Heat Stress Trial Research Articles

Glomerular filtration rate reserve is reduced during mild passive heat stress in healthy young adults.

We tested the hypothesis that, compared with normothermia, the increase in glomerular filtration rate (GFR) after an oral protein load (defined as the GFR reserve) is attenuated during moderate passive heat stress in young healthy adults. Sixteen participants (5 women; 26 ± 2 yr) completed two experimental visits, heat stress or a normothermic time-control, assigned in a block-randomized crossover design. During the heat stress trial, core temperature was increased by 0.6°C in the first hour before commencing a 2-min cold pressor test (CPT) to assess renal vasoconstrictor responses. One-hour post-CPT, subjects ingested a whey protein shake (1.2 g of protein/kg body wt), and measurements were taken pre-, 75, and 150 min postprotein. Segmental artery vascular resistance was calculated as the quotient of Doppler ultrasound-derived segmental artery blood velocity and mean arterial pressure and provided an estimate of renal vascular tone. GFR was estimated from creatinine clearance. The increase in segmental artery vascular resistance during the CPT was attenuated during heat stress (end CPT: 5.6 ± 0.9 vs. 4.7 ± 1.1 mmHg/cm/s, P = 0.024). However, the reduction in segmental artery vascular resistance in response to an oral protein load did not differ between heat stress (at 150 min: 1.9 ± 0.4 mmHg/cm/s) and normothermia (at 150 min: 1.8 ± 0.5 mmHg/cm/s; P = 0.979). The peak increase in creatinine clearance postprotein, independent of time, was attenuated during heat stress (+26 ± 19 vs. +16 ± 20 mL/min, P = 0.013, n = 13). GFR reserve is diminished by mild passive heat stress. Moreover, renal vasoconstrictor responses are attenuated by mild passive heat stress, but renal vasodilator responses are maintained.

Critical Environmental Limit Protocol: Validity and Reliability (PSU HEAT)

With increasing average global temperatures and greater frequency, duration, and severity of heat waves, there is an urgent need to better understand the specific environmental temperatures that place humans at greater risk of heat‐related morbidity and mortality. An incremental heat stress protocol can be used to establish critical environmental limits for human heat exchange, i.e., those combinations of ambient temperature and humidity above which heat stress becomes uncompensable and, therefore, unsafe. However, no studies have rigorously investigated the reliability and validity of this experimental paradigm.PURPOSEHere, we assessed the (1) between‐visit repeatability and (2) validity of an experimental paradigm that either holds ambient vapor pressure (Pa) constant and incrementally increases dry‐bulb temperature (Tdb) or vice versa.METHODSTwelve subjects (5M/7W; 25±4 yr) completed a progressive heat stress protocol during which they walked on a treadmill (2.2 mph, 3% gradient) in a controllable environmental chamber while gastrointestinal temperature (Tgi) was continuously monitored. After an equilibration period, the progressive heat stress protocol involved increasing Tdb every 5 min while Pa was held constant (Tcritexperiments), or increasing Pa every 5 min while Tdb was held constant (Pcritexperiments), until an upward inflection and continuous rise in Tgi was observed. The Tcrit or Pcrit was identified as the average Tdb or Pa, respectively, across the 2 min preceding the Tgi inflection point. For repeatability experiments, 11 subjects returned to the lab to repeat the same protocol as their first visit. For validity experiments, 10 subjects returned to the lab for a progressive heat stress trial in which Tdb or Pa was held constant at the Tcrit or Pcrit value from their first visit.RESULTSThe between‐visit repeatability for critical environmental limits was excellent (ICC = 0.98). Similarly, there was excellent agreement between original and validity trials for Tdb (ICC = 0.95) and Pa (ICC = 0.96) at the Tgi inflection point. Furthermore, the wet‐bulb temperature at the Tgiinflection point was not different during reliability (p = 0.78) or validity (p = 0.32) trials compared to original trials.CONCLUSIONTogether, these data provide strong evidence that this experimental paradigm is rigorous, reliable, and valid, supporting its use to investigate critical environmental limits to the maintenance of heat balance.

Ability of Thermal Work Limit (TWL) to Assess Sustainable Heat Stress Exposures.

