Days Of Heat Exposure Research Articles

Physiological responses to heat exposure in a general population cohort in Denmark: the Lolland-Falster Health Study.

Rising global temperatures due to climate change pose a health risk. Mortality and morbidity increase during heat events affects various organ systems. While warmer countries face higher risks, even colder regions show elevated mortality during hot periods. This study examines physiological responses to heat exposure using data from the general Danish population cohort Lolland-Falster Health Study (LOFUS) during the summers of 2016-2019. In this cross-sectional study, we analysed health data from 3804 individuals aged ≥15 years. Data were analysed across organ systems: cardiovascular system, lung function, renal system, inflammation, coagulation, and liver function. Meteorological data from the Danish Meteorological Institute provided information on temperature and humidity. Heat exposure was defined as one day ≥28°C heat index the day prior to examination. Adjusted multiple linear regression was applied to analyse differences between the two groups. There were 46 of 368 days with temperatures ≥28°C heat index. In total, 396 participants were heat-exposed (exposure group), while 3408 constituted the unexposed group. Heat exposure was associated with lower systolic blood pressure (-3.82 mm Hg [-5.72; -1.93]), higher heart rate (1.71 beats/min [0.45; 2.98]), lower oxygen saturation (-0.28% [-0.45; -0.10]), higher sodium (0.56 mmol/l [0.33; 0.79]), and higher urine albumin (0.14 mg/l [0.02; 0.27]). No significant differences were observed in inflammation, coagulation, or liver function. This study reveals early physiological responses to heat with one day of heat exposure ≥28°C, particularly in the cardiovascular, pulmonary, and renal systems. These findings underline the need for tailored strategies to mitigate health risks associated with rising temperatures.

Astaxanthin supplementation ameliorates simulated heat stress by regulating physio-biochemical responses in Sirohi goats.

The present study was undertaken to assess the ameliorative effect of dietary supplementation of astaxanthin in Sirohi goats under simulated heat stress conditions. Eighteen healthy female Sirohi goats were divided equally into three groups (n = 6): Heat-Stressed Control (HSC), Treatment 1 (T1), and Treatment 2 (T2). During the experiment, goats in the T1 group were supplemented with astaxanthin at the rate of 25mg/animal/day, while those in the T2 group received supplementation of 50mg/animal/day. The experiment was conducted for 42 days: 14 days of acclimatization period, next 21 days animals were exposed to 42ºC for 6h from 09:00h to 15:00h and 7 days of recovery period. On a daily basis, we recorded the physiological responses of goats and collected environmental data at the experimental site. Blood samples were collected 0 and 14th days of acclimatization, on 1st, 6th, 11th, 16th and 21st day of heat exposure and on the 7th day of the recovery period. The rectal temperature and respiration rates of the treatment groups were lower than those of the HSC group during the exposure period. Heat stress in the supplemented groups was associated with reduced levels of hepatic enzymes such as AST and ALT. Serum urea, creatinine and albumin levels were significantly (P < 0.05) different between control and treatment groups. It was thus concluded that dietary inclusion of antioxidant astaxanthin can ameliorate induced thermal load as evident from changes in physio-biochemical parameters in the Sirohi goats, that was more prominent at 50mg/ animal/day than 25mg/ animal/day.

Physiological and behavioural responses of Swedish domestic goats and their kids (Capra hircus) to 15 days of heat exposure

ABSTRACT Seven Swedish domestic goats (Capra hircus, 2–3 years) and their kids (37 ± 4 days) were subjected to indoor temperatures above 30°C during 15 days (periods H1–H4; periods without heat C1, C2) to study acclimation. Rectal temperature (RT) increased by 1.1°C during H1 to H3 (P < 0.001 vs. C1), but only by 0.6°C during H4 (P < 0.001 vs. C1; P < 0.024 vs. H1). Respiration rate (RR) increased less during H4 than during H1 (P < 0.001). Skin temperature increased during heat (P < 0.001), and skin evaporation (SE), which differed from C1 to H4 (P < 0.05). Goats increased water intake during heat, resulting in lowered milk osmolality while milk offtake was maintained. Kids' thermoregulatory responses resembled those of the goats. Thus, decreasing RT and RR simultaneously with increasing SE at the end of the heat indicate that goats had started to acclimate.

