Acute Heat Exposure Research Articles

Regularly drinking desert birds have greater evaporative cooling capacity and higher heat tolerance limits than non‐drinking species

Abstract Surface water is a critical resource for many birds inhabiting arid regions, but the implications of regular drinking and dependence on surface water for the evolution of thermal physiology remain largely unexplored. We hypothesized that avian thermoregulation in the heat has evolved in tandem with the use of surface water and predicted that (a) regularly drinking species have a greater capacity to elevate rates of evaporative water loss (EWL) compared to non‐drinking species, and (b) heat tolerance limits (HTLs) are higher among drinking species. To test these predictions, we quantified thermoregulatory responses to high air temperature (Ta) in 12 species of passerines from the South African arid zone and combined these with values for an additional five species. We categorized each species as either: (a) water‐dependent, regularly drinking, or (b) water‐independent, occasional‐/non‐drinking. In support of our predictions, both conventional and phylogenetically independent analyses revealed that evaporative scope (the ratio of maximum EWL to minimum thermoneutral EWL) during acute heat exposure was significantly higher among drinking species. Moreover, evaporative scope was significantly and positively related to HTL (i.e. maximum air temperature tolerated before the onset of severe hyperthermia). These findings offer new insights into the co‐evolution of water dependence, movement ecology and thermal physiology in the context of trade‐offs between dehydration avoidance and resistance to lethal hyperthermia in hot desert habitats. A free Plain Language Summary can be found within the Supporting Information of this article.

Differences in oxidative stress across seasons and ability to cope with environmental mismatch in muscle and brain of black‐capped chickadees Poecile atricapillus and rock pigeons Columba livia

Resident birds in temperate areas respond to seasonally fluctuating temperatures by adjusting their physiology so as to match thermogenic requirements of their environment. Climate change is predicted to increase the frequency of heat waves, increasing the likelihood that birds will face environmental mismatch. Changes in BMR due to seasonality or anomaly events should show effects to the oxidative stress system. We examined the effects of chronic and acute heat exposure on muscle and brain tissue total antioxidant capacity, enzymatic activities of catalase (CAT) and glutathione peroxidase (GPx) and lipid peroxidation (LPO) damage in two temperate bird species of differing body masses and ecological strategies, the black‐capped chickadee Poecile atricapillus and the rock pigeon Columba livia, across three seasons. We found that heat stress did not alter oxidative stress in either species or tissue. But, in muscle, rock pigeons and black‐capped chickadees demonstrated similar seasonal changes where peroxyl scavenging capacity was highest in the fall, hydroxyl scavenging capacity was higher in fall and summer. CAT activity was lowest in the fall and highest in the summer, GPx activity was highest in the fall, and LPO damage was highest in the summer but lowest in the fall. In brain, we found that scavenging capacity to hydroxyl radicals was highest in fall and summer for rock pigeons, whereas it was only elevated in the summer for black‐capped chickadees. Our data suggest that the oxidative stress system is slow to change seasonally.

Autophagy and Heat Shock Protein 70 Expression During Acute Heat Stress in Isosmotic and Hyperosmotic Conditions in Peripheral Blood Mononuclear Cells from Young Adults: Preliminary Data

Heat‐stress induced dehydration is associated with elevations in extracellular osmolality. To counteract the resultant osmotic stress, cells employ several stress response systems including the heat shock protein (HSP) and autophagy pathways. HSPs refold damaged proteins, whereas autophagy acts to degrade damaged cellular components, thereby promoting cellular survival. Accumulating evidence indicates a coordinated response between the HSP and autophagy systems, whereby both systems are activated under conditions of heat stress. However, it remains unknown whether elevated extracellular osmolality augments the HSP and autophagic response to whole‐body heat stress in humans. Thus, the purpose of this study was to examine changes in HSP (HSP70) and autophagy resulting from elevated intravascular osmolality during acute heat exposure. We hypothesized that both autophagy and HSP70 protein expression would be greater under hyperosmotic stress compared to isosmotic conditions. On separate days (separated by ~1 week), six young men (mean [SD]; 27 [5] years) received a 90‐min intravenous infusion with either isosmotic (ISO; 0.9% NaCl; 0.200 mL·kg−1·min−1) or hyperosmotic (HYP; 3.0% NaCl; 0.125 mL·kg−1·min−1) saline, followed by passive whole‐body heating to ~0.8°C above baseline esopha‐‐‐geal temperature using a water perfused suit. Serum osmolality was determined via freeze‐point depression from blood samples at baseline and at the end of passive heating. Peripheral blood mononuclear harvested at these time‐points were analyzed via Western blotting to assess changes in HSP70 protein and proteins indicative of autophagic activity including microtubule associated protein 1 light chain 3 beta‐II (LC3‐II) and p62/sequesterome‐1 (p62). All values were normalized to β‐actin and reported as fold changes relative to baseline. Data are presented as means and standard deviations (SD) and were compared between‐conditions at the end of passive heating using paired (2‐tailed) t‐tests (α=0.05). At the end of heating, serum osmolality was higher during HYP when compared to ISO (298 [SD 3] vs. 291 [SD 3]; p<0.001). During passive heating, LC3‐II was increased (2.20 [SD 2.12] vs. 1.62 [SD 1.47]; p=0.04) and p62 protein was reduced (0.47 [SD 0.33] vs. 1.20 [SD 0.56]; p=0.01) in HYP compared to ISO, indicating greater autophagic activation during HYP. Despite this, HSP70 protein was lower under HYP conditions following heating than ISO (0.72 [SD 0.24] vs. 1.20 [SD 0.19]; p=0.04). Contrary to our hypothesis, these preliminary findings indicate greater reliance on the autophagic response rather than simultaneous activation of HSP70 during acute heat exposure with super‐imposed hyperosmotic stress.Support or Funding InformationNational Science and Engineering Research Council of Canada