Thermal Work Limit (TWL) recommends a maximum metabolic rate for a given environmental condition, clothing ensemble, and acclimatization state so that thermal equilibrium can be sustained at or below the limiting metabolic rate. The purpose of this paper was to assess the ability of TWL to recommend maximum sustainable levels of heat stress using an existing database of progressive heat stress trials using four levels of clothing (woven clothing, particle barrier, water barrier, and vapor barrier), three levels of relative humidity, and three levels of metabolic rate. Each trial had a compensable and an uncompensable observation plus and observation at the transition point from compensable to uncompensable. Each observation was classified as a case (steady increase in rectal temperature) or non-case (steady rectal temperature). The data were used to compare the difference between the observed metabolic rate (Mobs) and the limiting metabolic rate of TWL (i.e., ∆LimitTWL = Mobs - TWL), where ∆LimitTWL > 0 was above the TWL limit. The sensitivity and specificity for each of the four clothing ensembles were about 0.96 and about 0.20, respectively. Logistic regression for all the data found that ∆LimitTWL, clothing, metabolic rate, and water vapor pressure were significant predictors of outcome. The ln(odds) equations for each clothing ensemble predicted a probability of an uncompensable exposure. The probability of an uncompensable outcome (case) when ∆LimitTWL = 0 was 0.14 for work clothes and particle barrier, and 0.22 for water barrier and vapor barrier. The probability of a case at ∆LimitTWL = 0 was greater than the probability of a case for the wet bulb globe temperature-based exposure limits where the probability of a case was 0.01. That is, the TWL was less restrictive than WBGT but with higher risk.

Heat Acclimation with or without Normobaric Hypoxia Exposure Leads to Similar Improvements in Endurance Performance in the Heat.

Background: Combining the key adaptation of plasma volume (PV) expansion with synergistic physiological effects of other acclimation interventions to maximise endurance performance in the heat has potential. The current study investigated the effects of heat acclimation alone (H), combined with normobaric hypoxia exposure (H+NH), on endurance athletic performance. Methods: Well-trained participants completed a heat-stress trial (30 °C, 80% relative humidity (RH), 20.8% fraction of inspired oxygen (FiO2)) of a 75 min steady-state cycling (fixed workload) and a subsequent 15 min cycling time trial for distance before and after intervention. Participants completed 12 consecutive indoor training days with either heat acclimation (H; 60 min·day−1, 30 °C, 80% RH; 20.8% FiO2) or heat acclimation and overnight hypoxic environment (H+NH; ~12 h, 60% RH; 16% FiO2 simulating altitude of ~2500 m). Control (CON) group trained outdoors with average maximum daily temperature of 16.5 °C and 60% RH. Results: Both H and H+NH significantly improved time trial cycling distance by ~5.5% compared to CON, with no difference between environmental exposures. PV increased (+3.8%) and decreased (−4.1%) following H and H+NH, respectively, whereas haemoglobin concentration decreased (−2%) and increased (+3%) in H and H+NH, respectively. Conclusion: Our results show that despite contrasting physiological adaptations to different environmental acclimation protocols, heat acclimation with or without hypoxic exposure demonstrated similar improvements in short-duration exercise performance in a hot environment.

Signals in the Anthropocene.