Effect of heat pre-conditioning on recovery following exercise-induced muscle damage.

This study investigated the influence of heat pre-conditioning on the recovery of muscle torque, microvascular function, movement economy and stride mechanics following exercise-induced muscle damage (EIMD). Twenty male participants were equally assigned to a control (CON) and an experimental group (HEAT), and performed a 30-min downhill run (DHR) to elicit EIMD. HEAT group received three consecutive days of heat exposure (45.1 ​± ​3.2 ​min of hot water immersion at 42 ​°C) prior to DHR. Microvascular function (near-infrared spectroscopy), maximal voluntary contraction (MVC) torque of the knee extensors, as well as two treadmill-based steady-state runs performed below (SSR-1) and above (SSR-2) the first ventilatory threshold were assessed prior to DHR and repeated for four consecutive days post-DHR (D1-POST to D4-POST). The decline in MVC torque following EIMD was attenuated in HEAT compared with CON at D1-POST (p ​= ​0.037), D3-POST (p ​= ​0.002) and D4-POST (p ​= ​0.022). Muscle soreness increased in both CON and HEAT, but was significantly attenuated in HEAT compared with CON at D2-POST (p ​= ​0.024) and D3-POST (p ​= ​0.013). Microvascular function decreased in CON from D1-POST to D3-POST (p ​= ​0.009 to 0.018), and was lower compared with HEAT throughout D1-POST to D3-POST (p ​= ​0.003 to 0.017). Pre-heat treatment decreased the magnitude of strength loss and muscle soreness, as well as attenuated the decline in microvascular function following EIMD. Heat treatment appears a promising pre-conditioning strategy when embarking on intensified training periods or competition.

The relation between liver damage and reproduction in female Japanese quail (Coturnix japonica) exposed to high ambient temperature

Reproductive failure associated with heat stress is a well-known phenomenon in poultry. High temperatures also induce various metabolic disturbances in many animals. Because the liver plays a central role in metabolism, the present study aimed to clarify the relationship between liver and reproduction in Japanese quails exposed to high temperatures. In the consecutive 20-D experimental period, quails were treated with 25°C (control) or 34°C (heat) from 12:00 to 16:00. Eggs were collected for hatching. On completion of the experimental period, quails were humanely euthanized for hormone analyses (e.g., serum and ovarian follicles). Serum metabolites were analyzed using GC/MS. Liver and ovary samples were collected for mRNA levels, histomorphology, and metabolic analysis. Ovary and oviduct weights significantly decreased after daily heat exposure. The number and weight of hierarchical follicles also decreased. Consequently, egg weight decreased. Although there was no difference in fertilization rate, chick birth weight significantly decreased in the heated group. Corticosterone and 17β-estradiol in the serum significantly increased in the heated group. Yolk corticosterone and 17β-estradiol concentration and content were higher in the heated group. Ovary sterologenic enzymes gene P450scc and estrogen receptor expression level increased. The FSH receptor decreased in heat-stressed quails. MetaboAnalyst analysis indicated that high temperature affects propanoate metabolism, beta-alanine metabolism, aspartate metabolism, and histidine metabolism. Triglyceride and cholesterol levels in the liver increased in the heated group. The heated group also had an increased mRNA expression of AGPAT5, apoptosis gene caspase3, and the immunocytokine genes IL-6 and TLR4. However, NF-κB gene expression decreased. These results suggest that high temperatures affect lipid metabolism and apoptosis and cause inflammation in the liver. High temperature induced ovarian dysfunction, which resulted in the decline of hierarchical follicle number and weight, egg weight, and chick birth weight. The increased level of 17β-estradiol suggests liver damage. Protecting liver function from damage may assist quails cope in summer.