Sex Differences in Hemodynamic Response to Acute Passive Heat Exposure

A single bout of passive heat stress elicits an increase in cardiac output, a redistribution of blood flow, and a subsequent increase in conduit vessel shear stress. This increased shear stress acutely improves vascular function in a dose‐dependent manner and potentiates many of the beneficial vascular adaptations that accompany chronic heat therapy. However, physical and physiologic differences exist between sexes and influence the thermoregulatory response to passive heat stress. It is unknown if these sex‐related thermoregulatory differences alter the adaptive shear stimulus accompanying passive heat stress.PurposeTo compare the hemodynamic response to acute passive heat exposure (APHE) between sexes.Methods10 women (W) and 11 men (M) between the ages of 18–31 years completed a one‐hour APHE session immersed to the level of the sternum in 40°C water. W were studied under low hormone conditions. Rectal temperature (Tre), mean arterial pressure (MAP), and brachial and carotid artery hemodynamics (ultrasound) were measured at baseline (seated rest before APHE) and every 15 min throughout APHE. Automated wall‐tracking software was used to determine brachial and carotid diameter, velocity, flow, and total shear rate. Data are reported as mean ± SEM. Subject characteristics, reported as mean ± SD, were compared using unpaired t‐tests. A 2 X 5 mixed model ANOVA was used to compare Tre, MAP, and brachial and carotid hemodynamics across time and between sexes.ResultsBoth body mass (W: 62.9 ± 8.1 kg, M: 74.2 ± 5.1 kg, P < 0.01) and body surface area (W: 1.71 ± 0.14 m2, M: 1.93 ± 0.10 m2, P < 0.001) were lower in W compared to M. W had a higher Tre than M (P < 0.05) at baseline (W: 37.5 ± 0.1°C, M: 37.2 ± 0.1°C) and after 60 min APHE (W: 38.7 ± 0.03°C, M: 38.5 ± 0.1°C). W had a lower MAP than M (P < 0.05) at baseline (W: 85 ± 2 mmHg, M: 88 ± 2 mmHg) and throughout APHE (W: 74 ± 2 mmHg, M: 82 ± 3 mmHg at 60 min APHE). W and M had a similar baseline brachial total shear rate (W: 170 ± 30 1/s, M: 105 ± 19 1/s). Brachial total shear rate was elevated to a greater extent in W than M during APHE (P < 0.01), reaching 651 ± 49 1/s and 396 ± 24 1/s at 60 min APHE, respectively. The sex difference in brachial shear response to APHE was the result of a greater increase in brachial velocity seen in W (+47 ± 6 cm/s) compared to M (+35 ± 4 cm/s) with APHE (P < 0.1). This elevated brachial velocity allowed for a similar increase in brachial blood flow between sexes with APHE (W: +339 ± 53 mL/min, M: +369 ± 37 mL/min) despite the smaller brachial diameter in W compared to M (P < 0.0001) at baseline (W: 0.31 ± 0.01 cm, M: 0.41 ± 0.01 cm) and throughout APHE (W: 0.37 ± 0.01 cm, M: 0.46 ± 0.01cm at 60 min APHE). In contrast, no differences were seen between sexes in carotid total shear rate, flow, velocity, or diameter at baseline or throughout APHE.ConclusionThese data indicate the presence of an artery‐specific sex difference in the hemodynamic response to a single bout of passive heat stress. Although a “threshold” or “dose‐response” relationship between shear stress and vascular adaptation has not been determined, these findings may have implications for sex‐specific vascular adaption accompanying chronic heat therapy.Support or Funding InformationAPS Porter Pre‐Doctoral Fellowship

The Impact of Acute Hot or Cold Water Immersion on Post‐Exercise Blood Pressure Regulation