Signals in the Anthropocene Adam Dickinson (bio) Anthropogenic pollution is rewriting our climate and the metabolism of our bodies. Chemical, noise, and light pollution, as well as gut microbiomes increasingly tuned to Western diets, have consequences for the hormonal conversations constantly taking place in the endocrine systems of humans and nonhumans. Poetry, as writing most concerned with the limits of writing, is, in my view, well-positioned to respond to these extraordinary acts of inscription, making them legible in ways that might influence prevailing cultural and political conversations around pollution and public health. Situated at the intersection between science and art, my poetic practice integrates creative writing with laboratory-based scientific experiments. My aim is to bring into focus the often inscrutable biological and cultural writing intrinsic to the Anthropocene by responding to the work of art in the work of art—that is, to the metabolic processes of human and nonhuman bodies and their inextricable link to the global metabolism of energy and capital.1 For example, my book Anatomic (Coach House Books, 2018) incorporates the results of chemical and microbial testing on my body. I looked into my blood, urine, and feces, and saw the Anthropocene staring back in the form of persistent organic pollutants and microbial species reflective of a modern, industrialized diet. I wrote about and with what I found. More recently, I have been investigating what it might mean to invite heat into the compositional process in the context of climate change. With laboratory assistance, I raised my internal body temperature by about 1.5°C through a series of heat stress trials that involved cycling on a stationary bicycle in hot and humid conditions (active heating) and wearing a specially designed hot water heated suit for several hours (passive heating). During these trials, I gathered information about changes to my core and skin temperature, blood pressure, brain blood flow, and CO2 uptake. I took cognitive tests at various intervals to measure effects on my memory and response time. I am also currently in the middle of a series of experiments with a [End Page 18] microbiologist, which involve employing a bioreactor that mimics the human colon. Inoculating the bioreactor with a sample of my own gut microbes, I will be looking at the effects of exposures to xenobiotics such as triclosan on the mobilization of antibiotic-resistant genes in my gut. I will also be inducing an "extinction event" in a sample of my own gut flora through the application of strong antibiotics. Following this process, I plan to observe the effects of artificial dyes and artificial sweeteners on the post-antibiotic-treated sample as compared to a control. What kind of microbial landscape, nourished entirely by artificial foods, would emerge in the wake of an antibiotic extinction event? While extreme, these speculative yet scientifically informed experiments engage with the kinds of medical, dietary, and commercial pressures at work in the Anthropocene. My recent poems respond directly and indirectly to these and other experiments. Shifting between microscopic and the macroscopic scales, between the personal and the global, and between procedural and thematic compositional methods, these pieces emerge from experimental protocols, research, and resulting data associated with various experiments. The two poems below respond specifically to antibiotic resistance and heat. "A Pump Is the Dream of Starting Over" is based in part on information I acquired from sequencing my microbiome, which revealed the presence of 45 distinct antibiotic-resistant genes in my gut, including several associated with efflux pumps, which are proteins capable of defensively pumping antibiotics out of bacterial cells. The poem explores the efflux pump in relation to antibiotic resistance acquired by my father during his final days in hospital before succumbing to leukemia, and in relation to the figure and function of pumps more generally as mechanisms for memory and thinking. "Asparagus" is a poem concerned with urine as both a transporter of body heat and as a signal. Urine carries within its warmth the products of the body's metabolic processes. It also carries metabolites that can activate other sense receptors. Asparagus produces a strong odor in the urine of those who consume it, as its volatile sulfurous byproducts evaporate...

Bread wheat genotypes phenotypic characterization under late sowing heat stress and genetic diversity analysis of selected heat tolerant genotypes

Wheat is one of the earliest cultivated plants and second major cereal crop of the world that contains human food essentials. Due to climatic variations, crop is exposed to severe environmental conditions. Rising global temperature is expected to result in severe climate shift in future. High temperature exerts negative effects on wheat phenology and grain production. Selection of heat tolerant wheat germplasm is the best stress management strategy. Present research was planned to conduct field-based evaluation of 100 wheat genotypes under normal and heat stress conditions. The data of twelve phenotypic traits was recorded under control and heat stress trials. There were diverse variations observed among genotypes for morphological characters. The high yielding selected wheat lines 68.111-56, CHEN-84, CHEN-74, IWA8611400-65, CHEN-95, CHEN-96, CHEN-86, CHEN-80, 68.111-60 and CHEN-92 were subjected to DNA fingerprinting with Simple Sequence Repeat markers viz; WMC 18, CFA2129, WMC 367, CFD 48, WMC44 and WMC 798. The genetic diversity ranged from 0 to 0.25 with an average value of 0.06. Unweighted pair group of arithmetic means cluster analysis grouped these lines into clusters. Most of the genetic diversity was observed for CHEN-74 and CHEN-96 in cluster. The study has identified genetically diverse, heat tolerant and high yielding wheat genotypes with possible exploitation in development of climate smart wheat varieties.