Assessment of Intraseasonal Variation in Hospitalization Associated With Heat Exposure in Brazil

The onset of the hot season is known to be adversely associated with a range of health outcomes. However, little is known about whether the association is constant over the course of the hot season. To quantify the change in the association between heat exposure and hospitalization from the early to late hot season in the Brazilian population. This time-stratified case-crossover study used daily data on hospitalization and weather conditions during the 2000 to 2015 hot seasons in 1814 Brazilian cities. There were 49 145 997 admissions during the study period. Data analysis was conducted between May 12, 2018, and July 2, 2018. Increase in daily mean temperature. Daily hospitalizations were recorded. Conditional quasi-Poisson regression with time-varying constrained distributed lag model was used to examine the city-specific association between heat and hospitalization in the early or late hot season. City-specific estimates were then pooled at the national level using random-effect meta-analysis. Stratified analyses were conducted by 5 regions, sex, 10 age groups, and 7 cause-specific categories. Of the 49 145 997 admissions (59% women), the median (interquartile range) age was 33.3 (19.8-55.7) years. At the national level, the risk of hospitalization increased by 4.6% (95% CI, 4.3%-4.9%) and 2.3% (95% CI, 1.9%-2.6%) for every 5°C increase in daily mean temperature in the early and late hot season, respectively. Exposure to early heat was associated with greater risk of hospitalization for residents in the northeast (6.4%; 95% CI, 5.5%-7.3%) and central west (7.1%; 95% CI, 6.1%-8.2%) compared with other regions. Children aged 0 to 9 years and elderly individuals (aged ≥80 years) were most susceptible. Admissions due to endocrine, nutritional, and metabolic diseases were most strongly associated with heat exposure. There was an attenuation in the heat-associated risk of hospitalization from the early to late hot season for all subgroups except young children and patients with hospitalization caused by respiratory illness. In this study, the association between heat exposure and hospitalization attenuated temporally for most of the Brazilian population. Preventive strategies to mitigate the association of high temperature with population health should focus in particular on the first few days of heat exposure.

Chronic Heat Stress Damages Small Intestinal Epithelium Cells Associated with the Adenosine 5'-Monophosphate-Activated Protein Kinase Pathway in Broilers.

Heat-stressed broilers usually reduce their feed intake, leading to energy imbalance and disturbing the homeostasis in the small intestine. This study was aimed to explore heat-stress-mediated physiological features that may be ascribed to impairments in the intestinal tract of broilers. The results revealed that heat exposure increased the activities of trypsin and Na+/K+-ATPase, while it decreased the activities of amylase, lipase, and maltase as well as the proliferating cell nuclear antigen cells in the jejunum after 14 days of heat exposure. Meanwhile, heat stress upregulated the mRNA expressions of AMPKα1, LKB1, and HIF-1α and protein expressions of p-AMPKαThr172 and p-LKB1Thr189 in the small intestine after 7 or 14 days of heat exposure. In conclusion, chronic heat exposure impeded the development of digestive organs, disordered the activities of intestinal digestive enzymes, and impaired the intestinal epithelial cells by increasing the cell apoptosis and declining cell proliferation, which might be correlated with the adenosine 5'-monophosphate-activated protein kinase signaling pathway. Additionally, heat stress upregulated the gene expression of HIF-1α, which indicated that heat stress may disturb the homeostasis in the intestine.

Heat-stress-modulated induction of NF-\u03baB leads to brucellacidal pro-inflammatory defense against Brucella abortus infection in murine macrophages and in a mouse model