Acute exercise, heat exposure, and cold exposure independently produce short‐term changes in blood pressure (BP). It is currently unknown whether post‐exercise hot water immersion (HWI) or cold water immersion (CWI) impact the magnitude or timeline of changes in BP observed following exercise. The objective of this study was to examine the impact of post‐exercise HWI and CWI on systolic (SBP), diastolic (DBP), and mean arterial pressure (MAP). Ten healthy (6M, 4F; BMI: 23.7±1.7; BP: 125±3/73±3 mmHg) individuals took part in 3 randomized, counterbalanced trials consisting of evening interval exercise (~7k treadmill walking and running with 8×400m high‐intensity intervals) followed by a 30 minute treatment of HWI (immersed to chest in 39–40°C tub), CWI (immersed to chest in 14–15°C tub) or time control (CON; seated passive recovery at room temperature). Brachial BP was measured in triplicate in a seated position pre‐exercise (Pre‐Ex), immediately post‐exercise (Post‐Ex), immediately post‐treatment (Post‐Tx), and following 12h overnight recovery (12h post). Results were analyzed using a 2‐way repeated measures ANOVA. Significant time by treatment interactions were observed for DBP (p=0.0070) and MAP (p=0.0059). Pre‐Ex and Post‐Ex, no differences were observed between groups. Post‐Tx, CWI resulted in increased DBP (+12 ± 3 mmHg; p<0.0001) and MAP (+9 ± 2 mmHg; p=0.0002) compared with Pre‐Ex, while DBP and MAP remained steady in HWI and CON. 12‐hr post‐exercise, both MAP (−6 ± 2mmHg; p=0.0431) and DBP (−7 ± 2mmHg; p=0.0159) were lower than Pre‐Ex in HWI, and no differences were seen in CWI or CON. These data indicate that post‐exercise CWI temporarily increases DBP and MAP, but does not affect blood pressure 12‐h post‐exercise. In contrast, post‐exercise HWI leads to prolonged reductions in DBP and MAP in healthy individuals. Those engaging in exercise to control or reduce blood pressure may experience a greater benefit with the addition of post‐exercise HWI. Future research should examine whether this effect is similarly observed in hypertensive individuals, as first‐morning blood pressure is an important indicator of disease severity and progression.

Heat Stress Nephropathy and Cardiovascular Surgery-Associated Renal Failure: Similarities and Implications

Climate changes associated with global warming are producing challenges increasingly relevant to clinicians. Rising temperatures and extended heat waves are associated with a growing incidence of a recently described condition termed heat sensitivity nephropathy. Considering all causes of acute kidney injury and chronic kidney disease, those producing renal dysfunction consequent to cardiovascular surgery may most closely overlap those tied to kidney disease following excessive chronic or acute heat exposure. In this review, heat sensitivity nephropathy and cardiovascular surgery related renal injury are characterized and compared. While both are global in distribution, the former has highest prevalence in remote, rural areas and difficult to study and quantify. Renal injury following cardiovascular surgery, occurring by contrast in relatively controlled settings, is more amenable to evaluation of diagnostic approaches, prognostic indicators, and potential treatments. Such findings may ultimately apply not only to surgically-related kidney damage but to heat sensitivity nephropathy as well. Despite many studies addressing post-cardiovascular surgery renal failure, no single management method has emerged as definitively superior. Nonetheless, reasonably standardized worldwide conduct of cardiac and vascular surgery provides fertile conditions for research that could lead to improved diagnostic and therapeutic approaches. Such findings may ultimately apply to not only surgically-related renal injury but perhaps also to heat sensitivity nephropathy. Instead of anticipating discovery of major isolated preventative or treatment methods applicable to either cause of renal failure, it is more realistic that a series of marginally successful measures employed in combination will engender the most nearterm progress. Potentially complimenting currently available options is biomarker analysis that may better guide both renal injury diagnosis and treatment efficacy assessment.

Effects of Acute Exposure to Heat Stress on Immunological and Lipid Parameters in Rats

Background: Exposure to heat stress can result in lipid parameters alterations as well as immunological responses. This study was aimed to investigate these alterations and responses at different humidity and temperatures levels under controlled laboratory conditions in adult male Sprague–Dawley rats. Methods: A total 15 adult male Sprague–Dawley rats, weighing between 200 and 250 g, 10-11 weeks of age, were used in the evaluation. After one week, animals were randomly divided into three equal groups of 5 animals each. Reference group (group1) was housed in the cage under WBGT of 20(1) according to experimental design. Also, animals were subjected to mild (WBGT of 29 ( 1)) and hotter (WBGT of 33(1)) conditions (8 hr/day for one day) in the exposure chamber as group2 and group3, respectively. At the end of exposure to heat stress, blood samples were collected from the heart of rats and different parameters were determined. Results: Based on results, acute heat exposure significantly caused a decrease in serum IgG, IgM, IgA of rats in the case group compared to control group (P<0.05). Conversely, acute heat exposure resulted in a significant increase in the levels of IgE (P<0.05). There was no statistical difference for the lipid parameters after exposure to acute heat stress compared with the control group (P > 0.05). Conclusion: Acute heat stress may affect immune responses depending on the intensity of the exposure. Higher environmental temperatures (WBGT≥32°C) cause more severe changes in plasma immunoglobulins.

Venous blood gas and chemistry components are moderately heritable in commercial white egg-laying hens under acute or chronic heat exposure.

ABSTRACTHeat stress has a large negative impact on poultry around the world in both intensive and small-scale production systems. Better understanding of genetic factors contributing to response to high ambient temperatures would provide a basis to develop strategies for alleviating negative impacts of heat on poultry production. The objective of this work was to characterize the genetic control (heritability estimate and quantitative trait loci (QTL)) of blood chemistry components before and after exposure to acute and chronic high ambient temperature in a commercial egg laying line Hy-Line W-36 female parent line mature hens were exposed to 4 wk of daily cyclic heat exposure. Blood was collected pre-heat, on the first day of heat, and 2 and 4 wk post heat initiation and analyzed immediately using an i-STAT® hand-held blood analyzer. Thirteen blood components were quantified at the 4 time points: pH, pCO2, pO2, HCO3, TCO2, sO2, iCa, Na, K, base excess, glucose, “hematocrit” (estimated from blood electrical conductivity, BEC), and “hemoglobin” (calculated from BEC). Heritabilities were estimated using genomic relationship information obtained from 600k SNP chip data. All 13 parameters exhibited a significant change after 5 h of heat exposure and most did not return to pre-heat levels throughout the duration of the study. Eight parameters (base excess, glucose, hemoglobin, HCO3, hematocrit, K, pCO2, TCO2) had heritability estimates differing from zero at one or more time points (0.21 to 0.45). The traits with significant heritability would be good candidates for use as biomarkers in a selection program if they are correlated with traits of economic importance that are more difficult to measure. QTL were identified for nine of the traits at one or more time point. These nine traits, however, did not have significant heritability estimates suggesting that while some QTL have been identified their effects are generally small.

