Heat Stress-induced Reduction Research Articles

Chlorogenic acid ameliorates the heat stress-induced impairment of porcine Sertoli cells by suppressing oxidative stress and apoptosis

Sertoli cells are an important type of somatic cell in the testis that are in direct contact with spermatogonia in vivo and play an important role in the process of spermatogenesis. Chlorogenic acid (CGA) plays a pivotal role in the regulation of the mammalian cell heat stress response. For example, CGA treatment protects porcine oocytes from heat stress-induced apoptosis and prevents reduced embryo quality. However, the role of CGA treatment in protecting porcine testicular Sertoli cells against heat-induced damage has rarely been studied. This study aimed to identify the protective effects of CGA on oxidative stress and apoptosis in Sertoli cells under heat stress. The present results demonstrated that the addition of CGA significantly inhibited the accumulation of reactive oxygen species (ROS) and apoptosis in Sertoli cells induced by heat stress and decreased the expression of CASP3 protein and the BAX/BCL-2 protein ratio. CGA pretreatment also prevented the heat stress-induced reductions in the mitochondrial membrane potential, PCNA protein expression, and SOD and CAT activities. Moreover, CGA treatment reversed S phase cell cycle arrest and increased the HSP70 protein expression levels. Overall, these results suggest that oxidative damage participates in the inhibition of the proliferation of Sertoli cells and the increase in their apoptosis induced by heat stress, and the protective effects of CGA treatment on Sertoli cells under heat stress provide a theoretical basis for preventing heat stress injury in animals.

Heat stress-induced intestinal epithelial cells necroptosis via TLR3-TRIF-RIP3 pathway was dependent on p53.

Heatstroke is a life-threatening disease. Present study was aimed to investigate the mechanism in heat induced intestinal epithelial cell death. Heat stress in vitro model was established on IEC cells with 42℃ for 2h. Caspase-8 inhibitor, Caspase-3 inhibitor, RIP3 inhibitor, TLR3 agonist, poly(I:C) and p53 knockdown were used to determine the signaling pathway. Heatstroke in vivo model was established on C57BL/6 mice, with a temperature of 35.5℃±0.5℃ and a relative humidity of 60% ± 5%. The intestine necroptosis and inflammatory cytokines were measured. Pifithrin α (3mg/kg) and p53 knockout mice were used to evaluate the role of p53. Heat stress-induced reduction of cell viability was remarkable reversed by RIP3 inhibitor. Heat stress induced upregulation of TLR3 and facilitate the formation of TRIF-RIP3 complex. The heat stress induced upregulation of RIP3 and p-RIP3 were normalized by the deletion of p53. Meanwhile, p53 knockout decreased TLR3 expression and blocked the formation of TLR3-TRIF complex. The deletion of p53 blocked the decreased cell viability and restored the activation of RIP3-MLKL signaling after heat stress, however, which were abolished by re-expression of p53 via Tp53 OE. Increased the expression of TLR3 in the p53-deficient cells could not affect the heat stress induced necrotic cell death, which suggests that heat stress induced necroptosis via TLR3-TRIF-RIP3 signaling pathway is dependent on p53. Heat stress promoted p53 phosphorylation, then upregulated TLR3 and enhanced the interaction of TRIF-RIP3, which would activate the RIP3-MLKL signaling pathway to mediate necroptosis in intestinal epithelial cells.

Carbohydrate, but not fat, oxidation is reduced during moderate-intensity exercise performed in 33 vs. 18°C at matched heart rates.