BackgroundBrucella causes a chronic and debilitating infection that leads to great economic losses and a public health burden. In this study, we demonstrated the brucellacidal effect of heat shock mediated by the induction of pro-inflammatory cytokines, reactive oxygen species (ROS) accumulation and apoptosis in murine macrophages and in mice.ResultsRAW264.7 cells were incubated at 43 °C, and BALB/c mice were subjected to whole body hyperthermia. The data showed a reduction in bacterial survival in the mice after daily heat exposure. This was accompanied by increased levels of cytokines TNF, IL-6, IL-1β and IFN-γ in the sera of the mice. Gene expression of NF-κB and inducible nitric oxide production were also induced in the mouse splenic cells. In parallel with the bacterial reduction in the mouse model, an increased bactericidal effect was observed in RAW264.7 cells after exposure to heat stress. In addition, the heat stress increased both the nuclear translocation of NF-κB and the expression of the heat shock proteins HSP70 and HSP90 in murine macrophages. Furthermore, heat exposure induced the increase of pro-inflammatory cytokines, ROS accumulation and apoptosis but did not affect the production of nitric oxide (NO) in macrophages.ConclusionThis study demonstrated the induction of innate immune responses by heat stress that significantly reduced the intracellular survival of B. abortus in vitro and in vivo. Transcriptional factor NF-κB, which is a master regulator, could be termed a key activator of heat-induced immunity against Brucella. The increase in the expression and activation of NF-κB in splenic cells and macrophages was followed by enhanced antimicrobial effectors, including cytokines, ROS and NO that may contribute to the reduction of bacterial survival.

Homoeolog-specific activation of genes for heat acclimation in the allopolyploid grass Brachypodium hybridum.

BackgroundAllopolyploid plants often show wider environmental tolerances than their ancestors; this is expected to be due to the merger of multiple distinct genomes with a fixed heterozygosity. The complex homoeologous gene expression could have been evolutionarily advantageous for the adaptation of allopolyploid plants. Despite multiple previous studies reporting homoeolog-specific gene expression in allopolyploid species, there are no clear examples of homoeolog-specific function in acclimation to a long-term stress condition.ResultsWe found that the allopolyploid grass Brachypodium hybridum and its ancestor Brachypodium stacei show long-term heat stress tolerance, unlike its other ancestor, Brachypodium distachyon. To understand the physiological traits of B. hybridum, we compared the transcriptome of the 3 Brachypodium species grown under normal and heat stress conditions. We found that the expression patterns of approximately 26% and approximately 38% of the homoeolog groups in B. hybridum changed toward nonadditive expression and nonancestral expression, respectively, under normal condition. Moreover, we found that B. distachyon showed similar expression patterns between normal and heat stress conditions, whereas B. hybridum and B. stacei significantly altered their transcriptome in response to heat after 3 days of stress exposure, and homoeologs that were inherited from B. stacei may have contributed to the transcriptional stress response to heat in B. hybridum. After 15 days of heat exposure, B. hybridum and B. stacei maintained transcriptional states similar to those under normal conditions. These results suggest that an earlier response to heat that was specific to homoeologs originating from B. stacei contributed to cellular homeostasis under long-term heat stress in B. hybridum.ConclusionsOur results provide insights into different regulatory events of the homoeo-transcriptome that are associated with stress acclimation in allopolyploid plants.

Chapter 28 - Neurogenesis in the thermoregulatory system

In response to various internal and external stimuli, neuronal progenitor cells in the hypothalamic area proliferate and differentiate to functionally working neurons even in adult animals. This is the case in the thermoregulatory system, especially in the process of heat acclimation. The heat acclimation process presents two different patterns, namely short-term and long-term heat acclimation. In rats, long-term heat acclimation is attained by exposing subjects to constant heat for more than 4 weeks, while short-term heat acclimation is established within several days of heat exposure. Heat exposure for more than 6 days facilitates cell proliferation in the ependymal layer of the third ventricle. The newborn cells then migrate into the hypothalamic parenchyma. After 33 days of heat exposure, the newborn cells abruptly differentiate to mature neurons. A part of the newborn cells are incorporated in a neuronal circuit in the hypothalamus. However, only 6 days of heat exposure hardly promote neuronal differentiation. An administration of mitosis inhibitor interferes with cell proliferation in the hypothalamic area and attenuates heat acclimation-induced improvement of heat tolerance. Long-term, but not short-term, heat acclimation may be established by generating new functional neurons in the hypothalamic area, which is where an important part of the thermoregulatory circuitry exists in rats.