Serum from young, sedentary adults who underwent passive heat therapy improves endothelial cell angiogenesis via improved nitric oxide bioavailability

ABSTRACTRationale: Passive heat therapy improves vascular endothelial function, likely via enhanced nitric oxide (NO) bioavailability, although the mechanistic stimuli driving these changes are unknown. Objective: To determine the isolated effects of circulating (serum) factors on endothelial cell function, particularly angiogenesis, and NO bioavailability. Methods and Results: Cultured human umbilical vein endothelial cells (HUVECs) were exposed to serum collected from 20 healthy young (22 ± 1 years) adults before (0 wk), after one session of water immersion (Acute HT), and after 8 wk of either heat therapy (N = 10; 36 sessions of hot water immersion; session 1 peak rectal temperature: 39.0 ± 0.03°C) or sham (N = 10; 36 sessions of thermoneutral water immersion). Serum collected following acute heat exposure and heat therapy improved endothelial cell angiogenesis (Matrigel bioassay total tubule length per frame, 0 wk: 69.3 ± 1.9 mm vs. Acute HT: 72.8 ± 1.4 mm, p = 0.04; vs. 8 wk: 73.0 ± 1.4 mm, p = 0.03), with no effects of sham serum. Enhanced angiogenesis was NO-mediated, as addition of the NO synthase (NOS) inhibitor L-NNA to the culture media abolished differences in tubule formation across conditions (0 wk: 71.3 ± 1.8 mm, Acute HT: 71.6 ± 1.9 mm, 8 wk: 70.5 ± 1.6 mm, p = 0.69). In separate experiments, we found that abundance of endothelial NOS (eNOS) was unaffected by Acute HT serum (p = 0.71), but increased by 8 wk heat therapy serum (1.4 ± 0.1-fold from 0 wk, p < 0.01). Furthermore, increases in eNOS were related to improvements in endothelial tubule formation (r2 = 0.61, p < 0.01). Conclusions: Passive heat therapy beneficially alters circulating factors that promote NO-mediated angiogenesis in endothelial cells and increase eNOS abundance. These changes may contribute to improvements in vascular function with heat therapy observed in vivo.Abbreviations: Ang-1: angiopoietin-1; ANOVA: analysis of variance; bFGF: basic fibroblast growth factor; CV: cardiovascular; CVD: cardiovascular diseases; eNOS: endothelial nitric oxide synthase; HSPs: heat shock proteins; HT: heat therapy; HUVECs: human umbilical endothelial cells; L-NNA: Nω-nitro-L-arginine; MnSOD: manganese superoxide dismutase; NO: nitric oxide; NOS: nitric oxide synthase; PBMCs: peripheral blood mononuclear cells; RM: repeated measures; sFlt-1: soluble VEGF receptor; SOD: superoxide dismutase; TGF-β: transforming growth factor- β; VEGF: vascular endothelial growth factor

Thermoregulatory Response to Acute Passive Heat Exposure in Individuals with Low‐level Spinal Cord Injury