Exposure to environmental heat stress increases carbohydrate oxidation and extracellular heat shock protein 70 (HSP70) concentrations during endurance exercise at matched absolute, external work rates. However, a reduction in absolute work rate typically occurs when unacclimated enduranceathletes train and/or compete in hot environments. We sought to determine the effect of environmental heat stress on carbohydrate oxidation rates and plasma HSP70 expression during exercise at matched heart rates (HR). Ten endurance-trained, male cyclists performed two experimental trials in an acute, randomised, counterbalanced cross-over design. Each trial involved a 90-min bout of cycling exercise at 95% of the HR associated with the first ventilatory threshold in either 18 (TEMP) or 33°C (HEAT), with ~ 60% relative humidity. Mean power output (17 ± 11%, P < 0.001) and whole-body energy expenditure (14 ± 8%, P < 0.001) were significantly lower in HEAT. Whole-body carbohydrate oxidation rates were significantly lower in HEAT (19 ± 11%, P = 0.002), while fat oxidation rates were not different between-trials. The heat stress-induced reduction in carbohydrate oxidation was associated with the observed reduction in power output (r = 0.64, 95% CI, 0.01, 0.91, P = 0.05) and augmented sweat rates (r = 0.85, 95% CI, 0.49, 0.96, P = 0.002). Plasma HSP70 and adrenaline concentrations were not increased with exercise in either environment. These data contribute to our understanding of how moderate environmental heat stress is likely to influence substrate oxidation and plasma HSP70 expression in an ecologically-valid model of endurance exercise.

Genetic and molecular mechanisms underlying root architecture and function under heat stress-A hidden story.

Heat stress events are resulting in a significant negative impact on global food production. The dynamics of cellular, molecular and physiological homoeostasis in aboveground parts under heat stress are extensively deciphered. However, root responses to higher soil/air temperature or stress signalling from shoot to root are limited. Therefore, this review presents a holistic view of root physio-morphological and molecular responses to adapt under hotter environments. Heat stress reprogrammes root cellular machinery, including crosstalk between genes, phytohormones, reactive oxygen species (ROS) and antioxidants. Spatio-temporal regulation and long-distance transport of phytohormones, such as auxin, cytokinin and abscisic acid (ABA) determine the root growth and development under heat stress. ABA cardinally integrates a signalling pathway involving heat shock factors, heat shock proteinsand ROS to govern heat stress responses. Additionally, epigenetic modifications by transposable elements, DNA methylationand acetylation also regulate root growth under heat stress. Exogenous application of chemical compounds or biological agents such as ascorbic acid, metal ion chelators, fungi and bacteria can alleviate heat stress-induced reduction in root biomass. Future research should focus on the systemic effect of heat stress from shoot to root with more detailed investigations to decipher the molecular cues underlying the roots architecture and function.

Stability of Heart Rate at Physiological Thresholds Between Temperate and Heat Stress Environments in Endurance-Trained Males.

Many endurance athletes perform specific blocks of training in hot environments in "heat stress training camps." It is not known if physiological threshold heart rates measured in temperate conditions are reflective of those under moderate environmental heat stress. A total of 16 endurance-trained cyclists and triathletes performed incremental exercise assessments in 18°C and 35°C (both 60% relative humidity) to determine heart rates at absolute blood lactate and ventilatory thresholds. Heart rate at fixed blood lactate concentrations of 2, 3, and 4mmol·L-1 and ventilatory thresholds were not significantly different between environments (P > .05), despite significant heat stress-induced reductions in power output of approximately 10% to 17% (P < .05, effect size = 0.65-1.15). The coefficient of variation for heart rate at these blood lactate concentrations (1.4%-2.9%) and ventilatory thresholds (2.3%-2.7%) between conditions was low, with significant strong positive correlations between measurements in the 2 environments (r = .92-.95, P < .05). These data indicate heart rates measured at physiological thresholds in temperate environments are reflective of measurements taken under moderate environmental heat stress. Therefore, endurance athletes embarking on heat stress training camps can use heart rate-based thresholds ascertained in temperate environments to prescribe training under moderate environmental heat stress.