The Effect of Moderate Heat on Rat Pituitary ACTH Cells: Histomorphometric, Immunofluorescent and Hormonal Study

AbstractIn areas with moderate continental climate, increased average ambient temperature during the summer represents a stressogenic factor that affects the hypothalamo-pituitaryadrenocortical axis in mammals. Therefore, we wanted to examine the effects of 4 days of constant exposure to moderately elevated ambient temperature (35 ± 1oC) on the histomorphometric and immunofl uorescent characteristics, as well as on the hormonal secretion of pituitary corticotropes (ACTH) cells in adult male rats. In comparison with the controls kept at 20 ± 2oC, a signifi cant increase (p&lt;0.05) of the absolute and relative pituitary weight (23.1% and 36.1%, respectively) was registered after exposure to heat. The localization, as well as the shape of the ACTH cells in the heat exposed group was not signifi cantly altered, but their immunopositivity was weaker. After 4 days of heat exposure, a weaker signal confi rmed the relative fl uorescence intensity of the ACTH cells (15.3%, p&lt;0.05). In heat exposed rats, an increase of the cellular and nuclear volumes of immunolabelled ACTH cells and decrease of their volume density (6.9%, 14.3% and 20.0%, respectively; p&lt;0.05) was registered. Observed histomorphometric and immunofl uorescent features of the pituitary ACTH cells were in accordance with the increased (p&lt;0.05) value of plasma adrenocorticotropic hormone (ACTH) by 23.7% compared to the control rats. It can be concluded that the 4-day exposure to moderately elevated ambient temperature intensifi es pituitary ACTH secretion in adult male rats.

Chronic Heat Stress Impairs the Quality of Breast-Muscle Meat in Broilers by Affecting Redox Status and Energy-Substance Metabolism.

We investigated the molecular mechanisms by which chronic heat stress impairs the breast-meat quality of broilers. Broilers were assigned to three groups: the normal control (NC) group, heat-stress (HS) group, and pair-fed (PF) group. After 7 days of heat exposure (32 °C), the high temperature had caused oxidative stress; elevated the activity of citrate synthase (CS), the mRNA expression of M-CPT1, and the phosphorylation level of AMPKα; and reduced the mRNA expression of avUCP. After 14 days of heat exposure, the heat stress had increased the lightness and drip loss and decreased the pH and shear force of the breast meat. Additionally, the heat exposure had increased the mRNA expressions of FAS, ACC, and PDK4; the content of lipids; and the activities of lactic dehydrogenase and pyruvate kinase, and it had decreased the mRNA expression of M-CPT1 and the activity of CS. In conclusion, chronic heat stress impairs meat quality by causing mitochondria to malfunction and affecting energy-substance aerobic metabolism, resulting in increased glycolysis and intramuscular fat deposition.

Heat acclimation causes a linear decrease in sweat sodium ion concentration

The purpose of this study was to determine the time course for the previously reported reduction in sweat sodium ion concentration during heat acclimation. Four healthy volunteers completed 7 consecutive days of heat acclimation which included 2h of treadmill walking in a 40°C and 40% relative humidity environment. A modified constant hyperthermia protocol was used as workloads were increased each day to maintain a constant core temperature over the 7 days of heat acclimation. Forearm sweat was collected 3 times during each 2h exercise bout on days 1, 3, 5, and 7 of heat acclimation. Forearm sweat rate and sweat sodium ion concentration were determined from each sample. The results showed that there was a significant (p < 0.05) downward shift in the mean sweat rate vs. sweat sodium ion concentration relationship on days 3, 5, and 7 of heat acclimation, as compared to the pre-heat acclimation (day 1) data. Thus, at any given sweat rate, heat acclimation resulted in a significantly lower sweat sodium ion concentration. The response was very rapid and occurred following only 2 consecutive days of heat exposure (i.e., day 3 vs. day 1 data). Furthermore, the calculated sweat sodium ion concentration, at a sweat rate of 1µl/cm2/min, decreased linearly (r = − 0.50, p < 0.05) during the 7 days of heat acclimation. Such results suggest that heat acclimation rapidly improves sodium ion reabsorption from the eccrine sweat gland duct as evidenced by significant reductions in the sweat sodium ion concentration.