Spinal cord injury (SCI) impacts both the afferent and efferent pathways of the thermoregulatory system and may result in delayed and/or diminished sweating, skin blood flow, and ventilatory responses to whole body heating. Because the magnitude of these impairments is largely related to the level and severity of injury, it is possible that individuals with low‐level SCI initiate an appropriate thermoregulatory response that supports the maintenance of core temperature within a safe range during acute heat exposure.PurposeTo characterize and compare the thermoregulatory response to acute passive heat exposure (APHE) in individuals with low‐level SCI and the able‐bodied (AB) population. We hypothesized that individuals with low‐level SCI would display attenuated skin blood flow and ventilatory responses to heating compared to AB individuals, but that these responses would be sufficient to maintain core temperature within a safe range during a one‐hour bout of APHE.MethodsFour individuals (1F) with low‐level SCI (T8‐T11) and 8 AB individuals (4 F) completed a one‐hour APHE session immersed to the level of the sternum in 40°C water. During a period of seated rest, baseline values of skin red blood cell (RBC) flux, ventilation (V̇E), and rectal temperature (Tre) were measured. RBC flux, measured at two sites on the ventral forearm (laser Doppler flowmetry), was divided by mean arterial pressure to calculate cutaneous vascular conductance (CVC). Local heating to 44°C was performed following APHE, and data are presented as a percentage of maximal CVC (% CVCmax). Throughout APHE, average CVC was assessed every 5 minutes, V̇E was measured every 20 minutes, and Tre was recorded every 5 minutes. Data are reported as mean ± SEM. Statistical analyses were conducted via paired and unpaired t‐tests where appropriate.ResultsBaseline CVC was similar between groups at rest (SCI: 11 ± 6% CVCmax and AB: 9 ± 2% CVCmax, P = 0.54) and after 60 minutes of APHE (both SCI and AB: 48 ± 4% CVCmax, P = 0.94). However, the time course of cutaneous vasodilation was delayed in individuals with SCI as CVC increased to only 19 ± 6% CVCmax in individuals with SCI by 20 minutes APHE compared to 39 ± 3% CVCmax in AB individuals (P = 0.01). Baseline V̇E was similar between groups (SCI: 7.9 ± 0.8 L·min−1 and AB: 9.4 ± 1.1 L·min−1, P = 0.39). Within group comparisons revealed that V̇E increased with heating in AB individuals (12.2 ± 1.4 L·min−1 at 60 minutes APHE, P &lt; 0.01) but not in individuals with SCI (SCI: 9.2 ± 0.5 L·min−1 at 60 minutes APHE, P = 0.15). There was no difference in baseline Tre between groups (SCI: 36.98 ± 0.31°C and AB: 37.36 ± 0.11°C, P = 0.17). Tre tended to increase more in individuals with SCI (+1.48 ± 0.36°C) than AB individuals (+1.18 ± 0.04°C) (P = 0.25) throughout heating, but by 60 minutes APHE Tre increased to a similar, safe level in both groups (SCI: 38.45 ± 0.19°C and AB: 38.54 ± 0.08°C, P = 0.63).ConclusionThese data indicate that although individuals with low‐level SCI exhibit a delayed rise in skin blood flow and an attenuated ventilatory response to heating compared to AB individuals, both groups similarly maintain Tre within a safe range during a one‐hour APHE session.Support or Funding InformationAmerican Heart Association 16GRNT31330014This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Sex-specific stress tolerance, proteolysis, and lifespan in the invertebrate Tigriopus californicus.

Because stress tolerance and longevity are mechanistically and phenotypically linked, the sex with higher acute stress tolerance might be expected to also live longer. On the other hand, the association between stress tolerance and lifespan may be complicated by tradeoffs between acute tolerance and long-term survival. Here we use the copepod Tigriopus californicus to test for sex differences in stress resistance, proteolytic activity and longevity. Unlike many model organisms, this species does not have sex chromosomes. However, substantial sex differences were still observed. Females were found to have superior tolerance to a range of acute stressors (high temperature, high salinity, low salinity, copper and bisphenol A (BPA)) across a variety of treatments including different populations, pure vs. hybrid crosses, and different shading environments. Upregulation of proteolytic capacity - one molecular mechanism for responding to acute stress - was also found to be sexually dimorphic. In the combined stress treatment of chronic copper exposure followed by acute heat exposure, proteolytic capacity was suppressed for males. Females, however, maintained a robust proteolytic stress response. While females consistently showed greater tolerance to short-term stress, lifespan was largely equivalent between the two sexes under both benign conditions and mild thermal stress. Our findings indicate that short-term stress tolerance does not predict long-term survival under relatively mild conditions.

Testosterone mediates hyperthermic response of mice to heat exposure

AimsTestosterone is implicated as a potential contributing factor to heat-induced injury. We examined effects of testosterone on thermal response of mice to heat exposure. Main methodsAdult C57BL/6J male mice received gonadectomy or sham surgery subsequent vehicle (Gnx) or testosterone implants (Gnx+T). Body core temperature (Tc) of mice was recorded telemetrically during acute heat exposure. Thermal responses to heat exposure were also examined in age-matched female mice at each stage of the estrous cycle. Key findingsBasal Tc was lower in sham male mice than females, but did not differ among sham, Gnx or Gnx+T males. No alterations in expression of uncoupling proteins 2 and 3 in the gastrocnemius muscle were found in either Gnx or Gnx+T mice compared to sham males. During heat exposure, sham male mice had a faster and greater rise in Tc, compared to females. This rapid hyperthermic response to heat was abolished in Gnx males, but not in Gnx+T males. No significant correlation was revealed between peak Tc values and plasma testosterone concentrations in Gnx+T males treated with either low- or high-dose testosterone. No effects of estrous cycle phase on the thermal response to heat exposure were detected in female mice. SignificanceWe found that male mice were more susceptible to development of heat-induced hyperthermia than females and this was prevented by castration, not by castration with testosterone replacement. These results suggest that testosterone mediates heat-induced hyperthermia and is a heat stress susceptibility factor.