Renal Vasoconstrictor, but Not Vasodilator, Responses are Modified by Mild Passive Heat Stress in Humans

Purpose The effect of heat stress on renal vascular control is not well studied. For instance, moderate passive heat stress attenuates the renal segmental artery vasoconstrictor response to the cold pressor test (CPT), a sympathoexcitatory stimulus. Whether this occurs with mild passive heat stress is unknown. Additionally, the vasodilatory response of the kidneys has never been studied during heat stress. Oral protein loading is a common approach used to elicit increases in renal blood flow. The purpose of this study was to test the hypothesis that both renal segmental artery vasoconstriction and vasodilation are attenuated during mild passive heat stress. Methods Twelve healthy adults (26 ± 1 y, 3 females) completed two experimental visits where they underwent passive heat stress or a normothermic time control trial in a randomized crossover design. In the heat stress trial, core temperature was increased ~0.5°C within the first hour and was maintained thereafter. Subjects completed a CPT one hour into heat stress which involved subjects immersing their right hand in an agitated ice slurry for 2 min. One hour post-CPT, subjects ingested a whey protein shake (1.2 g of protein/kg of body weight mixed with water). Renal segmental artery blood velocity (BV, Doppler ultrasound) and beat-to-beat blood pressure (Penaz method) were measured pre-CPT, in the final minute of CPT, pre-protein, and 150 min post-protein. Segmental artery vascular resistance (VR) was calculated as mean arterial pressure (MAP) divided by segmental artery BV. Data are presented as mean ± SD. Results Core temperature was higher pre-CPT (37.6 ± 0.5 vs 37.1 ± 0.5°C, P<0.01) and pre-protein (37.7 ± 0.4 vs 37.0 ± 0.4°C, P<0.01), and body fluid loss was greater (3.0 ± 0.9% vs. 1.5 ± 0.4%, P<0.01) in heat stress compared to normothermia. MAP did not differ pre-CPT between heat stress (80 ± 11 mmHg) and normothermia (84 ± 9 mmHg, P=0.76), but during the CPT was lower during heat stress (88 ± 18 vs. 113 ± 14 mmHg, P<0.01). Segmental BV did not differ pre-CPT between heat stress (22 ± 3 cm/s) and normothermia (22 ± 4 cm/s, P=0.99) or during the CPT (P = 0.56). Segmental VR pre-CPT did not differ between heat stress (3.8 ± 0.6 mmHg/cm/s) and normothermia (4.0 ± 0.7 mmHg/cm/s, P=0.91) but was lower in heat stress during the CPT (5.7 ± 1.1 vs. 4.6 ± 1.5 mmHg/cm/s, P=0.01). MAP did not differ pre-protein between heat stress (83 ± 9 mmHg) and normothermia (85 ± 9 mmHg, P=0.93), or post-protein (P=0.94). Segmental BV did not differ pre-protein between heat stress (22 ± 3 cm/s) and normothermia (22 ± 3 cm/s, P=0.99), or post-protein (P=0.36). Segmental VR was not different pre-protein between heat stress (3.9 ± 0.8 mmHg/cm/s, P=0.97) and normothermia (3.9 ± 0.6 mmHg/cm/s). Segmental VR decreased post-protein (P=0.03) but did not differ between heat stress (3.4 ± 0.9 mmHg/cm/s) and normothermia (3.5 ± 0.5 mmHg/cm/s, P=0.98). Conclusion Compared to normothermia, renal segmental artery vasoconstriction during a sympathetic stimulus is attenuated, but renal segmental artery vasodilation following a protein load is not affected by mild passive heat stress.

Gene expression differences between abalone that are susceptible and resilient to a simulated heat wave event

Sudden increases in water temperature can lead to mortality of cultured and wild mollusc communities during the summer months. The frequency and severity of mortality events are expected to increase as climate changes. The molecular basis for individual survival ability is poorly understood. To better understand signatures and mechanisms affecting survival we analyzed the gene expression profiles of greenlip abalone (Haliotis laevigata) classified as susceptible or resilient to laboratory induced heat stress both prior to, and at three time points throughout, the heat stress event. We detected 487 genes that were significantly differentially expressed between resilient and susceptible abalone (28 of these were significantly differentially expressed over all three time points and 26 were significantly differentially expressed throughout two of the three heat stress trial sampling points). These 54 genes also demonstrated a similar relative expression level difference between resilient and susceptible abalone in samples collected six months prior to the heat stress event. Three distinct co-expression networks incorporating these genes were also identified. The most informative transcriptomic differences between resilient and susceptible abalone throughout the heat stress trial were associated with metabolism (e.g. Mitofusin 1) and immune process (e.g. Multiple epidermal growth factor-like domain 10, Lysozyme). These functional mechanisms may enable resilient individuals to endure heat wave events. These signatures could be used to predict an individual's resilience. The findings have application in aiding stock selection for the aquaculture industry, to provide greater resilience to global climate change.