Excess burden of non-communicable disease years of life lost from heat in rural Burkina Faso: a time series analysis of the years 2000–2010

ObjectivesInvestigate the association of heat exposure on years of life lost (YLL) from non-communicable diseases (NCD) in Nouna, Burkina Faso, between 2000 and 2010.DesignDaily time series regression analysis using distributed...

Spontaneously hypertensive rats are sensitive to thoracic aorta damage induced by a hot and humid environment.

The purpose of this study was to investigate the effect of a hot and humid environment on thoracic aorta damage in spontaneously hypertensive rats (SHRs). Wistar-Kyoto (WKY) rats were randomly divided into three groups (n=8 in each group): Control group (WKY-CN), heat exposure for 8 h group (WKY-8) and heat exposure for 24 h group (WKY-24). The CN group was exposed to room temperature (24°C); WKY-8 and WKY-24 group were exposed to heat (32°C) and 65% relative humidity for 8 and 24 h, respectively. Accordingly, SHRs were randomly divided into three groups (n=8 each group): SHR-CN, SHR-8 and SHR-24. After 7 days of heat exposure, the weight, food consumption and blood pressure of rats was measured. Noradrenaline (NA)-induced contraction of aorta rings was measured using an organ bath system, and vascular morphology was observed. Expression levels of apoptotic genes and proteins in the thoracic aorta were also measured. The experimental results indicated that, in the heat exposure environment, rat food intake was reduced. Rat weight was significantly increased in all groups except SHR-24 (all P<0.01 except SHR-8, P<0.05). Heat exposure significantly increased the blood pressure of rats in the WKY-24 (P<0.01 for systolic; P<0.05 for diastolic), SHR-8 and SHR-24 (all P<0.01) groups. This effect was more notable in SHR compared with WKY. NA-induced contraction of aorta rings significantly increased in the SHR-CN group, compared with the WKY-CN group (P<0.01). Heat exposure significantly elevated the NA-induced contraction in both 8 h groups compared with the CN groups (P<0.01). This effect was accompanied by structural damage to the thoracic aorta and increased expression of apoptotic genes and proteins. In conclusion, thoracic aorta damages in SHRs were more sensitive to heat exposure. The enhanced NA-induced contraction may have partly been due to increased apoptosis in the thoracic aorta.

Estimating population heat exposure and impacts on working people in conjunction with climate change.

Increased environmental heat levels as a result of climate change present a major challenge to the health, wellbeing and sustainability of human communities in already hot parts of this planet. This challenge has many facets from direct clinical health effects of daily heat exposure to indirect effects related to poor air quality, poor access to safe drinking water, poor access to nutritious and safe food and inadequate protection from disease vectors and environmental toxic chemicals. The increasing environmental heat is a threat to environmental sustainability. In addition, social conditions can be undermined by the negative effects of increased heat on daily work and life activities and on local cultural practices. The methodology we describe can be used to produce quantitative estimates of the impacts of climate change on work activities in countries and local communities. We show in maps the increasing heat exposures in the shade expressed as the occupational heat stress index Wet Bulb Globe Temperature. Some tropical and sub-tropical areas already experience serious heat stress, and the continuing heating will substantially reduce work capacity and labour productivity in widening parts of the world. Southern parts of Europe and the USA will also be affected. Even the lowest target for climate change (average global temperature change=1.5°C at representative concentration pathway (RCP2.6) will increase the loss of daylight work hour output due to heat in many tropical areas from less than 2% now up to more than 6% at the end of the century. A global temperature change of 2.7°C (at RCP6.0) will double this annual heat impact on work in such areas. Calculations of this type of heat impact at country level show that in the USA, the loss of work capacity in moderate level work in the shade will increase from 0.17% now to more than 1.3% at the end of the century based on the 2.7°C temperature change. The impact is naturally mainly occurring in the southern hotter areas. In China, the heat impact will increase from 0.3 to 2%, and in India, from 2 to 8%. Especially affected countries, such as Cambodia, may have losses going beyond 10%, while countries with most of the population at high cooler altitude, such as Ethiopia, may experience much lower losses.