Heat Shock Protein Expression is Upregulated after Acute Heat Exposure in Three Species of Australian Desert Birds

Desert birds must cope with occasional and unpredictable heat waves, which are slowly becoming more frequent with climate change. Different orders of birds have different physiological and behavioural capacities that may aid survival during a heat wave. To date, the expression of genes related to heat exposure have not been studied across different bird orders. We hypothesised that acutely exposing native Australian birds whose natural habitat include arid environments to a high temperature (45 °C), similar to during a heat wave, would result in the upregulation of genes with protective effects against cell damage (BCL-2, VEGFA and heat shock proteins) and inflammation (interleukins), as well as the downregulation of genes involved in the coagulation pathway (fibrinogen). We used eight each of captive-bred Budgerigars (Melopsittacus undulatus), Zebra Finches (Taeniopygia guttata) and Diamond Doves (Geopelia cuneata). Four birds of each species were exposed to a temperature that was within the zone of thermal neutrality (35 °C), while the other four birds were exposed to a higher temperature (45 °C). The mRNA expression of selected genes were then measured using high-throughput qPCR platform (Fluidigm®, BioMark™). The results supported the hypothesis that acute exposure to a high temperature would result in the upregulation of heat shock protein (HSP) genes, but there was no significant upregulation of other genes with protective effects against cell damage nor genes associated with inflammation. The results also do not support the hypothesis that acute heat exposure would result in downregulation of the genes involved in the coagulation pathway in these birds. Among all the tissues that were analysed, the gastrointestinal tissue had the highest number of upregulated HSP genes, possibly indicating that this tissue requires the most protection to continue functioning. Diamond Dove organs also had the highest number of HSP genes upregulated, possibly a reflection of their ability to better protect their cells at high temperatures.

Effects of acute or chronic heat exposure, exercise and dehydration on plasma cortisol, IL-6 and CRP levels in trained males

This study examined the acute and chronic effects of euhydrated and hypohydrated heat exposure, on biomarkers of stress and inflammation. Eight trained males [mean (SD) age: 21 (3) y; mass: 77.30 (4.88) kg; V̇O2max: 56.9 (7.2) mL kg−1 min−1] undertook two heat acclimation programmes (balanced cross-over design), once drinking to maintain euhydration and once with restricted fluid-intake (permissive dehydration). Days 1, 6, and 11 were 60 min euhydrated exercise-heat stress tests (40 °C; 50% RH, 35% peak power output), days 2–5 and 7–10 were 90 min, isothermal-strain (target rectal temperature: 38.5 °C) exercise-heat sessions. Plasma was obtained pre- and post- exercise on day 1, 2, and 11 and analysed for cortisol, interleukin-6 (IL-6), and C-reactive protein (CRP). Cortisol and CRP were also assessed on day 6. IL-6 was elevated following the initial (acute) 90 min isothermal heat strain exercise-heat exposure (day 2) with permissive dehydration ((pre exercise: 1.0 pg mL−1 [0.9], post-exercise: 1.8 pg mL−1 [1.0], P = .032) and when euhydrated (pre-exercise: 1.0 pg mL−1 [1.4], post-exercise: 1.6 pg mL−1 [2.1], P = .048). Plasma cortisol levels were also elevated but only during permissive dehydration (P = .032). Body mass loss was strongly correlated with Δcortisol (r = −0.688, P = .003). Although there was a trend for post-exercise cortisol to be decreased following both heat acclimation programmes (chronic effects), there were no within or between intervention differences in IL-6 or CRP. In conclusion, acute exercise in the heat increased IL-6 and cortisol only when fluid-intake is restricted. There were no chronic effects of either intervention on biomarkers of inflammation as evidenced by IL-6 and CRP returning to basal level at the end of heat acclimation.

Expression of Mn-SOD and Cu,Zn-SOD of Sahiwal and Karan-Fries in response to acute heat exposure

The present study aimed to investigate the expression of Mn-SOD and Cu,Zn-SOD mRNA in lymphocytes of Sahiwal and Karan-Fries during acute thermal exposure. Six numbers each of Sahiwal and Karan-Fries heifers in the age group of 2–2.5 years were exposed at 40±1°C and 50% relative humidity inside a psychrometric chamber for 4 h in a day. Respiration rate, heart rate and rectal temperatures were recorded to calculate heat tolerance index by calculating Dairy Search Index (DSI). Blood samples were collected at 0, 1, 2, 3 and 4 h of heat exposure for estimation of Mn-SOD and Cu,Zn-SOD mRNA expression by RT-PCR. DSI of Sahiwal was not influenced by heat exposure even after 4 h of heat exposure. After 1 h of heat exposure, DSI of Karan-Fries increased which further escalated after 3 h of exposure in Karan-Fries. Mn-SOD expression increased after 4 h and 2 h of heat exposure in Sahiwal and Karan-Fries respectively, however the expression declined after 3 h of exposure in Karan-Fries. Expression of Cu,Zn-SOD mRNA of Sahiwal and Karan-Fries was not influenced by heat exposure. The study revealed better equipped antioxidant system of Sahiwal than Karan-Fries in response to acute thermal exposure.

Thermoregulatory and Cardiovascular Adjustments to Acute Passive Heat Exposure in Low‐level Spinal Cord Injury