Thermoregulatory adaptations with progressive heat acclimation are predominantly evident in uncompensable, but not compensable, conditions.

This study assessed whether, notwithstanding lower resting absolute core temperatures, alterations in time-dependent changes in thermoregulatory responses following partial and complete heat acclimation (HA) are only evident during uncompensable heat stress. Eight untrained individuals underwent 8 wk of aerobic training (i.e., partial HA) followed by 6 days of HA in 38°C/65% relative humidity (RH) (i.e., complete HA). On separate days, esophageal temperature (Tes), arm (LSRarm), and back (LSRback) sweat rate, and whole body sweat rate (WBSR) were measured during a 45-min compensable (37°C/30% RH) and 60-min uncompensable (37°C/60% RH) heat stress trial pre-training (PRE-TRN), post-training (POST-TRN), and post-heat acclimation (POST-HA). For compensable heat stress trials, resting Tes was lower POST-TRN (36.74 ± 0.27°C, P = 0.05) and POST-HA (36.60 ± 0.27°C, P = 0.001) compared with PRE-TRN (36.99 ± 0.19°C); however, ΔTes was similar in all trials (PRE-TRN:0.40 ± 0.23°C; POST-TRN:0.42 ± 0.20°C; POST-HA:0.43 ± 0.12°C, P = 0.97). While LSRback was unaltered by HA (P = 0.94), end-exercise LSRarm was higher POST-TRN (0.70 ± 0.14 mg·cm-2·min-1, P < 0.001) and POST-HA (0.75 ± 0.16 mg·cm-2·min-1, P < 0.001) compared with PRE-TRN (0.61 ± 0.15 mg·cm-2·min-1). Despite matched evaporative heat balance requirements, steady-state WBSR (31st-45th min) was greater POST-TRN (12.7 ± 1.0 g/min, P = 0.02) and POST-HA (12.9 ± 0.8 g/min, P = 0.004), compared with PRE-TRN (11.7 ± 0.9 g/min). For uncompensable heat stress trials, resting Tes was lower POST-TRN (36.77 ± 0.22°C, P = 0.05) and POST-HA (36.62 ± 0.15°C, P = 0.03) compared with PRE-TRN (36.86 ± 0.24°C). But ΔTes was smaller POST-TRN (0.77 ± 0.19°C, P = 0.05) and POST-HA (0.75 ± 0.15°C, P = 0.04) compared with PRE-TRN (1.10 ± 0.32°C). LSRback and LSRarm increased with HA (P < 0.007), supporting the greater WBSR with HA (POST-TRN:14.4 ± 2.4 g/min, P < 0.001; POST-HA:16.8 ± 2.8 g/min, P < 0.001) compared with PRE-TRN (12.7 ± 3.2 g/min). In conclusion, the thermal benefits of HA are primarily evident when conditions challenge the physiological capacity to dissipate heat.NEW & NOTEWORTHY We demonstrate that neither partial nor complete heat acclimation alters the change in core temperature during compensable heat stress compared with an unacclimated state, despite a marginally greater whole body sweat rate. However, the greater local and whole body sweat rate with partial and complete heat acclimation reduced the rise in core temperature during 60 min of uncompensable heat stress compared with an unacclimated state, suggesting the improvements in heat dissipation associated with heat acclimation are best observed when the upper physiological limits for evaporative heat loss are challenged.

