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Exercise in the heat increases the slope of the relation between minute ventilation and carbon dioxide elimination (V̇E/V̇co2 slope) in young healthy adults. An indispensable role for skin temperature in modulating the ventilatory response to exercise is noted, contradicting common belief that internal/core temperature acts independently as a controller of ventilation during hyperthermia.

Compared with younger adults, passive heating induced increases in cardiac output are attenuated by ∼50% in older adults. This attenuated response may be associated with older individuals’ inability to maintain stroke volume through ionotropic mechanisms and/or through altered chronotropic mechanisms. The purpose of this study was to identify the interactive effect of age and hyperthermia on cardiac responsiveness to dobutamine-induced cardiac stimulation. Eleven young (26 ± 4 yr) and 8 older (68 ± 5 yr) participants underwent a normothermic and a hyperthermic (baseline core temperature +1.2°C) trial on the same day. In both thermal conditions, after baseline measurements, intravenous dobutamine was administered for 12 min at 5 µg/kg/min, followed by 12 min at 15 µg/kg/min. Primary measurements included echocardiography-based assessments of cardiac function, gastrointestinal and skin temperatures, heart rate, and mean arterial pressure. Heart rate responses to dobutamine were similar between groups in both thermal conditions ( P > 0.05). The peak systolic mitral annular velocity (S′), i.e., an index of left ventricular longitudinal systolic function, was similar between groups for both thermal conditions at baseline. While normothermic, the increase in S′ between groups was similar with dobutamine administration. However, while hyperthermic, the increase in S′ was attenuated in the older participants with dobutamine ( P < 0.001). Healthy, older individuals show attenuated inotropic, but maintained chronotropic responsiveness to dobutamine administration during hyperthermia. These data suggest that older individuals have a reduced capacity to increase cardiomyocyte contractility, estimated by changes in S′, via β1-adrenergic mechanisms while hyperthermic.

Aerobic exercise is important in the rehabilitation of individuals with prior burn injuries, but no studies have examined whether adult burn survivors demonstrate cardiac remodeling to long-term aerobic exercise training. In this study, we tested the hypothesis that 6 months of progressive exercise training would improve cardiac magnetic resonance imaging-based measures of cardiac structure and function in well-healed burn survivors. Our findings highlight the ability of exercise training to modify cardiac structure and function in well-healed burn survivors and nonburned sedentary controls alike.

The human body constantly exchanges heat with the environment. Temperature regulation is a homeostatic feedback control system that ensures deep body temperature is maintained within narrow limits despite wide variations in environmental conditions and activity-related elevations in metabolic heat production. Extensive research has been performed to study the physiological regulation of deep body temperature. This review focuses on healthy and disordered human temperature regulation during heat stress. Central to this discussion is the notion that various morphological features, intrinsic factors, diseases, and injuries independently and interactively influence deep body temperature during exercise and/or exposure to hot ambient temperatures. The first sections review fundamental aspects of the human heat stress response, including the biophysical principles governing heat balance and the autonomic control of heat loss thermoeffectors. Next, we discuss the effects of different intrinsic factors (morphology, heat adaptation, biological sex, and age), diseases (neurological, cardiovascular, metabolic, and genetic), and injuries (spinal cord injury, deep burns, and heat stroke), with emphasis on the mechanisms by which these factors enhance or disturb the regulation of deep body temperature during heat stress. We conclude with key unanswered questions in this field of research.

Exercise training reduces cardiovascular disease risk, partly due to arterial blood pressure (BP) lowering at rest and during fixed-load exercise. However, it is unclear whether exercise training can reduce BP at rest and during exercise in adults with well-healed burn injuries. Therefore, the purpose of this investigation was to test the hypothesis that 6 mo of unsupervised exercise training reduces BP at rest and during lower-body cycle ergometry in adults with well-healed burn injuries. Thirty-nine adults (28 with well-healed burn injuries and 11 controls) completed 6 mo of unsupervised, progressive exercise training including endurance, resistance, and high-intensity interval components. Before and after exercise training, we measured BP at rest, during fixed-load submaximal exercise (50 and 75 W), during fixed-intensity submaximal exercise (40% and 70% of V̇o

The purpose of this study was to evaluate whether burn survivors have lower adherence compared to non-burned control individuals during a 6-month community-based exercise program. In burn survivors we sought to answer if there was a relation between the size of the burn injury and dropout frequency. Fifty-two burn survivors and 15 non-burned controls (n=67) were recruited for a 6-month community-based (i.e., non-supervised), progressive, exercise training program. During the exercise program, 27% (i.e., 4 of 15 enrolled) of the non-burned individuals dropped out of the study, while 37% (i.e., 19 of 52) of the burn survivors dropped out from the study. There was no difference in the percentage of individuals who dropped out between groups (p = 0.552). There was no difference in size of the burn injury, expressed as percent body surface area burned (%BSA) between the burn-survivors that dropped out versus those who completed the exercise regimen (p = 0.951). We did not observe a relation between %BSA burned and dropouts (log odds = -0.15-0.01(%BSA), B= -0.01, SE = 0.015, p = 0.541). There was no effect of %BSA burned on the probability of dropout [Exp (B) = 0.991, 95% CI (0.961, 1.020)] and there were no differences in the percentage of individuals who dropped out of the study based on %BSA burned (χ2(1) = 0.44, p = 0.51). These data demonstrate that burn survivors have similar exercise adherence relative to a non-burned group and the extent of a burn injury does not affect exercise program adherence.

Skin grafting following a burn injury attenuates/abolishes sweat production within grafted areas. It is presently unknown whether the thermoregulatory consequences of skin grafting depend on anatomical location.Purpose: To test the hypothesis that a simulated burn injury on the torso will be no more or less detrimental to core temperature control than on the limbs during uncompensable exercise-heat stress.Methods: Nine non-burned individuals (7 males, 2 females) completed the protocol. On separate occasions, burn injuries of identical surface area (0.45 ± 0.08 m2 or 24.4% ± 4.4% of total body surface area) were simulated on the torso or the arms/legs using an absorbent, vapor-impermeable material that impedes sweat evaporation in those regions. Participants performed 60 min of treadmill walking at 5.3 km·h-1 and a 4.1% ± 0.8% grade, targeting 6 W·kg-1 of metabolic heat production in 40.1°C ± 0.2°C and 19.6% ± 0.6% relative humidity conditions. Rectal temperature, heart rate, and perceptual responses were measured.Results: Rectal temperature increased to a similar extent with simulated injuries on the torso and limbs (condition-by-time interaction: P = 0.86), with a final rectal temperature 0.9 ± 0.3°C above baseline in both conditions. No differences in heart rate, perceived exertion, or thermal sensation were observed between conditions (condition-by-time interactions: P ≥ 0.50).Conclusion: During uncompensable exercise-heat stress, sized-matched simulated burn injuries on the torso or limbs evoke comparable core temperature, heart rate, and perceptual responses, suggesting that the risk of exertional heat illness in such environmental conditions is independent of injury location.