Effects of dietary supplementation of the osmolyte betaine on growing pig performance and serological and hematological indices during thermoneutral and heat-stressed conditions.

The present study was designed to evaluate the effects of dietary betaine on pig performance and serological and hematological indices during thermoneutral and heat-stressed conditions. Individually housed pigs ( = 64; 39.0 ± 1.5 kg BW) were assigned within weight blocks and sex to 1 of 8 treatments. Treatments consisted of 2 environmental conditions (thermoneutral or heat-stressed) and 4 levels of betaine (0, 0.10, 0.15, and 0.20%). Room temperatures followed a daily pattern with a low of 14°C and a high of 21°C for the thermoneutral environment and a low of 28°C and a high of 35°C for the heat-stressed environment. Experimental diets were fed from d -7 (7 d prior to imposing temperature treatments; constant 21°C) until 28. Respiration rate and rectal temperature were measured on d 0, 1, 2, 3, 7, 14, 21, and 28, and blood samples were collected on d 3 and 28. Heat stress reduced ( ≤ 0.008) ADG (0.710 vs. 0.822 kg/d) and ADFI (1.81 vs. 2.27 kg/d) and increased G:F ( = 0.036; 0.391 vs. 0.365). Betaine tended to quadratically increase G:F ( = 0.071; 0.377, 0.391, 0.379, and 0.366 for 0, 0.10, 0.15, and 0.20% betaine, respectively), regardless of environment. Heat stress increased ( ≤ 0.001) respiration rate (48 vs. 23 breaths/30 s) and rectal temperature (39.47 vs. 38.94°C) throughout d 1 to 28. Betaine at 0.10% reduced rectal temperature in heat-stressed pigs but not in control pigs (interaction, = 0.040). Heat stress increased serum cysteine and triglycerides and reduced Ca, alkaline phosphatase, and lipase, regardless of day of sampling ( ≤ 0.048). Heat stress increased serum creatine phosphokinase (CPK) and K and reduced osmolarity, Na, urea N, methionine, homocysteine, the albumin:globulin ratio, and blood eosinophil count on d 3 but not on d 28 (interaction, ≤ 0.013). Heat stress increased serum Mg, globulin, creatinine, amylase, and γ-glutamyltranspeptidase and reduced , the urea N:creatinine ratio, alanine aminotransferase, NEFA, hemoglobin, hematocrit, and red blood cells on d 28 but not on d 3 (interaction, ≤ 0.034). Betaine increased serum osmolarity and NEFA and reduced CPK and K on d 3 but not on d 28 (interaction, ≤ 0.060) and increased serum creatinine and reduced amylase on d 28 but not on d 3 (interaction ≤ 0.057). Heat stress reduced growth, disturbed ion balance, and increased markers of muscle damage. Betaine had a minor impact on alleviating heat stress with the possible exception of early days of heat exposure. The beneficial effect of betaine was diminished by pig adaptation.

Effect of dehydration heat exposure on thoracic aorta reactivity in rats.