Impact of Fan Use on Physical Work Capacity in Extreme Heat

Emerging evidence suggests that electric fan use can reduce thermoregulatory and cardiovascular strain at air temperatures as high as 42°C during rest. However, there is a dearth of empirical evidence relating to the safety limits for fan use at various combinations of air temperatures and humidity, and how their use impacts physical work capacity (PWC). PURPOSE: The aim of the current study is to provide new threshold limit values for electric fan use during physical work. METHODS: Sixteen young adult males (heterogenous in fitness and anthropological characteristics) performed ~20 trials, consisting of 1 hour of treadmill walking at a fixed heart rate of 130 beats·min-1. The first experimental trial was conducted in a reference environment with no heat-stress (15°C, 50% rh). The remaining trials were conducted at the same fixed heart rate for a maximum of 1 hour at 30-50°C at various humidities. Each experimental trial was conducted with and without electric fans. The PWC in each heat-stress trial was defined as the total energy expended during 1 hour of treadmill walking and was expressed relative (%) to that expended during the reference condition. The study cohort was split into two subgroups with one group performing trials in minimal clothing (shorts only) whilst the second group undertook trials wearing protective clothing covering the legs, torso and arms (e.g. coveralls). RESULTS: Based on individual responses to fan exposure during moderate to heavy work undertaken wearing minimal clothing, forced convection was always beneficial at air temperatures ≤34°C. Between 34 and 43°C, a consistent fan benefit was only observed between 40 and 60% relative humidity, with lowered PWC above and below. In contrast, when protective clothing was worn, the beneficial impact of fans between 34 and 43°C was eroded with negligible effects on PWC observed. PWC was consistently impaired by fan use at air temperatures >43°C. CONCLUSION: These empirical data will facilitate the formulation of comprehensive threshold limit values for fan use during physical work based on biophysical parameters. Funding was provided by ‘Heat-Shield’, European Union's Horizon 2020 research and innovation programme under the Grant agreement no. 668786.

Ability to Discriminate Between Sustainable and Unsustainable Heat Stress Exposures-Part 2: Physiological Indicators.

There are times when it is not practical to assess heat stress using environmental metrics and metabolic rate, and heat strain may provide an alternative approach. Heat strain indicators have been used for decades as tools for monitoring physiological responses to work in hot environments. Common indicators of heat strain are body core temperature (assessed here as rectal temperature Tre), heart rate (HR), and average skin temperature (Tsk). Data collected from progressive heat stress trials were used to (1) demonstrate if physiological heat strain indicators (PHSIs) at the upper limit of Sustainable heat stress were below generally accepted limits; (2) suggest values for PHSIs that demonstrate a Sustainable level of heat stress; (3) suggest alternative PHSIs; and (4) determine if metabolic rate was an effect modifier. Two previous progressive heat stress studies included 176 trials with 352 pairs of Sustainable and Unsustainable exposures over a range of relative humidities and metabolic rates using 29 participants. To assess the discrimination ability of PHSIs, conditional logistic regression and stepwise logistic regression were used to find the best combinations of predictors of Unsustainable exposures. The accuracy of the models was assessed using receiver operating characteristic curves. Current recommendations for physiological heat strain limits were associated with probabilities of Unsustainable greater than 0.5. Screening limits for Sustainable heat stress were Tre of 37.5°C, HR of 105 bpm, and Tsk of 35.8°C. Tsk alone resulted in an area under the curve of 0.85 and the combination of Tsk and HR (area under the curve = 0.88) performed the best. The adjustment for metabolic rate was statistically significant for physiological strain index or ∆Tre-sk as main predictors, but its effect modification was negligible and could be ignored. Based on the receiver operating characteristic curve, PHSIs (Tre, HR, and Tsk) can accurately predict Unsustainable heat stress exposures. Tsk alone or in combination with HR has a high sensitivity, and makes better discriminations than the other PHSIs under relatively constant exposure (metabolic rate and environment) for an hour or so. Screening limits with high sensitivity, however, have low thresholds that limit utility. To the extent that the observed strain is low, there is good evidence that the exposure is Sustainable.

Mapping QTLs associated with agronomic and physiological traits under terminal drought and heat stress conditions in wheat (Triticum aestivum L.).