KEY POINTS Low dose ketamine is a leading medication used to provide analgesia in pre-hospital and hospital settings. Low dose ketamine is increasingly used off-label to treat conditions such as depression. In animals, ketamine stimulates the sympathetic nervous system and increases blood pressure, but these physiological consequences have not been studied in conscious humans. Our data suggest that low dose ketamine administration blunts pain perception and reduces blood pressure, but not muscle sympathetic nerve activity burst frequency, responses during a cold pressor test in healthy humans. These mechanistic, physiological results inform risk-benefit analysis for clinicians administering low dose ketamine in humans. ABSTRACT Low dose ketamine is an effective analgesic medication. However, our knowledge of the effects of ketamine on autonomic cardiovascular regulation is primarily limited to animal experiments. Notably, it is unknown if low dose ketamine influences autonomic cardiovascular responses during painful stimuli in humans. We tested the hypothesis that low dose ketamine blunts perceived pain, and blunts subsequent sympathetic and cardiovascular responses during an experimental noxious stimulus. Twenty-two adults (10F/12M; 27 ± 6 years; 26 ± 3 kg m-2 , mean ± SD) completed this randomized, crossover, placebo-controlled trial during two laboratory visits. During each visit, participants completed cold pressor tests (CPT; hand in ∼0.4°C ice bath for 2 min) pre- and 5 min post-drug administration (20 mg ketamine or saline). We compared pain perception (100 mm visual analogue scale), muscle sympathetic nerve activity (MSNA; microneurography, 12 paired recordings), and beat-to-beat blood pressure (BP; photoplethysmography) during the pre- and post-drug CPTs separately using paired, two-tailed t tests. For the pre-drug CPT, perceived pain (P = 0.4378), MSNA burst frequency responses (P = 0.7375), and mean BP responses (P = 0.6457) were not different between trials. For the post-drug CPT, ketamine compared to placebo administration attenuated perceived pain (P

INTRODUCTION: Although evaporative heat loss capacity is reduced in burn-injured individuals with extensive skin grafts, the thermoregulatory strain due to a prior burn injury during exercise-heat stress may be negligible if the burn is located underneath protective clothing with low vapor permeability. PURPOSE: To test the hypothesis that heat strain during exercise in a hot-dry environment while wearing protective clothing would be similar with and without a simulated torso burn injury. METHODS: Ten healthy individuals (8M/2F) underwent three trials wearing: Uniform (combat uniform, tactical vest, and replica torso armor plates), Uniform with a 20% total body surface area (TBSA) simulated torso burn (Uniform + Burn), or shorts (and sports bra) only (Control). Exercise consisted of treadmill walking (5.3 km·h(–1); 3.7 ± 0.9% grade) for 60 min at a target heat production of 6.0 W·kg(−1) in 40.0 ± 0.1°C; 20.0 ± 0.6% relative humidity conditions. Measurements included rectal temperature, heart rate, rating of perceived exertion, and thermal sensation. RESULTS: No differences in rectal temperature (P ≥ 0.85), heart rate (P ≥ 0.99), thermal sensation (P ≥ 0.73), or rating of perceived exertion (P ≥ 0.13) occurred between Uniform + Burn and Uniform trials. In the Control trial, however, core temperature, heart rate, thermal sensation, and rating of perceived exertion were lower compared to the Uniform and Uniform + Burn trials (P ≤ 0.04 for all). CONCLUSION: A 20% TBSA simulated torso burn injury does not further exacerbate heat strain when wearing a combat uniform. These findings suggest that the physiological strain associated with torso burn injuries is not different from non-injured individuals when wearing protective clothing during an acute exercise-heat stress.

Each year, within the United States, tens of thousands of individuals are hospitalized for burn-related injuries. The treatment of deep burns often involves skin grafts to accelerate healing and reduce the risk of infection. The grafting procedure results in a physical disruption between the injured and subsequently debrided host site and the skin graft placed on top of that site. Both neural and vascular connections must occur between the host site and the graft for neural modulation of skin blood flow to take place. Furthermore, evaporative cooling from such burn injured areas is effectively absent, leading to greatly impaired thermoregulatory responses in individuals with large portions of their body surface area burned. Hospitalization following a burn injury can last weeks to months, with cardiovascular and metabolic consequences of such injuries having the potential to adversely affect the burn survivor for years postdischarge. With that background, the objectives of this article are to discuss 1) our current understanding of the physiology and associated consequences of skin grafting, 2) the effects of skin grafts on efferent thermoregulatory responses and the associated consequences pertaining to whole body thermoregulation, 3) approaches that may reduce the risk of excessive hyperthermia in burn survivors, 4) the long-term cardiovascular consequences of burn injuries, and 5) the extent to which burn survivors can “normalize” otherwise compromised cardiovascular responses. Our primary objective is to guide the reader toward an understanding that severe burn injuries result in significant physiological consequences that can persist for years after the injury.

We tested the hypothesis that thermal behavior resulting in reductions in mean skin temperature alleviates thermal discomfort and mitigates the rise in core temperature during light-intensity exercise. In a 27 ± 0°C, 48 ± 6% relative humidity environment, 12 healthy subjects (6 men, 6 women) completed 60 min of recumbent cycling. In both trials, subjects wore a water-perfused suit top continually perfusing 34 ± 0°C water. In the behavior trial, subjects maintained their upper body thermally comfortable by pressing a button to perfuse cool water (2.2 ± 0.5°C) through the top for 2 min per button press. Metabolic heat production (control: 404 ± 52 W, behavior: 397 ± 65 W; P = 0.44) was similar between trials. Mean skin temperature was reduced in the behavior trial (by −2.1 ± 1.8°C, P < 0.01) because of voluntary reductions in water-perfused top temperature ( P < 0.01). Whole body ( P = 0.02) and local sweat rates were lower in the behavior trial ( P ≤ 0.05). Absolute core temperature was similar ( P ≥ 0.30); however, the change in core temperature was greater in the behavior trial after 40 min of exercise ( P ≤ 0.03). Partitional calorimetry did not reveal any differences in cumulative heat storage (control: 554 ± 229, behavior: 544 ± 283 kJ; P = 0.90). Thermal behavior alleviated whole body thermal discomfort during exercise (by −1.17 ± 0.40 arbitrary units, P < 0.01). Despite lower evaporative cooling in the behavior trial, similar heat loss was achieved by voluntarily employing convective cooling. Therefore, thermal behavior resulting in large reductions in skin temperature is effective at alleviating thermal discomfort during exercise without affecting whole body heat loss. NEW & NOTEWORTHY This study aimed to determine the effectiveness of thermal behavior in maintaining thermal comfort during exercise by allowing subjects to voluntarily cool their torso and upper limbs with 2°C water throughout a light-intensity exercise protocol. We show that voluntary cooling of the upper body alleviates thermal discomfort while maintaining heat balance through convective rather than evaporative means of heat loss.