Alpha lipoic acid improves heat stress-induced reduction of serum oestradiol and progesterone levels by affecting oxidative and endoplasmic reticulum stress in hens

Alpha lipoic acid (ALA), a natural lipophilic compound, plays an important role in regulating several metabolic pathways due to its antioxidant properties. This study aims to investigate whether ALA could be used as a feed additive to enhance the antioxidant capacity of the ovary tissue in hens exposed to heat stress (HS). One hundred and sixty 128-days-old female chickens were randomly assigned into four groups: the control group (Con), ALA treatment group (ALA), ALA and HS treatment group (ALA + HS), and HS treatment group (HS). The ALA and ALA + HS groups were fed a basal diet with 0.25% ALA, whereas the Con and HS groups were fed a basal diet only. Serum oestradiol, progesterone levels, biomarkers of antioxidant capacity, and endoplasmic reticulum (ER) stress markers were detected in the ovaries of heat-stressed chickens. HS decreased serum oestradiol and progesterone concentrations compared with the control group, whereas dietary ALA (0.25%) increased oestradiol and progesterone levels in the serum of heat-stressed hens. Malondialdehyde concentration in the ovary was higher in the HS group than that of the ALA + HS group. Compared with the HS group, ALA increased the enzymatic activities of superoxide dismutase, glutathione peroxidase, and catalase in the ovaries of ALA + HS group. Simultaneously, ALA enhanced the total antioxidative capacity of the ovaries of heat-stressed hens. Moreover, ALA also significantly inhibited the increased expression of glucose-regulated protein 78 and CCAAT/enhancer-binding protein homologous protein, which are two markers of ER stress, and heat shock protein 70, a key biomarker of heat stress, in the ovaries of the ALA + HS group as compared to those of the HS group. This work implied that dietary ALA supplementation improved the antioxidant capacity and attenuated the HS-induced reduction of serum oestradiol and progesterone levels and modulated the oxidative and ER stress, which are involved in the protective effect of ALA in hens exposed to hyperthermia.

Outdoor heat stress and cognition: Effects on those over 40 years old in China

With the increases in hot weather frequency and intensity induced by observed and predicted climate change, heat exposure is an evolving challenge. We estimated a fixed effect econometric model to data on 5,404 individuals drawn from the China Health and Retirement Longitudinal Study database. These observations were used to examine the effect of heat stress on cognitive performance for those above 40 years of age who are often household decision-makers. We found today's heat stress decreases performance on verbal and math test scores, and that cumulative heat exposure over the last 3 days adversely affects verbal test scores. We also found that middle-aged women and people in rural areas exhibit substantial heat stress-induced reductions on cognitive test scores. This finding implies that continuing climate change may well diminish decision-making capacity and effectiveness.

256 Heat stress and β-adrenergic agonists alter the adipose transcriptome and fatty acid mobilization in ruminant livestock

Abstract Heat stress (HS) negatively impacts livestock performance and carcass traits while beta-adrenergic agonist (βAA) supplementation improves animal production and efficiency; both can stimulate lipolysis in adipose. The objective of this study was to understand the independent and interacting effects of HS and βAA on the subcutaneous adipose transcriptome in lambs and on visceral adipose fatty acid mobilization in steers. For study 1, 24 wethers were assigned to thermal neutral (TN THI = 65) or HS (THI = 80) conditions and supplemented without (NS) or with ractopamine hydrochloride (RH) for 30d in a 2 x 2 factorial. TN lambs were pair-fed the average intake of HS. RNA collected from subcutaneous fat at harvest was sequenced. Differential expression (DE) analyses identified 71 (Padj &amp;lt; 0.05) loci altered due to the interaction of environment and supplement. No DE genes were observed for the main effect of supplement, but HS reduced expression (P &amp;lt; 0.05) of RBM3 and increased expression (P &amp;lt; 0.05) of ATXN7L1. HS was predicted by pathway analyses to impair adipogenesis and fatty acid mobilization. In study 2, 24 steers were assigned to TN (THI = 65) or HS (THI = 83) and NS or zilpaterol hydrochloride (ZH) treatments for 21d in a 2 x 2 factorial. TN steers were pair-fed the intake of their HS cohort. Ex vivo fatty acid mobilization from visceral adipose in response to 0 or 1µM epinephrine was quantified at harvest. Fatty acid mobilization did not differ among groups when unstimulated, but epinephrine-stimulated mobilization was less (P = 0.05) in HS and greater (P &amp;lt; 0.01) in ZH steers. These findings indicate that heat stress-induced reduction of fatty acid mobilization from adipose may be associated with increased expression of stress-responsive genes. Moreover, the stimulatory effect of ZH on epinephrine-induced fatty acid mobilization was present after chronic treatment. Our data have yet to identify an interaction between HS and βAA supplementation that demonstrably impacts well-being.