Spinal cord injury (SCI) results in complete or partial loss of sensory, motor, and autonomic function below the level of the lesion. Because SCI impacts both the afferent and efferent pathways of the thermoregulatory system, it can impair the accurate sensation of and adequate response to heat stress. Impairments in heat dissipation through vasodilation of cutaneous microvessels and sweating could lead to unsafe rises in core temperature in individuals with SCI during heat stress. Due to the reduced muscle pump activity and attenuation of sympathetically mediated redistribution of blood flow in individuals with SCI, heat stress may also present a challenge to blood pressure regulation. However, because the magnitude of these impairments is related to the level and severity of injury, heat stress may be well tolerated in individuals with low‐level SCI. Therefore, this study sought to characterize and compare the thermoregulatory and cardiovascular adjustments to acute passive heat exposure (APHE) in individuals with low‐level SCI and the able‐bodied (AB) population. We hypothesized that a one‐hour water immersion APHE session in 40°C water would result in similar core temperature and blood pressure responses in subjects with low‐level SCI and AB subjects. Two individuals (1F) with low‐level SCI (below T6 vertebra) (Body Mass: 70.45 ± 2.57 kg) and 8 AB individuals (4F) (Body Mass: 70.18 ± 2.53 kg) underwent APHE. Resting and APHE values of rectal temperature (Tre), brachial mean arterial pressure (MAP), and cardiac output (Q̇c) (open circuit acetylene uptake) were collected. Tre and MAP were recorded every 5 minutes and Q̇c was measured every 20 minutes throughout APHE. Total peripheral resistance (TPR) was calculated as (MAP/Q̇c). Due to the low number of volunteers with SCI, no statistical comparisons were made between groups. Subjects with SCI and AB subjects had a similar Tre at rest, but Tre increased slightly more in those with SCI (+1.70°C) than AB (+1.18°C) throughout heating. However, by 60 minutes APHE Tre remained within safe limits in both groups (SCI: 38.75 ± 0.05°C and AB: 38.54 ± 0.08°C). Those with SCI had a slightly lower MAP at rest than AB subjects (SCI: 80 ± 4 mmHg vs AB: 85 ± 2 mmHg) and MAP was similarly reduced throughout heating (SCI: 70 ± 4 mmHg and AB: 74 ± 3 mmHg by 60 minutes APHE). In subjects with SCI compared to AB subjects, resting Q̇c was slightly higher (SCI: 6.58 ± 0.97 L·min−1 vs AB: 5.65 ± 0.31 L·min−1) and TPR was slightly lower (SCI: 12.34 ± 1.21 mmHg·min·L−1 vs AB: 15.30 ± 0.86 mmHg·min·L−1). Heating similarly impacted Q̇c and TPR in subjects with SCI and in AB subjects as Q̇c nearly doubled (SCI: 10.86 ± 1.45 L·min−1 and AB: 10.15 ± 0.56 L·min−1) and TPR fell by ~50% (SCI: 6.49 ± 0.53 mmHg·min·L−1 and AB: 7.41 ± 0.52 mmHg·min·L−1) by 60 minutes APHE in both groups. Consistent with our hypothesis, one‐hour APHE elicits similar changes in Tre, Q̇c, MAP, and TPR in individuals with SCI and in AB subjects. These findings are of particular relevance as chronic passive heat therapy emerges as a means of improving cardiometabolic health in patient populations.Support or Funding InformationSupported by American Heart Association 16GRNT31330014This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Acute Heat Exposure Results in an Appropriate Initial Decrease in Core Body Temperature in Subjects with Higher Levels of Spinal Cord Injury, but the Thermal Homeostatic Response to More Prolonged Heat Exposure is Insufficient

Study ObjectiveTo determine the initial (30 minutes) and more prolonged (60 &amp; 90 minutes) response to heat exposure in individuals with higher levels of spinal cord injury (Hi‐SCI; ≥thoracic level‐4).MethodsSixteen persons with Hi‐SCI (C4‐T4, AIS A‐B) and 16 age and body mass index‐matched AB controls were acclimated in a 27°C baseline (BL) room before being transitioned to a 35°C chamber for 90 minutes (Heat Challenge). Tcore (rectal temperature) was continuously measured throughout the Heat Challenge, and sweat rates of the upper extremities (SRUE) and lower extremities (SRLE) were measured at BL and then at 30‐minute intervals.ResultsAt BL, the average Tcore of the Hi‐SCI group was lower than that of the AB group (36.8±0.45°C vs. 37.35±0.27°C; p=0.0003, respectively). From BL to 30 minutes of Heat Challenge, in both Hi‐SCI and AB groups, a significant decrease (p&lt;0.001) in Tcore (Hi‐SCI and AB: 36.57±0.47°C; 37.07±0.20°C, respectively) was accompanied by increases in SRUE for both Hi‐SCI and AB groups (63.77±83.15%; p=0.008 and 202.98±412.47%; p=0.068, respectively). SRLE also increased in the AB group from BL to 30 minutes (138.25±227.96%; p=0.028). From 30–60 minutes of Heat Challenge in the Hi‐SCI group, SRUE increased significantly (32.34±54.53%; p=0.031), but SRLE did not. From 60–90 minutes of Heat Challenge in the Hi‐SCI group, SRUE and SRLE failed to increase, which was associated with progressive increases in Tcore to BL values at 60 minutes (36.74±0.45°C) and above BL values at 90 minutes (37.01±0.45°C vs. 36.8±0.45°C; p=0.01). In the AB group, both SRUE and SRLE incrementally and significantly increased at each 30 minute interval of Heat Challenge, and Tcore remained lower than the BL value at 90 minutes (37.17±0.23 vs. 37.35±0.27°C; p=0.003).ConclusionsIn the Hi‐SCI group, we speculate that during the first 30 minutes of Heat Challenge, residual sympathetic sudomotor control allowed for increased SRUE, which resulted in a dip in Tcore that was similar to the dip observed in the AB group. However, because of limited sympathetic integrity in the upper and lower extremities, persons with Hi‐SCI were unable to mount a meaningful increase in SRUE from 60–90 minutes or in SRLE from BL to 90 minutes. The insufficient thermal homeostatic response to more prolonged Heat Challenge in the Hi‐SCI group resulted in a Tcore rise above BL values. Thus, prolonged exposure (&gt;60 minutes) to elevated ambient temperatures poses a risk to persons with higher levels of SCI.Support or Funding Information: Department of Veterans Affairs Rehabilitation Research and Development Service (I21RX001734).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Physiological responses to heat stress in two genetically distinct chicken inbred lines