Although the severity of a burn injury is often associated with the percentage of total body surface area burned (%TBSA), the thermoregulatory consequences of a given %TBSA injury do not account for the interactive effects of body morphology and metabolic heat production (H(prod)). PURPOSE: Using a simulated burn injury model to mimic the detrimental effect of a 40% TBSA injury on whole-body evaporative heat dissipation, core temperature response to exercise in physiologically uncompensable conditions between morphologically-disparate groups were examined at (i) an absolute H(prod) (watts, W), and (ii) a mass-specific H(prod) (watts per kilogram of body mass, W·kg(−1)). METHODS: Healthy, young, non-burned individuals of small (SM, n = 11) or large (LG, n = 11) body size cycled for 60 min at 500 W or 5.3 W·kg(−1) of H(prod) in 39°C and 20% relative humidity conditions. A 40% burn injury was simulated by affixing a highly absorbent, vapor-impermeable material across the torso (20% TBSA), arms (10% TBSA), and legs (10% TBSA) to impede evaporative heat loss in those regions. RESULTS: While the elevation in core temperature was greater in SM compared to LG at a H(prod) of 500 W (SM: 1.69 ± 0.26°C, LG: 1.05 ± 0.26°C, P < 0.01), elevations in core temperature were not different at a H(prod) of 5.3 W·kg(−1) between groups (SM: 0.99 ± 0.32°C, LG: 1.05 ± 0.26°C, P = 0.66). CONCLUSION: These data suggest that among individuals with a 40% TBSA burn injury, a smaller body size leads to exacerbated elevations in core temperature during physical activities eliciting the same absolute H(prod) (non-weight-bearing tasks) but not activities eliciting the same mass-specific H(prod) (weight-bearing tasks).

For thermal physiologists, calorimetry is an important methodological tool to assess human heat balance during heat or cold exposures. A whole body direct calorimeter remains the gold standard instrument for assessing human heat balance; however, this equipment is rarely available to most researchers. A more widely accessible substitute is partitional calorimetry, a method by which all components of the conceptual heat balance equation—metabolic heat production, conduction, radiation, convection, and evaporation—are calculated separately based on fundamental properties of energy exchange. Since partitional calorimetry requires relatively inexpensive equipment (vs. direct calorimetry) and can be used over a wider range of experimental conditions (i.e., different physical activities, laboratory or field settings, clothed or seminude), it allows investigators to address a wide range of problems such as predicting human responses to thermal stress, developing climatic exposure limits and fluid replacement guidelines, estimating clothing properties, evaluating cooling/warming interventions, and identifying potential thermoregulatory dysfunction in unique populations. In this Cores of Reproducibility in Physiology (CORP) review, we summarize the fundamental principles underlying the use of partitional calorimetry, present the various methodological and arithmetic requirements, and provide typical examples of its use. Strategies to minimize estimation error of specific heat balance components, as well as the limitations of the method, are also discussed. The goal of this CORP paper is to present a standardized methodology and thus improve the accuracy and reproducibility of research employing partitional calorimetry.

INTRODUCTION. Vasodilator function is impaired in individuals with well-healed burn injuries, but therapeutic interventions that lessen or reverse this maladaptation are lacking. The purpose of this study was to test the hypothesis that a 6-month community-based exercise training program would increase microvascular dilator function in individuals with well healed burn injuries irrespective of the magnitude of the injured body surface area. Further, we hypothesize that macrovascular dilator function would remain unchanged post-training. METHODS. Microvascular function, (forearm reactive hyperemia), macrovascular function (brachial artery flow-mediated dilation), and the maximal vasodilatory response following ischemic handgrip exercise (an estimate of microvascular remodeling) were assessed before and after exercise training in non-burned control subjects (N = 11) and individuals with burn injuries covering a moderate body surface area (26 ± 7 %; N = 13) and a high body surface area (59 ± 15 %; N = 19). RESULTS. Peak vascular conductance and area under the curve during post-occlusive reactive hyperemia increased from pre- to post-training in control and burn injury groups (both P < 0.05), the magnitude of which did not differ between groups (both P = 0.6). Likewise, the maximal vasodilatory response following ischemic handgrip exercise increased in all groups after exercise training (P < 0.05). Macrovascular dilator function did not differ across time or between groups (P = 0.8). CONCLUSION. These data suggest that a community-based exercise training program improves microvascular function in individuals with well-healed burn injuries, which may be due in part to vascular remodeling.

New findings What is the central question of this study? Does dietary nitrate supplementation with beetroot juice attenuate thermoregulatory and cardiovascular strain in older adults during severe heat stress? What is the main finding and its importance? A 7-day nitrate supplementation regimen lowered resting mean arterial pressure in thermoneutral conditions. During heat stress, core and mean skin temperatures, vasodilatory responses, sweat loss, heart rate and left ventricular function were unchanged, and mean arterial pressure was only transiently reduced, post-supplementation. These data suggest nitrate supplementation with beetroot juice does not mitigate thermoregulatory or cardiovascular strain in heat-stressed older individuals. Abstract This study tested the hypothesis that dietary nitrate supplementation with concentrated beetroot juice attenuates thermoregulatory and cardiovascular strain in older individuals during environmental heat stress. Nine healthy older individuals (six females, three males; aged 67 ± 5 years) were exposed to 42.5 ± 0.1°C and 34.0 ± 0.5% relative humidity conditions for 120 min before (CON) and after 7 days of dietary nitrate supplementation with concentrated beetroot juice (BRJ; 280 ml, ∼16.8 mmol of nitrate daily). Core and skin temperatures, body mass changes (indicative of whole-body sweat loss), skin blood flow and cutaneous vascular conductance, forearm blood flow and vascular conductance, heart rate, arterial blood pressures and indices of cardiac function were measured. The 7-day beetroot juice regimen increased plasma nitrate/nitrite levels from 27.4 ± 15.2 to 477.0 ± 102.5 μmol l-1 (P 0.05). Mean arterial pressure was lower in BRJ vs. CON during heat stress (treatment-by-time interaction: P = 0.02). Overall, these findings suggest that dietary nitrate supplementation with concentrated beetroot juice does not attenuate thermoregulatory or cardiovascular strain in older individuals exposed to severe ambient heat stress.