Heat stress induces apoptosis through disruption of dynamic mitochondrial networks in dairy cow mammary epithelial cells.

Heat stress-induced reductions in milk yield and the dysfunction of mammary glands are economically important challenges that face the dairy industry, especially during summer. The aim of the present study is to investigate the effects of heat stress on mitochondrial function by using dairy cow mammary epithelial cells (DCMECs) as an in vitro model. Live cell imaging shows that the mitochondria continually change shape through fission and fusion. However, heat stress induces the fragmentation of mitochondria, as well as the decreased of ATP level, membrane potential, and anti-oxidant enzyme activity and the increased of respiratory chain complex I activity. In addition, the cytosolic Ca2+ concentration and cytochrome c expression (Cyto-c) were increased after heat stress treatment. Both qRT-PCR and western blot analysis indicate that mitofusin1/2 (Mfn1/2) and optic atrophy protein-1 (Opa-1) are downregulated after heat stress, whereas dynamin-related protein 1 (Drp1) and fission 1 (Fis-1) are upregulated, which explains the observed defect of mitochondrial network dynamics. Accordingly, the present study indicated that heat stress induced the dysfunction of DCMEC through disruption of the normal balance of mitochondrial fission and fusion.

MiR-130a-3p Inhibits PRL Expression and Is Associated With Heat Stress-Induced PRL Reduction.

MicroRNAs (MiRNAs) play critical roles in the regulation of pituitary function. MiR-130a-3p has previously been found to be down-regulated in prolactinoma, but its roles in prolactin (PRL) regulation and the underlying mechanisms are still unclear. Heat stress has been shown to induce alteration of endocrine hormones and miRNAs expressions. However, there is limited information regarding the emerging roles of miRNAs in heat stress response. In this study, we transfected miR-130a-3p mimic into the pituitary adenoma cells (GH3 cells) to investigate the function of miR-130a-3p in regulating PRL. Our results showed that miR-130a-3p overexpression significantly decreased the PRL expression at both mRNA and protein levels. Subsequently, estrogen receptor α (ERα) was identified as a direct target of miR-130a-3p by bioinformatics prediction, luciferase reporter assay and western blotting assay. Furthermore, the inhibition of ERα caused by estrogen receptor antagonist significantly reduced the PRL expression. Overexpression of ERα rescued the suppressed expression of PRL caused by miR-130a-3p mimic. Besides, we also studied the effect of heat stress on PRL and miRNAs expressions. Interestingly, we found that heat stress reduced PRL and ERα expressions while it increased miR-130a-3p expression both in vitro and in vivo. Taken together, our results indicate that miR-130a-3p represses ERα by targeting its 3'UTR leading to a decrease in PRL expression, and miR-130a-3p is correlative with heat stress-induced PRL reduction, which provides a novel mechanism that miRNAs are involved in PRL regulation.

