. By combining scintigraphy (gamma camera imaging) with technetium-99m labelled red blood cells, Crandall et al. (2012) examined changes in central blood volume in heat stressed individuals during a simulated haemorrhagic challenge induced by lower body negative pressure. As passive heat stress itself reduces central blood volume (Crandall et al. 2008), the novel aspect of their study consisted of performing the simulated haemorrhagic challenge with (colloid volume infusion) and without prior restoration of central blood volume. Building upon previous research demonstrating that volume loading returned orthostatic tolerance during heat stress to levels similar to when normothermic (Keller et al. 2009), it was hypothesized that colloid volume loading sufficient to restore central blood volume to pre-heat stress levels would attenuate the reductions in central blood volume during a subsequent haemorrhagic challenge. Contrary to this hypothesis, however, decreases in central blood volume were similar whether volume loading was performed or not prior to the haemmorrhagic challenge. To reconcile the seemingly contradictory observations that volume loading can improve orthostatic tolerance, yet does not attenuate decreases in central blood volume, the authors nicely point out that warm blood vessels have a remarkable capacity to increase blood volume under an elevated state of hyperthermia. As such, the added central blood volume provided by colloid infusion is simply absorbed by the dilated vasculature of the lower limbs. Aggravating the problem is also a lower vasoconstrictor responsiveness of the heat stressed cutaneous vasculature (Wilson et al. 2002), which effectively keeps the infused volume within the ‘sink’ created by the heated lower limbs. That being said, volume infusion does elevate cardiac output to greater levels prior to initiating the simulated haemorrhagic challenge; such that volume loaded individuals maintain a greater cardiac output for a given level of lower body negative pressure while heat stressed. This is likely to be the mechanism by which volume loading can maintain orthostatic tolerance, despite having little effect on decreases in central blood volume. These findings raise the important question as to whether volume loading alone is an adequate intervention treatment to maintain both central blood volume and consciousness during haemorrhage under stress. It might be that greater infusion volumes than the one used in the current study are needed to significantly limit decreases in central blood volume in such scenarios. However, the capacity of warm blood vessels to increase blood volume might require the use of unreasonably large infusion volumes. In contrast, future studies might consider interventions that target both the decreases in central blood volume and the ‘sink’ created by the warm vascular beds. For example, skin surface cooling results in similar cardiovascular adjustments as colloid volume infusion, such as a rightward shift of the operating point of the Frank–Starling relationship toward a flatter portion of the curve (Wilson et al. 2009), resulting in greater orthostatic tolerance to a simulated haemorrhagic challenge. Skin surface cooling would also be expected to induce vasoconstriction of the peripheral vascular beds and re-distribute blood towards the central circulation. The distinct advantage of skin surface cooling, however, might also be to limit the accumulation of blood in the compliant venous system, possibly making a given volume loading more effective by keeping a greater proportion of it within the central circulation. Although body warming of haemorrhagic patients has long been advocated to avoid the complications of potential hypothermia, it must be kept in mind that the thermal and cardiovascular consequences of hyperthermia might allow for combined skin surface cooling and volume loading to be an effective treatment strategy in heat stressed individuals.