KEY POINTS Haemorrhage is the leading cause of battlefield and civilian trauma deaths. Given that a haemorrhagic injury on the battlefield is almost always associated with pain, it is paramount that the administered pain medication does not disrupt the physiological mechanisms that are beneficial in defending against the haemorrhagic insult. Current guidelines from the US Army's Committee on Tactical Combat Casualty Care (CoTCCC) for the selection of pain medications administered to a haemorrhaging soldier are based upon limited scientific evidence, with the clear majority of supporting studies being conducted on anaesthetized animals. Specifically, the influence of low-dose ketamine, one of three analgesics employed in the pre-hospital setting by the US Army, on haemorrhagic tolerance in humans is unknown. For the first time in conscious males and females, the findings of the present study demonstrate that the administration of an analgesic dose of ketamine does not compromise tolerance to a simulated haemorrhagic insult. Increases in muscle sympathetic nerve activity during progressive lower-body negative pressure were not different between trials. Despite the lack of differences for muscle sympathetic nerve activity responses, mean blood pressure and heart rate were higher during moderate hypovolemia after ketamine vs. placebo administration. ABSTRACT Haemorrhage is the leading cause of battlefield and civilian trauma deaths. For a haemorrhaging soldier, there are several pain medications (e.g. ketamine) recommended for use in the prehospital, field setting. However, the data to support these recommendations are primarily limited to studies in animals. Therefore, it is unknown whether ketamine adversely affects physiological mechanisms responsible for maintenance of arterial blood pressure (BP) during haemorrhage in humans. In humans, ketamine has been demonstrated to raise resting BP, although it has not been studied with the concomitant central hypovolemia that occurs during haemorrhage. Thus, the present study aimed to test the hypothesis that ketamine does not impair haemorrhagic tolerance in humans. Thirty volunteers (15 females) participated in this double-blinded, randomized, placebo-controlled trial. A pre-syncopal limited progressive lower-body negative pressure (LBNP; a validated model for simulating haemorrhage) test was conducted following the administration of ketamine (20 mg) or placebo (saline). Tolerance was quantified as a cumulative stress index and compared between trials using a paired, two-tailed t test. We compared muscle sympathetic nerve activity (MSNA; microneurography), beat-to-beat BP (photoplethysmography) and heart rate (electrocardiogram) responses during the LBNP test using a mixed effects model (time [LBNP stage] × drug). Tolerance to the LBNP test was not different between trials (Ketamine: 635 ± 391 vs. Placebo: 652 ± 360 mmHg‧min, p = 0.77). Increases in MSNA burst frequency (time: P

The present study evaluated whether wearing a water-soaked t-shirt, with or without electric fan use, mitigates thermal and cardiovascular strain in older individuals exposed to hot and moderately humid conditions. Nine healthy older individuals (68 ± 4 yr; five women) completed three 120-min heat exposures (42.4 ± 0.2°C, 34.2 ± 0.9% relative humidity) on separate days while wearing a dry t-shirt (CON), a t-shirt soaked with 500 ml of tap water (WET), or a t-shirt soaked with 500 ml of tap water while facing an electric fan (2.4 ± 0.4 m/s; WET+FAN). Measurements included core and skin temperatures, evaporative mass losses, heart rate, and blood pressure. In the WET condition, elevations in core temperature were attenuated compared with DRY from 30 to 120 min and compared with WET+FAN from 30 to 90 min ( P < 0.05). Evaporative mass losses (inclusive of sweat and water losses from the shirt) were greatest in WET+FAN, followed by WET, and then DRY ( P < 0.01). Sweat losses were lowest in WET, followed by DRY, and then WET+FAN ( P < 0.01). Heart rate was lower only at 60 min in WET versus DRY ( P = 0.01). No differences in mean arterial pressure were observed ( P = 0.51). In conclusion, wearing a water-soaked t-shirt without, but not with, electric fan use is an effective heat management strategy to mitigate thermal strain and lower sweat losses in older individuals exposed to hot and moderately humid conditions. NEW & NOTEWORTHY In older individuals exposed to hot and moderately humid environments, electric fan use coupled with a water-soaked t-shirt exacerbates sweat losses without mitigating heat strain compared with a dry t-shirt. However, wearing a water-soaked t-shirt without fan use reduces sweat losses and attenuates heat strain compared with a dry t-shirt and a fan/water-soaked t-shirt combination. These findings suggest wearing a water-soaked t-shirt is an effective heat-management strategy for older individuals during heat waves when air conditioning is inaccessible.

New findings What is the central question of this study? Hypoxia reportedly does not impair thermoregulation during exercise in compensable heat stress conditions: does it have an impact on maximal heat dissipation and therefore the critical environmental limit for the physiological compensability of core temperature? What is the main finding and its importance? Although skin blood flow was higher in hypoxia, no differences in sweat rates or the critical environmental limit for the physiological compensability of core temperature - an indicator of maximal heat loss - were found compared to exercise in normoxia, indicating no influence of normobaric hypoxia on thermoregulatory capacity in warm conditions. Abstract Altered control of skin blood flow (SkBF) in hypoxia does not impair thermoregulation during exercise in compensable conditions, but its impact on maximal heat dissipation is unknown. This study therefore sought to determine whether maximum heat loss is altered by hypoxia during exercise in warm conditions. On separate days, eight males exercised for 90 min at a fixed heat production of ∼500 W in normoxia (NORM) or normobaric hypoxia (HYP, F I O 2 = 0.13) in a 34°C environment. Ambient vapour pressure was maintained at 2.13 kPa for 45 min, after which it was raised 0.11 kPa every 7.5 min. The critical ambient vapour pressure at which oesophageal temperature inflected upward (Pcrit ) indicated that maximum heat dissipation had been reached. Neither local sweat rates on the upper arm, back and forehead (average NORM: 1.46 (0.15) vs. HYP: 1.41 (0.16) mg cm-2 min-1 ; P = 0.59) nor whole-body sweat losses (NORM: 1029 (137) g vs. HYP: 1025 (150) g; P = 0.95) were different between trials. Laser-Doppler flux values (LDF; arbitrary units), an index of SkBF, were not different between NORM and HYP on the forearm (P = 0.23) or back (P = 0.73); however, when normalized as a percentage of maximum, LDF values tended to be higher in HYP compared to NORM at the forearm (condition effect, P = 0.05) but not back (P = 0.19). Despite potentially greater SkBF in hypoxia, there was no difference in Pcrit between conditions (NORM: 3.67 (0.35) kPa; HYP: 3.46 (0.39) kPa; P = 0.22). These findings suggest that hypoxia does not independently alter thermoregulatory capacity during exercise in warm conditions.