&lt;i&gt;Angelica keiskei&lt;/i&gt; (Ashitaba) powder and its functional compound xanthoangelol prevent heat stress-induced impairment in sperm density and quality in mouse testes

Recently, gradual decline in human sperm production has become a serious worldwide concern because it leads to increased rates of infertility. Endocrine disrupters, lifestyle changes, and varicocele, all of which elevate testicular temperature, are thought to be the main causes of this decline. The present study aimed to determine whether the dietary phytochemicals Angelica keiskei (Ashitaba) powder (57.5 mg/kg) and its functional component, xanthoangelol (3 mg/kg), can prevent heat stress-induced impairment in sperm density and quality in mice. Sperm parameters were analyzed 28 days after mice exposure to heat. Supplementation with Ashitaba powder completely prevented heat-induced impairment in sperm parameters, including densities of motile sperms and progressive sperms (> 25 μm/sec), and amplitude of lateral head displacement. Xanthoangelol did not exert a complete protective effect; nevertheless, it significantly prevented heat stress-induced reduction in most parameters. Both Ashitaba powder and xanthoangelol elevated the expression of the widely expressed heat shock proteins (HSPs) Hspa1a and Hsp40 and the antioxidant enzyme glutathione synthase in non-stressed testes. Ashitaba powder significantly prevented heat stress-induced reduction in the expression of Hspa1l and Hspa2, which are highly expressed in the testes and critical for fertility. Our results showed that Ashitaba powder and xanthoangelol protected testicular cells from heat stress, probably by elevating the levels of antioxidant enzymes and HSPs. Supplementation with dietary functional phytochemicals may help prevent heat stress-induced male infertility.

COMT1 Silencing Aggravates Heat Stress-Induced Reduction in Photosynthesis by Decreasing Chlorophyll Content, Photosystem II Activity, and Electron Transport Efficiency in Tomato.

Despite a range of initiatives to reduce global carbon emission, the mean global temperature is increasing due to climate change. Since rising temperatures pose a serious threat of food insecurity, it is important to further explore important biological molecules that can confer thermotolerance to plants. Recently, melatonin has emerged as a universal abiotic stress regulator that can enhance plant tolerance to high temperature. Nonetheless, such regulatory roles of melatonin were unraveled mainly by assessing the effect of exogenous melatonin on plant tolerance to abiotic stress. Here, we generated melatonin deficient tomato plants by silencing of a melatonin biosynthetic gene, CAFFEIC ACID O-METHYLTRANSFERASE 1 (COMT1), to unveil the role of endogenous melatonin in photosynthesis under heat stress. We examined photosynthetic pigment content, leaf gas exchange, and a range of chlorophyll fluorescence parameters. The results showed that silencing of COMT1 aggravated heat stress by inhibiting both the light reactions and the carbon fixation reactions of photosynthesis. The photosynthetic pigment content, light absorption flux, trapped energy flux, energy dissipation, density of active reaction center per photosystem II (PSII) cross-section, the photosynthetic electron transport rate, the maximum photochemical efficiency of PSII photochemistry, and the rate of CO2 assimilation all decreased in COMT1-silenced plants compared with that of non-silenced plants particularly under heat stress. However, exogenous melatonin alleviated heat-induced photosynthetic inhibition in both genotypes, indicating that melatonin is essential for maintaining photosynthetic capacity under stressful conditions. These findings provide genetic evidence on the vital role of melatonin in photosynthesis and thus may have useful implication in horticultural crop management in the face of climate change.

Elevated skin and core temperatures both contribute to reductions in tolerance to a simulated haemorrhagic challenge.