High ambient temperature is one of the most important environmental factors negatively impacting poultry production and health. Genetics is an important contributor in mitigating the stress response to heat. Two genetically distinct highly inbred lines of similar body size (Leghorn and Fayoumi) were characterized for phenotypic differences in response to heat. At 14 days of age, birds were exposed to 38°C with 50% humidity for 4 hours, then 35°C until the conclusion of the experiment. Non-treated individuals were kept at 29.4°C for the first week and then 25°C throughout the experiment. Birds in the heat-stress group were inoculated at day (d) 21 with Newcastle disease virus (NDV) La Sota strain to investigate the effects of heat stress and NDV infection. Thirteen blood parameters were measured using the iSTAT blood analyzer at three stages: 4h, 6 d, and 9 d post heat-stress treatment, representing acute heat (AH) exposure, chronic heat (CH1) exposure, and chronic heat exposure after virus infection (CH2), respectively. Most blood parameters were significantly changed with heat stress in Leghorns at AH and in Fayoumis at CH1 and CH2. The Leghorn line had significant acute responses with disrupted acid-base balance and metabolic disorders. The heat-resilient Fayoumis maintained a relatively well-balanced acid-base balance. The current study provides the comprehensive profile of biomarker signatures in blood associated with heat tolerance and suggests that PO2, TCO2, HCO3, and base excess can be served as potential biomarkers that can be used to genetically improve heat tolerance in poultry.

Antioxidant response to heat stress in seagrasses. A gene expression study

Seawater warming associated to the ongoing climate change threatens functioning and survival of keystone coastal benthic species such as seagrasses. Under elevated temperatures, the production of reactive oxygen species (ROS) is increased and plants must activate their antioxidant defense mechanisms to protect themselves from oxidative damage. Here we explore from a molecular perspective the ability of Mediterranean seagrasses to activate heat stress response mechanisms, with particular focus on antioxidants. The level of expression of targeted genes was analyzed in shallow and deep plants of the species Posidonia oceanica and in shallow plants of Cymodocea nodosa along an acute heat exposure of several days and after recovery. The overall gene expression response of P. oceanica was more intense and complete than in C. nodosa and reflected a higher oxidative stress level during the experimental heat exposure. The strong activation of genes with chaperone activity (heat shock proteins and a luminal binding protein) just in P. oceanica plants, suggested the higher sensitivity of the species to increased temperatures. In spite of the interspecific differences, genes from the superoxide dismutase (SOD) family seem to play a pivotal role in the thermal stress response of Mediterranean seagrasses as previously reported for other marine plant species. Shallow and deep P. oceanica ecotypes showed a different timing of response to heat. Shallow plants early responded to heat and after a few days relaxed their response which suggests a successful early metabolic adjustment. The response of deep plants was delayed and their recovery incomplete evidencing a lower resilience to heat in respect to shallow ecotypes. Moreover, shallow ecotypes showed some degree of pre-adaptation to heat as most analyzed genes showed higher constitutive expression levels than in deep ecotypes. The recurrent exposure of shallow plants to elevated summer temperatures has likely endowed them with a higher basal level of antioxidant defense and a faster responsiveness to warming than deep plants. Our findings match with previous physiological studies and supported the idea that warming will differently impact Mediterranean seagrass meadows depending on the species as well as on the depth (i.e. thermal regimen) at which the meadow grows. The increase in the incidence of summer heat waves could therefore produce a significant change in the distribution and composition of Mediterranean seagrass meadows with considerable consequences for the functioning of the whole ecosystem and for the socio-economic services that these ecosystems offer to the riverine populations.

Disruption of TRPV3 Impairs Heat-Evoked Vasodilation and Thermoregulation: A Critical Role of CGRP

Sensing environmental temperature is a key factor allowing individuals to maintain thermal homeostasis via thermoregulatory mechanisms, including changes to skin blood flow. Among transient receptor potential channels, transient receptor potential vanilloid 3 (TRPV3) is a heat-activated cation channel highly expressed in keratinocytes. However, the role of TRPV3 in triggering heat-evoked cutaneous vasodilation is unknown. Using a murine invivo model of local acute environmental heat exposure in the skin, we show that TRPV3 is involved in the local thermoregulatory control of skin blood flow by initiating the release of calcitonin gene-related peptide and nitric oxide in response to local heating of the skin. In addition to their contribution in local heat-evoked vasodilation, TRPV3, calcitonin gene-related peptide, and nitric oxide also contribute to internal body temperature stability during passive whole-body heating. This study provides invivo demonstration of the role of TRPV3 as a strong modulator of cutaneous vascular thermoregulatory mechanisms.