Objective To determine if a healthy newborn's age in hours (3, 6, or 9 hours after birth) affects thermoregulatory status after the first bath as indicated by axillary and skin temperatures. Design Quasi-experimental, mixed-model (between subjects and within subjects) design with hours of age as the nonrepeated variable and prebath and postbath temperatures as the repeated variables. Setting Family-centered care unit at an urban hospital in the southwestern United States. Participants Healthy newborns (N = 75) 37 weeks or more completed gestation. Methods Mothers chose time of first bath based on available time slots (n = 25 newborns in each age group). Research nurses sponge bathed the newborns in the mothers' rooms. Axillary temperature, an index of core temperature, was measured with a digital thermometer, and skin temperature, an index of body surface temperature, was measured with a thermography camera. Temperatures were taken before the bath; immediately after the bath; and 5, 30, 60, and 120 minutes after the bath. Immediately after the bath, newborns were placed in skin-to-skin care (SSC) for 60 or more minutes. Results We found a difference (p = .0372) in axillary temperatures between the 3- and 9-hour age groups, although this difference was not clinically significant (0.18 °F [0.10 °C]). We found no statistically significant differences in skin temperatures among the three age groups. Regardless of age group, axillary and skin temperatures initially decreased and then recovered after the bath. Conclusion For up to 2 hours postbath, axillary and skin temperatures were not different between healthy newborns bathed at 3, 6, or 9 hours of age. Thermography holds promise for learning about thermoregulation, bathing, and SSC.

Skeletal muscle blood flow is attenuated in aged humans performing dynamic exercise, which is due, in part, to impaired local vasodilatory mechanisms. Recent evidence suggests that folic acid improves cutaneous vasodilation during localized and whole body heating through nitric oxide-dependent mechanisms. However, it is unclear whether folic acid improves vasodilation in other vascular beds during conditions of increased metabolism (i.e., exercise). The purpose of this study was to test the hypothesis that folic acid ingestion improves skeletal muscle blood flow in aged adults performing graded handgrip and plantar flexion exercise via increased vascular conductance. Nine healthy, aged adults (two men and seven women; age: 68 ± 5 yr) performed graded handgrip and plantar flexion exercise before (control), 2 h after (acute, 5 mg), and after 6 wk (chronic, 5 mg/day) folic acid ingestion. Forearm (brachial artery) and leg (superficial femoral artery) blood velocity and diameter were measured via Duplex ultrasonography and used to calculate blood flow. Acute and chronic folic acid ingestion increased serum folate (both P < 0.05 vs. control). During handgrip exercise, acute and chronic folic acid ingestion increased forearm blood flow (both conditions P < 0.05 vs. control) and vascular conductance (both P < 0.05 vs. control). During plantar flexion exercise, acute and chronic folic acid ingestion increased leg blood flow (both P < 0.05 vs. control), but only acute folic acid ingestion increased vascular conductance ( P < 0.05 vs. control). Taken together, folic acid ingestion increases blood flow to active skeletal muscle primarily via improved local vasodilation in aged adults.NEW & NOTEWORTHY Our findings demonstrate that folic acid ingestion improves blood flow via enhanced vascular conductance in the exercising skeletal muscle of aged humans. These findings provide evidence for the therapeutic use of folic acid to improve skeletal muscle blood flow, and perhaps exercise and functional capacity, in human primary aging.Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/folic-acid-and-exercise-hyperemia-in-aging/ .

This study sought to assess the within-subject influence of acute hypoxia on exercise-induced changes in core temperature and sweating. Eight participants [1.75 (0.06) m, 70.2 (6.8) kg, 25 (4) yr, 54 (8) ml·kg−1·min−1] completed 45 min of cycling, once in normoxia (NORM; [Formula: see text] = 0.21) and twice in hypoxia (HYP1/HYP2; [Formula: see text]= 0.13) at 34.4(0.2)°C, 46(3)% RH. These trials were designed to elicit 1) two distinctly different %V̇o2peak [NORM: 45 (8)% and HYP1: 62 (7)%] at the same heat production (Hprod) [NORM: 6.7 (0.6) W/kg and HYP1: 7.0 (0.5) W/kg]; and 2) the same %V̇o2peak [NORM: 45 (8)% and HYP2: 48 (5)%] with different Hprod [NORM: 6.7 (0.6) W/kg and HYP2: 5.5 (0.6) W/kg]. At a fixed %V̇o2peak, changes in rectal temperature (ΔTre) and changes in esophageal temperature (ΔTes) were greater at end-exercise in NORM [ΔTre: 0.76 (0.19)°C; ΔTes: 0.64 (0.22)°C] compared with HYP2 [ΔTre: 0.56 (0.22)°C, P < 0.01; ΔTes: 0.42 (0.21)°C, P < 0.01]. As a result of a greater Hprod ( P < 0.01) in normoxia, and therefore evaporative heat balance requirements, to maintain a similar %V̇o2peak compared with hypoxia, mean local sweat rates (LSR) from the forearm, upper back, and forehead were greater (all P < 0.01) in NORM [1.10 (0.20) mg·cm−2·min−1] compared with HYP2 [0.71 (0.19) mg·cm−2·min−1]. However, at a fixed Hprod, ΔTre [0.75 (0.24)°C; P = 0.77] and ΔTes [0.63 (0.29)°C; P = 0.69] were not different in HYP1, compared with NORM. Likewise, mean LSR [1.11 (0.20) mg·cm−2·min−1] was not different ( P = 0.84) in HYP1 compared with NORM. These data demonstrate, using a within-subjects design, that hypoxia does not independently influence thermoregulatory responses. Additionally, further evidence is provided to support that metabolic heat production, irrespective of %V̇o2peak, determines changes in core temperature and sweating during exercise. NEW & NOTEWORTHY Using a within-subject design, hypoxia does not independently alter core temperature and sweating during exercise at a fixed rate of heat production. These findings also further contribute to the development of a methodological framework for assessing differences in thermoregulatory responses to exercise between various populations and individuals. Using the combined environmental stressors of heat and hypoxia we conclusively demonstrate that exercise intensity relative to aerobic capacity (i.e., %V̇o2max) does not influence changes in thermoregulatory responses.