What is the central question of this study? Combined increases in skin and core temperatures reduce tolerance to a simulated haemorrhagic challenge. The aim of this study was to examine the separate and combined influences of increased skin and core temperatures upon tolerance to a simulated haemorrhagic challenge. What is the main finding and its importance? Skin and core temperatures increase during many occupational settings, including military procedures, in hot environments. The study findings demonstrate that both increased skin temperature and increased core temperature can impair tolerance to a simulated haemorrhagic challenge; therefore, a soldier's tolerance to haemorrhagic injury is likely to be impaired during any military activity that results in increased skin and/or core temperatures. Tolerance to a simulated haemorrhagic insult, such as lower-body negative pressure (LBNP), is profoundly reduced when accompanied by whole-body heat stress. The aim of this study was to investigate the separate and combined influence of elevated skin (Tskin ) and core temperatures (Tcore ) on LBNP tolerance. We hypothesized that elevations in Tskin as well as Tcore would both contribute to reductions in LBNP tolerance and that the reduction in LBNP tolerance would be greatest when both Tskin and Tcore were elevated. Nine participants underwent progressive LBNP to presyncope on four occasions, as follows: (i)control, with neutral Tskin (34.3±0.5°C) and Tcore (36.8±0.2°C); (ii)primarily skin hyperthermia, with high Tskin (37.6±0.2°C) and neutral Tcore (37.1±0.2°C); (iii)primarily core hyperthermia, with neutral Tskin (35.0±0.5°C) and high Tcore (38.3±0.2°C); and (iv)combined skin and core hyperthermia, with high Tskin (38.8±0.6°C) and high Tcore (38.1±0.2°C). The LBNP tolerance was quantified via the cumulative stress index (in millimetres of mercury×minutes). The LBNP tolerance was reduced during the skin hyperthermia (569±151mmHgmin) and core hyperthermia trials (563±194 mmHgmin) relative to control conditions (1010±246mmHgmin; both P<0.05). However, LBNP tolerance did not differ between skin hyperthermia and core hyperthermia trials (P=0.92). The lowest LBNP tolerance was observed during combined skin and core hyperthermia (257±106mmHgmin; P<0.05 relative to all other trials). These data indicate that elevated skin temperature, as well as elevated core temperature, can both contribute to reductions in LBNP tolerance in heat-stressed individuals. However, heat stress-induced reductions in LBNP tolerance are greatest in conditions when both skin and core temperatures are elevated.

Hormonal regulation of reproductive growth under normal and heat-stress conditions in legume and other model crop species.

Legume crops are grown throughout the world and provide an excellent food source of digestible protein and starch, as well as dietary fibre, vitamins, minerals, and flavonoids. Fruit and seeds from legumes are also an important source of vegetables for a well-balanced diet. A trend in elevated temperature as a result of climate change increases the risk of a heat stress-induced reduction in legume crop yield. High temperatures during the crop reproductive development phase are particularly detrimental to fruit/seed production because the growth and development of the reproductive tissues are sensitive to small changes in temperature. Hormones are signalling molecules that play important roles in a plant's ability to integrate different environmental inputs and modify their developmental processes to optimize growth, survival, and reproduction. This review focuses on the hormonal regulation of reproductive development and heat stress-induced alteration of this regulation during (i) pollination, (ii) early fruit set, and (iii) seed development that affects fruit/seed yield in legume and other model crops. Further understanding of hormone-regulated reproductive growth under non-stress and heat-stress conditions can aid in trait selection and the development of gene modification strategies and cultural practices to improve heat tolerance in legume crops contributing to improved food security.

Enhanced economic connectivity to foster heat stress-related losses.

Assessing global impacts of unexpected meteorological events in an increasingly connected world economy is important for estimating the costs of climate change. We show that since the beginning of the 21st century, the structural evolution of the global supply network has been such as to foster an increase of climate-related production losses. We compute first- and higher-order losses from heat stress-induced reductions in productivity under changing economic and climatic conditions between 1991 and 2011. Since 2001, the economic connectivity has augmented in such a way as to facilitate the cascading of production loss. The influence of this structural change has dominated over the effect of the comparably weak climate warming during this decade. Thus, particularly under future warming, the intensification of international trade has the potential to amplify climate losses if no adaptation measures are taken.