The aim of the present study was to investigate the effect of one week dehydration heat exposure on thoracic aorta reactivity in rats. Eighteen Male Sprague-Dawley rats were randomly divided into 3 groups (n=6 each group): Control group (CN), heat exposure group (HE), dehydration heat exposure group (DHE). The CN group was exposed to a room temperature of 24°C, while the HE and DHE groups were exposed to a heat temperature of 32°C. After 7 days of heat exposure, the heart rate and blood pressure of the rats were measured, and the noradrenaline (NA)-induced contraction on the aorta rings was measured by tension recording. The average contents of malondialdehyde (MDA) and superoxide dismutase (SOD) in serum were detected using ELISA. The expression of apoptotic genes in the thoracic aorta was measured using RT-PCR. Compared with CN, the heart rate in the HE and DHE groups had a tendency to become retarded, but there was no significant difference (P>0.05). In the HE group, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) of the rats were significantly higher than that of the CN (P<0.05). In the DHE group, the SBP of rats was significantly higher than that of the CN (P<0.05), while the SBP, DBP, and MAP of the rats were decreased compared to the rats in the HE group, although there was no statistical significance (P>0.05). In the HE and DHE groups, the NA-induced contraction on the rats thoracic aorta ring was larger than that of the CN (P<0.05), albeit there was no significant difference between the HE and DHE groups (P>0.05). The serum SOD content decreased in the HE and DHE groups, however, the reduction was significant only in the DHE group (P<0.05). The content of MDA in serum was significantly increased in the DHE group (P<0.05). The expression of BAX was significantly upregulated whereas Bcl2 expression was decreased in the DHE group (P<0.05). The results showed that a high temperature was harmful to the body, especially in the case of lack of food and water. Additionally, the heat exposure elevated blood pressure, and increased arterial reactivity, which were related to the elevated production of MDA, led to the impaired production of SOD, and an increase of cell apoptosis. These findings are useful to understand the influence of dehydrated heat exposure on the vascular function, and they provide certain theoretical and experimental guidance for protection under high temperature.

Intermittent heat exposure and thirst in rats.

Adequate water intake, supporting both cardiovascular function and evaporative cooling, is a critical factor in mitigating the effects of heat waves, which are expected to increase with global warming. However, the regulation of water intake during periods of intermittent heat exposure is not well understood. In this study, the effects of access to water or no access during intermittent heat exposure were assessed using male Sprague‐Dawley rats exposed to 37.5°C for 4 h/day. After 7 days of intermittent heat exposure, reductions in evaporative water loss were observed in all animals and reductions in water intake following heat exposure occurred as the days of heat exposure increased. Rats that were not allowed water during the 7 days of exposure had decreased rehydration levels, however, rats allowed access to water increased water intake during exposure and exhibited higher overall rehydration levels over the same time period. Peripheral administration of angiotensin II, mimicking activation of volemic thirst, or hypertonic saline solution, activating intracellular thirst, did not result in alteration of water intake in rats exposed to heat with access to water compared to control rats. In contrast, rats exposed to heat without access to water had reduced water intake after administration of hypertonic saline and increased water intake after administration of angiotensin II compared to control rats. These experiments demonstrate that thirst responses to intermittent heat exposure are altered by providing water during heat exposure and that intermittent heat exposure without access to water alters drinking responses to both intracellular and extracellular thirst challenges.

Multiple Days of Heat Exposure on Firefighters' Work Performance and Physiology.

This study assessed the accumulated effect of ambient heat on the performance of, and physiological and perceptual responses to, intermittent, simulated wildfire fighting tasks over three consecutive days. Firefighters (n = 36) were matched and allocated to either the CON (19°C) or HOT (33°C) condition. They performed three days of intermittent, self-paced simulated firefighting work, interspersed with physiological testing. Task repetitions were counted (and converted to distance or area) to determine work performance. Participants were asked to rate their perceived exertion and thermal sensation after each task. Heart rate, core temperature (Tc), and skin temperature (Tsk) were recorded continuously throughout the simulation. Fluids were consumed ad libitum. Urine volume was measured throughout, and urine specific gravity (USG) analysed, to estimate hydration. All food and fluid consumption was recorded. There was no difference in work output between experimental conditions. However, significant variation in performance responses between individuals was observed. All measures of thermal stress were elevated in the HOT, with core and skin temperature reaching, on average, 0.24 ± 0.08°C and 2.81 ± 0.20°C higher than the CON group. Participants’ doubled their fluid intake in the HOT condition, and this was reflected in the USG scores, where the HOT participants reported significantly lower values. Heart rate was comparable between conditions at nearly all time points, however the peak heart rate reached each circuit was 7 ± 3% higher in the CON trial. Likewise, RPE was slightly elevated in the CON trial for the majority of tasks. Participants’ work output was comparable between the CON and HOT conditions, however the performance change over time varied significantly between individuals. It is likely that the increased fluid replacement in the heat, in concert with frequent rest breaks and task rotation, assisted with the regulation of physiological responses (e.g., heart rate, core temperature).