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.

Introduction Excision of burned skin and subsequent grafting removes sweat glands and thereby impairs thermoregulation. Consequently, rehabilitation and associated exercise may be accompanied by a greater risk of hyperthermia, depending on exercise duration, intensity and environmental temperature. Current physical activity guidelines recommend adults perform at least 150 min of moderate-intensity exercise per week, which is often divided into 30-min daily sessions. This project tested the hypothesis that burn survivors could exercise for 30 min without excessive elevations in core body temperature, regardless of the total body surface area (%TBSA) burned or environmental temperature. Methods Ten subjects cycled for 60 min at 1) a moderate intensity (97±8 watts) in a thermoneutral environment (24°C, MOD_NEU), 2) a moderate intensity (100±17 watts) in a hot environment (39°C, MOD_HOT), and 3) a low intensity (65±10 watts) in a hot environment (39°C, LOW_HOT). Burn injuries were simulated by covering 0%, 20%, 40%, or 60% of the individual’s TBSA with an absorbent material that prevented sweat evaporation. Changes in gastrointestinal temperature (ΔTcore) were analyzed at 15-min increments throughout exercise. Results For the MOD_NEU trial, there were no differences in ΔTcore between the %TBSA coverage bouts at any time point during exercise. For the MOD_HOT trial, there were no differences in ΔTcore at 15 and 30 min of exercise regardless of the %TBSA coverage, while ΔTcore was appreciably elevated (P< 0.05) at 45 and 60 min of exercise for 20%+ TBSA bouts. For the MILD_HOT trial, there were no differences in ΔTcore at any time point between %TBSA bouts, with the sole exception of 60% simulated burn having a slightly greater ΔTcore (0.3±0.34°C; P< 0.05) at 60 min of exercise relative to the 0% TBSA bout. Conclusions These data indicate that individuals with up to 60% of their TBSA burned could exercise at a moderate intensity for 30 min, even in hot environmental conditions, without excessive elevations in body core temperature. Applicability of Research to Practice Individuals with significant burn injuries can benefit from exercise, without the risk of excessive hyperthermia, for up to 30 min in the heat or at least 60 min in an air conditioned space. Funding: DOD W81XWH-15-1-0647

Vast improvements in the survival rates following burn injuries has led to a greater number of patients living with a wide range of long-term impairments, activity limitations, and participation constraints. Therefore, long-term care is critical in this clinical population and necessitates appropriate rehabilitation strategies to maximize an individual's overall health. The purpose of this study was to test the hypothesis that the extent to which outcomes within the International Classification of Functioning, Disability, and Health (ICF) framework are improved following 6 months of unsupervised exercise training is influenced by the severity of a burn injury (i.e., percent body surface area injured). Outcome variables representing the dimensions of the ICF, body functions & structure, activity, and participation, were collected pre- and post- 6 months of exercise training in three groups of participants: non-injured control subjects (N = 11), subjects with moderate-level well-healed burn injuries (N = 13, 26 ± 6% body surface area burned), and subjects with high-level well-healed burn injuries (N = 20, 58 ± 15% body surface area burned). Exercise training improved lower extremity strength (changes in peak torque/kg body mass at 90 degrees/sec flexion: 30 ± 5% and extension: 36 ± 4%, p < 0.05) and functional activities (changes in sit to stand: -9 ± 4% and ascend stairs: -4 ± 1%; p < 0.05) in all groups. For outcome variables representing ICF levels of body functions & structure and activity, there were no differences at baseline or improvements made between the groups after training. That said, with the exception of the domain of functional activity (reported 17 ± 34% improvement in the high-level burn cohort, p < 0.05), no changes were revealed in the participation level of ICF indexed by health-related quality of life questionnaires. These findings support the utilization of a 6-month unsupervised exercise training program in the long-term rehabilitation of individuals with burn injuries; that is, improvements in body functions & structure and activity can be achieved with an exercise regimen regardless of the severity of burn injury.

The U.S. Army’s Standards of Medical Fitness (AR 40-501) states: “Prior burn injury (to include donor sites) involving a total body surface area of 40 percent or more does not meet the standard”. However, the standard does not account for the interactive effect of burn injury size and air temperature on exercise thermoregulation. PURPOSE: To evaluate whether the detrimental effect of a simulated burn injury on exercise thermoregulation is dependent upon air temperature. METHODS: On eight occasions, nine males cycled for 60 min at a fixed metabolic heat production (6 W·kg(−1)) in air temperatures of 40°C or 25°C with simulated burn injuries of 0% (Control), 20%, 40%, or 60% of total body surface area (TBSA). Burn injuries were simulated by covering the skin with an absorbent, vapor-impermeable material to impede evaporation from the covered areas. Core temperature was measured in the gastrointestinal tract via telemetric pill. RESULTS: In 40°C conditions, greater elevations in core temperature were observed with 40% and 60% TBSA simulated burn injuries vs. Control (P < 0.01). However, at 25°C, core temperature responses were not different vs. Control with 20%, 40%, and 60% TBSA simulated injuries (P = 0.97). The elevation in core temperature at the end of exercise was greater in the 40°C environment with 20%, 40% and 60% TBSA simulated burn injuries (P ≤ 0.04). CONCLUSION: Simulated burn injuries ≥20% TBSA exacerbate core temperature responses in hot, but not temperate, air temperatures. These findings suggest that the U.S. Army’s standard for inclusion of burned soldiers is appropriate for hot conditions, but could lead to the needless discharge of soldiers who could safely perform their duties in cooler training/operational settings.

Long-term rehabilitative strategies are important for individuals with well-healed burn injuries. Such information is particularly critical because patients are routinely surviving severe burn injuries given medical advances in the acute care setting. The purpose of this study was to test the hypothesis that a 6-mo community-based exercise training program will increase maximal aerobic capacity (V̇o2max) in subjects with prior burn injuries, with the extent of that increase influenced by the severity of the burn injury (i.e., percent body surface area burned). Maximal aerobic capacity (indirect calorimetry) and skeletal muscle oxidative enzyme activity (biopsy of the vastus lateralis muscle) were measured pre- and postexercise training in noninjured control subjects ( n = 11) and in individuals with well-healed burn injuries ( n = 13, moderate body surface area burned; n = 20, high body surface area burned). Exercise training increased V̇o2max in all groups (control: 15 ± 5%; moderate body surface area: 11 ± 3%; high body surface area: 11 ± 2%; P < 0.05), though the magnitude of this improvement did not differ between groups ( P = 0.7). Exercise training also increased the activity of the skeletal muscle oxidative enzymes citrate synthase ( P < 0.05) and cytochrome c oxidase ( P < 0.05), an effect that did not differ between groups ( P = 0.2). These data suggest that 6 mo of progressive exercise training improves V̇o2max in individuals with burn injuries and that the magnitude of body surface area burned does not lessen this adaptive response.