Corrigendum

CorrigendaCorrigendumPublished Online:15 May 2013https://doi.org/10.1152/japplphysiol.zdg-0617-corr.2013Original articleMoreSectionsPDF (83 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Lee JF, Harrison ML, Brown SR, Brothers RM. The magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage. J Appl Physiol 114: , 2013. First published November 8, 2012; doi:10.1152/japplphysiol.00878.2012.—On page 38, right column, Experimental protocols, sentence beginning on line 11 should read: “LBNP is commonly used to simulate hypovolemia and is an effective model to study cardiovascular responses to acute hemorrhage in humans (9, 10).”This article has no references to display. Download PDF Previous Back to Top FiguresReferencesRelatedInformation Related ArticlesThe magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage 01 Jan 2013Journal of Applied PhysiologyCited ByCompensatory hemodynamic changes in response to central hypovolemia in humans: lower body negative pressure: updates and perspectives15 November 2022 | Journal of Muscle Research and Cell Motility, Vol. 7 More from this issue > Volume 114Issue 10May 2013Pages 1492-1492 Copyright & PermissionsCopyright © 2013 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.zdg-0617-corr.2013History Published online 15 May 2013 Published in print 15 May 2013 Metrics

The magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage

The mechanisms responsible for heat stress-induced reductions in tolerance to a simulated hemorrhage are unclear. Although a high degree of variability exists in the level of reduction in tolerance amongst individuals, syncope will always occur when cerebral perfusion is inadequate. This study tested the hypothesis that the magnitude of reduction in cerebral perfusion during heat stress is related to the reduction in tolerance to a lower body negative pressure (LBNP) challenge. On different days (one during normothermia and the other after a 1.5°C rise in internal temperature), 20 individuals were exposed to a LBNP challenge to presyncope. Tolerance was quantified as a cumulative stress index, and the difference in cumulative stress index between thermal conditions was used to categorize individuals most (large difference) and least (small difference) affected by the heat stress. Cerebral perfusion, as indexed by middle cerebral artery blood velocity, was reduced during heat stress compared with normothermia (P < 0.001); however, the magnitude of reduction did not differ between groups (P = 0.51). In the initial stage of LBNP during heat stress (LBNP 20 mmHg), middle cerebral artery blood velocity and end-tidal PCO(2) were lower; whereas, heart rate was higher in the large difference group compared with small difference group (P < 0.05 for all). These data indicate that variability in heat stress-induced reductions in tolerance to a simulated hemorrhage is not related to reductions in cerebral perfusion in this thermal condition. However, responses affecting cerebral perfusion during LBNP may explain the interindividual variability in tolerance to a simulated hemorrhage when heat stressed.

Sweat loss during heat stress contributes to subsequent reductions in lower‐body negative pressure tolerance

The contribution of sweating to heat stress-induced reductions in haemorrhagic tolerance is not known. This study tested the hypothesis that fluid loss due to sweating contributes to reductions in simulated haemorrhagic tolerance in conditions of heat stress. Eight subjects (35 ± 8 years old; 77 ± 5 kg) underwent a normothermic time control and two heat stress trials (randomized). The two heat stress trials were as follows: (i) with slow intravenous infusion of lactated Ringer solution sufficient to offset sweat loss (IV trial); or (ii) without intravenous infusion (dehydration; DEH trial). Haemorrhage was simulated via progressive lower-body negative pressure (LBNP) to presyncope after core body (intestinal) temperature was raised by ~1.5 °C using a water-perfused suit or a normothermic time control period. The LBNP tolerance was quantified via a cumulative stress index. Middle cerebral artery blood velocity (transcranial Doppler) and mean blood pressure (Finometer®) were measured continuously. Relative changes in plasma volume were calculated from haematocrit and haemoglobin. Increases in core body temperature and sweat loss (~1.6% body mass deficit) were similar (P > 0.05) between heat stress trials. Slow intravenous infusion (1.2 ± 0.3 litres) prevented heat-induced reductions in plasma volume (IV trial, -0.6 ± 6.1%; and DEH trial, -6.6 ± 5.1%; P = 0.01). Intravenous infusion improved LBNP tolerance (632 ± 64 mmHg min) by ~20% when compared with the DEH trial (407 ± 117 mmHg min; P = 0.01), yet tolerance remained 44% lower in the IV trial relative to the time control normothermic trial (1138 ± 183 mmHg min; P < 0.01). These data indicate that although sweat-induced dehydration impairs simulated haemorrhagic tolerance, this impairment is secondary to the negative impact of heat stress itself.

Heat Stress-Induced Cell Death, Changes in Antioxidants, Lipid Peroxidation, and Protease Activity in Wheat Leaves

Six wheat genotypes were evaluated for heat tolerance in terms of seedling growth, antioxidant response and cell death. Based on the heat susceptibility index (HSI), response of the genotypes varied from heat tolerant (Inqilab-91) to heat sensitive (Sitta) along with moderately tolerant (Nesser and Sarsabz) and sensitive (Fareed and FD-83). Heat stress-induced programmed cell death (probably necrosis) in wheat leaves was evident by DNA smear. MDA content increased above twofold in most of genotypes under heat stress, with the lowest increase in the heat-tolerant genotype Nesser. Catalase activity diminished under heat stress in all genotypes. Peroxidase, superoxide dismutase (SOD), protease, and ascorbate peroxidase (APX) activities increased under heat stress. Apparently, heat stress-induced reduction in catalase activity was compensated by a parallel increase in peroxidases to quench H2O2. Heat stress-induced decrease (%) in catalase and increase in protease activities showed significant positive correlations, whereas increase (%) in APX activity showed a significant negative correlation with HSI or relative heat tolerance of genotypes. All these correlations signify that catalase, protease and ascorbate peroxidase can be used efficiently as biochemical markers to assess the relative heat stress tolerance of wheat genotypes at the seedling stage. In conclusion, using a multiparametric approach involving morphophysiological and biochemical assays, the sensitivity of wheat genotypes to heat stress could be evaluated to a sufficient level of certainty at the seedling stage.

End-tidal carbon dioxide tension reflects arterial carbon dioxide tension in the heat-stressed human with and without simulated hemorrhage

End-tidal carbon dioxide tension (Pet(CO(2))) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is dependent on Pet(CO(2)) being an accurate surrogate for arterial carbon dioxide tension (Pa(CO(2))), the latter being the physiologically relevant variable. This study tested the hypothesis that Pet(CO(2)) provides an accurate assessment of Pa(CO(2)) during the aforementioned conditions. Comparisons between these measures were made: 1) after two levels of heat stress (N = 11); 2) during combined heat stress and simulated hemorrhage [via lower-body negative pressure (LBNP), N = 8]; and 3) during an end-tidal clamping protocol to attenuate heat stress-induced reductions in Pet(CO(2)) (N = 7). Pet(CO(2)) and Pa(CO(2)) decreased during heat stress (P < 0.001); however, there was no group difference between Pa(CO(2)) and Pet(CO(2)) (P = 0.36) nor was there a significant interaction between thermal condition and measurement technique (P = 0.06). To verify that this nonsignificant trend for the interaction was not due to a type II error, Pet(CO(2)) and Pa(CO(2)) at three distinct thermal conditions were also compared using paired t-tests, revealing no difference between Pa(CO(2)) and Pet(CO(2)) while normothermic (P = 0.14) and following a 1.0 ± 0.2°C (P = 0.21) and 1.4 ± 0.2°C (P = 0.28) increase in internal temperature. During LBNP while heat stressed, measures of Pet(CO(2)) and Pa(CO(2)) were similar (P = 0.61). Likewise, during the end-tidal carbon dioxide clamping protocol, the increases in Pet(CO(2)) (7.5 ± 2.8 mmHg) and Pa(CO(2)) (6.6 ± 3.4 mmHg) were similar (P = 0.31). These data indicate that mean Pet(CO(2)) reflects mean Pa(CO(2)) during the evaluated conditions.