The U.S. Army’s Standards of Medical Fitness, AR 40–501, state that “Prior burn injury (to include donor sites) involving a total body surface area of 40 percent or more does not meet the standard”. Inclusion of donor sites (sites harvested for skin grafts) in this Standard implies that thermoregulatory function is impaired within donor sites during exercise-heat stress; however, supporting evidence is currently lacking. PURPOSE: To test the hypothesis that well-healed donor and non-injured sites demonstrate similar elevations in skin blood flow and sweating during exercise-induced hyperthermia. METHODS: Twenty burn survivors (>1 year post-injury; four females) cycled for 60 min in a 39.7 ± 0.3°C and 21.1 ± 3.3% relative humidity environment at ~50% of maximal aerobic capacity. Core and mean skin temperatures were recorded throughout exercise. Skin blood flow (laser-Doppler imaging) was measured at baseline and after exercise within donor (LDF(DON)) and adjacent non-injured control (LDF(CON)) sites. At 45 min of exercise, local sweat rates (Technical Absorbents) were measured within the same donor (LSR(DON)) and non-injured (LSR(CON)) areas. RESULTS: After 60 min of exercise, core and skin temperatures reached 38.2 ± 0.4°C and 35.5 ± 1.2°C, respectively. The increase in skin blood flow from baseline to end-exercise (LDF(DON): 91.6 ± 44.5 AU; LDF(CON): 106.0 ± 61.6 AU; P = 0.17) and local sweat rates (LSR(DON): 0.46 ± 0.26 mg cm(−2) min(−1); LSR(CON): 0.53 ± 0.25 mg cm(−2) min(−1); P = 0.14) were not different between donor and non-injured control sites. CONCLUSION: Well-healed donor sites retain the ability to increase skin blood flow and sweating during exercise-heat stress, providing evidence against the inclusion of donor sites when determining whether a burn injury meets the Army’s Standards of Medical Fitness.

Long-term burn survivors have reduced aerobic capacity, placing them at increased risk for cardiovascular disease, morbidity, and mortality. However, the exact mechanism contributing to a reduced aerobic capacity remains incompletely understood, but may be related to adverse cardiovascular remodeling. Therefore, it was hypothesized that well-healed burn survivors would exhibit adverse left ventricular (LV) remodeling and impaired LV function. To test this hypothesis, 22 well-healed moderately burned individuals (age: 41 ± 14 years; BMI: 27.7 ± 5.4 kg/m(2); male/female: 12/10; extent of burn: 37 ± 12 %BSA), 11 well-healed severely burned individuals (age: 43 ± 12 years; BMI: 29.5 ± 5.8 kg/m(2); male/female: 8/3; extent of burn: 73 ± 11 %BSA), and 12 healthy, age-matched controls (age: 34 ± 9 years; BMI: 28.6 ± 5.2 kg/m(2); male/female: 5/7) were enrolled in the study. All subjects were sedentary, performing less than 30 minutes of aerobic exercise per day, 3 days per week. LV morphology and function were assessed via cardiac magnetic resonance imaging. In contrast to the hypothesis, neither the presence nor severity of burn injury adversely affected LV morphology or function, when compared with equally sedentary nonburned controls. However, of note, LV mass of all three groups was in the lowest 5th percentile compared with normative values. Finally, group differences in LV morphology were largely explained by differences in aerobic capacity. Taken together, these data suggest a prior burn injury itself does not result in pathological remodeling of the LV and support a role for aerobic exercise training to improve cardiac function.

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.

Humans maintain a relatively constant core temperature through the dynamic balance between endogenous heat production and heat dissipation to the surrounding environment. In response to metabolic or environmental disturbances to heat balance, the autonomic nervous system initiates cutaneous vasodilation and eccrine sweating to facilitate higher rates of dry (primarily convection and radiation) and evaporative transfer from the body surface; however, absolute heat losses are ultimately governed by the properties of the skin and the environment. Over the duration of a heat exposure, the cumulative imbalance between heat production and heat dissipation leads to body heat storage, but the consequent change in core temperature, which has implications for health and safety in occupational and athletic settings particularly among certain clinical populations, involves a complex interaction between changes in body heat content and the body's morphological characteristics (mass, surface area, and tissue composition) that collectively determine the body's thermal inertia. The aim of this review is to highlight the biophysical aspects of human core temperature regulation by outlining the principles of human energy exchange and examining the influence of body morphology during exercise and environmental heat stress. An understanding of the biophysical factors influencing core temperature will enable researchers and practitioners to better identify and treat individuals/populations most vulnerable to heat illness and injury during exercise and extreme heat events. Further, appropriate guidelines may be developed to optimize health, safety, and work performance during heat stress.

NEW FINDINGS What is the central question of this study? Does folic acid supplementation alleviate thermoregulatory and cardiovascular strain of older adults during exposure to extreme heat and humidity? What is the main finding and its importance? Folic acid supplementation for 6 weeks did not affect whole-limb blood flow/vasodilatation, core and skin temperatures, heart rate, blood pressure and cardiac output. Thus, 6 weeks of folic acid supplementation does not alleviate thermoregulatory or cardiovascular strain of healthy older adults exposed to extreme heat and humidity. ABSTRACT Folic acid supplementation reverses age-related reductions in cutaneous vasodilatation during passive heating. However, it is unknown if folic acid supplementation alleviates thermoregulatory and cardiovascular strain experienced by older adults during heat exposure. We evaluated the effect of folic acid supplementation on thermoregulatory and cardiovascular responses of nine healthy older adults (61-72 years, 3 males/6 females) exposed to extreme heat and humidity. Participants rested at 42°C while relative humidity was increased from 30% to 70% in 2% increments every 5 min. The protocol was performed before (CON) and after (FOLIC) 6 weeks of folic acid supplementation (5 mg day-1 ). Local cutaneous vascular conductance (CVC, laser-Doppler flowmetry), forearm vascular conductance (FVC, Doppler ultrasound), mean skin and oesophageal temperatures, heart rate, blood pressure and cardiac output were measured. Folic acid supplementation increased fasting serum folate concentrations (P

Acute acetaminophen (ACT) ingestion has been reported to reduce thermal strain during cycling in the heat. In this study, nine active participants ingested 20 mg of ACT per kg of total body mass (ACT) or a placebo (PLA), 60 min prior to cycling at a fixed rate of metabolic heat production (ACT: 8.3 ± 0.3 W/kg; PLA: 8.5 ± 0.5 W/kg), which was equivalent to 55 ± 6% VO2max , for 60 min at 34.5 ± 0.1 °C, 52 ± 1% relative humidity. Resting rectal temperature (Tre ; ACT: 36.70 ± 0.17 °C; PLA: 36.80 ± 0.16 °C, P = 0.24), esophageal temperature (Tes ; ACT: 36.54 ± 0.22 °C; PLA: 36.61 ± 0.17 °C, P = 0.50) and mean skin temperature (Tsk ; ACT: 34.00 ± 0.14 °C; PLA: 33.96 ± 0.20 °C, P = 0.70) were all similar among conditions. At end-exercise, no differences in ΔTre (ACT: 1.12 ± 0.15 °C; PLA: 1.11 ± 0.21 °C, P = 0.92), ΔTes (ACT: 0.90 ± 0.28 °C; PLA: 0.88 ± 0.23 °C, P = 0.84), ΔTsk (ACT: 0.80 ± 0.39 °C; PLA: 0.70 ± 0.46 °C, P = 0.63), mean local sweat rate (ACT: 1.02 ± 0.15 mg/cm(2) /min; PLA: 1.02 ± 0.13 mg/cm(2) /min, P = 0.98) and whole-body sweat loss (ACT: 663 ± 83 g; PLA: 663 ± 77 g, P = 0.995) were evident. Furthermore, ratings of perceived exertion and thermal sensation and thermal comfort were not different between ACT and PLA conditions. In conclusion, ACT ingested 60 min prior to moderate intensity exercise in hot-humid conditions does not alter physiologic thermoregulatory control nor perceived strain.

Heat waves continue to claim lives, with the elderly and poor at greatest risk. A simple and cost-effective intervention is an electric fan, but public health agencies warn against their use despite no evidence refuting their efficacy in heat waves. A conceptual human heat balance model can be used to estimate the evaporative requirement for heat balance, the potential for evaporative heat loss from the skin, and the predicted sweat rate, with and without an electrical fan during heat wave conditions. Using criteria defined by the literature, it is clear that fans increase the predicted critical environmental limits for both the physiological compensation of endogenous/exogenous heat, and the onset of cardiovascular strain by an air temperature of ∼3-4 °C, irrespective of relative humidity (RH) for the young and elderly. Even above these critical limits, fans would apparently still provide marginal benefits at air temperatures as high as 51.1 °C at 10%RH for young adults and 48.1 °C at 10%RH for the elderly. Previous concerns that dehydration would be exacerbated with fan use do not seem likely, except under very hot (>40 °C) and dry (

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.

The effect of acute increases in cardiac contractility on cerebral blood flow (CBF) remains unknown. We hypothesized that the external carotid artery (ECA) downstream vasculature modifies the direct influence of acute increases in heart rate and cardiac function on CBF regulation. Twelve healthy subjects received two infusions of dobutamine [first a low dose (5 μg·kg−1·min−1) and then a high dose (15 μg·kg−1·min−1)] for 12 min each. Cardiac output, blood flow through the internal carotid artery (ICA) and ECA, and echocardiographic measurements were performed during dobutamine infusions. Despite increases in cardiac contractility, cardiac output, and arterial pressure with dobutamine, ICA blood flow and conductance slightly decreased from resting baseline during both low- and high-dose infusions. In contrast, ECA blood flow and conductance increased appreciably during both low- and high-dose infusions. Greater ECA vascular conductance and corresponding increases in blood flow may protect overperfusion of intracranial cerebral arteries during enhanced cardiac contractility and associated increases in cardiac output and perfusion pressure. Importantly, these findings suggest that the acute increase of blood perfusion attributable to dobutamine administration does not cause cerebral overperfusion or an associated risk of cerebral vascular damage. NEW & NOTEWORTHY A dobutamine-induced increase in cardiac contractility did not increase internal carotid artery blood flow despite an increase in cardiac output and arterial blood pressure. In contrast, external carotid artery blood flow and conductance increased. This external cerebral blood flow response may assist with protecting from overperfusion of intracranial blood flow.

We sought to identify the appropriate exercise intensity for unbiased comparisons of changes in rectal temperature (ΔT re ) and local sweat rates (LSR) between groups unmatched for body size during uncompensable heat stress. Sixteen males vastly different in body morphology were separated into two equal groups [small (SM): 65.8 ± 6.2 kg, 1.8 ± 0.1 m 2 ; large (LG): 100.0 ± 13.1 kg, 2.3 ± 0.1 m 2 ], but matched for sudomotor thermosensitivity (SM: 1.3 ± 0.6; LG: 1.1 ± 0.4 mg·cm −2 ·min −1 ·°C −1 ). The maximum potential for evaporation (E max ) for each participant was assessed using an incremental humidity protocol. On separate occasions, participants then completed 60 min of cycling in a 35°C and 70% RH environment at (1) 50% of VO 2max , (2) a heat production (H prod ) of 520 W, (3) H prod relative to mass (6 W·kg −1 ), and (4) H prod relative to mass above E max (3 W·kg −1 >E max ). E max was similar between LG (347 ± 39 W, 154 ± 15 W·m −2 ) and SM (313 ± 63 W, 176 ± 34 W·m −2 , P > 0.12). ΔT re was greater in SM compared to LG at 520 W (SM: 1.5 ± 0.5; LG 0.8 ± 0.3°C, P 0.001) and at 50% of VO 2max (SM: 1.4 ± 0.5; LG 0.9 ± 0.3°C, P 0.001). However, ΔT re was similar between groups when H prod was either 6 W·kg −1 (SM: 0.9 ± 0.3; LG 0.9 ± 0.2°C, P = 0.98) and 3 W·kg −1 >E max (SM: 1.4 ± 0.5; LG 1.3 ± 0.4°C, P = 0.99). LSR was similar between LG and SM irrespective of condition, suggesting maximum LSR was attained (SM: 1.10 ± 0.23; LG: 1.07 ± 0.35 mg·cm −2 ·min −1 , P = 0.50). In conclusion, systematic differences in ΔT re and LSR between groups unmatched for body size during uncompensable heat stress can be avoided by a fixed H prod in W·kg −1 or W·kg −1 >E max .