Wheat crops frequently experience a combination of abiotic stresses in the field, but most quantitative trait loci (QTL) studies have focused on the identification of QTLs for traits under single stress field conditions. A recombinant inbred line (RIL) population derived from SeriM82 × Babax was used to map QTLs under well-irrigated, heat, drought, and a combination of heat and drought stress conditions in two years. A total of 477 DNA markers were used to construct linkage groups that covered 1619.6 cM of the genome, with an average distance of 3.39 cM between adjacent markers. Moderate to relatively high heritability estimates (0.60-0.70) were observed for plant height (PHE), grain yield (YLD), and grain per square meter (GM2). The most important QTLs for days to heading (DHE), thousand grain weight (TGW), and YLD were detected on chromosomes 1B, 1D-a, and 7D-b. The prominent QTLs related to canopy temperature were on 3B. Results showed that common QTLs for DHE, YLD, and TGW on 7D-b were validated in heat and drought trials. Three QTLs for chlorophyll content in SPAD unit (on 1A/6B), leaf rolling (ROL) (on 3B/4A), and GM2 (on 1B/7D-b) showed significant epistasis × environment interaction. Six heat- or drought-specific QTLs (linked to 7D-acc/cat-10, 1B-agc/cta-9, 1A-aag/cta-8, 4A-acg/cta-3, 1B-aca/caa-3, and 1B-agc/cta-9 for day to maturity (DMA), SPAD, spikelet compactness (SCOM), TGW, GM2, and GM2, respectively) were stable and validated over two years. The major DHE QTL linked to 7D-acc/cat-10, with no QTL × environment (QE) interaction increased TGW and YLD. This QTL (5.68 ≤ LOD ≤ 10.5) explained up to 19.6% variation in YLD in drought, heat, and combined stress trials. This marker as a candidate could be used for verification in other populations and identifying superior allelic variations in wheat cultivars or its wild progenitors to increase the efficiency of selection of high yielding lines adapted to end-season heat and drought stress conditions.

The effect of elevations in internal temperature on event-related potentials during a simple cognitive task in humans.

The effect of hyperthermia on cognitive function remains equivocal, perhaps because of methodological discrepancy. Using electroencephalographic event-related potentials (ERPs), we tested the hypothesis that a passive heat stress impairs cognitive processing. Thirteen volunteers performed repeated auditory oddball paradigms under two thermal conditions, normothermic time control and heat stress, on different days. For the heat stress trial, these paradigms were performed at preheat stress (i.e., normothermic) baseline, when esophageal temperature had increased by ∼0.8°C, when esophageal temperature had increased by ∼2.0°C, and during cooling following the heat stress. The reaction time and ERPs were recorded in each session. For the time control trial, subjects performed the auditory oddball paradigms at approximately the same time interval as they did in the heat stress trial. The peak latency and amplitude of an indicator of auditory processing (N100) were not altered regardless of thermal conditions. An indicator of stimulus classification/evaluation time (latency of P300) and the reaction time were shortened during heat stress; moreover an indicator of cognitive processing (the amplitude of P300) was significantly reduced during severe heat stress (8.3 ± 1.3 μV) relative to the baseline (12.2 ± 1.0 μV, P < 0.01). No changes in these indexes occurred during the time control trial. During subsequent whole body cooling, the amplitude of P300 remained reduced, and the reaction time and latency of P300 remained shortened. These results suggest that excessive elevations in internal temperature reduce cognitive processing but promote classification time.

Myocardial functional responses do not contribute to maximal exercise performance in the heat.

BackgroundBoth the extent and means by which maximal oxygen uptake (dot{V}{text{O}}_{ 2hbox{max} }) is depressed by elevated ambient temperature are uncertain. Particularly, information is currently unavailable regarding the possible influence of alterations in myocardial function on dot{V}{text{O}}_{ 2hbox{max} } and performance during exercise in the heat. This study investigated the effects of environmental heat on dot{V}{text{O}}_{ 2hbox{max} }, peak work capacity, and myocardial function during a standard, progressive cycle test to exhaustion. Twelve euhydrated men (aged 20.7 ± 1.7 years) performed a maximal cycle test in an environmental chamber in both heat stress [35°C, 30% relative humidity (RH)] and temperate (20°C, 30% RH) conditions with measurement of standard gas exchange variables, core temperature, and echocardiographic measures of cardiac function.ResultsA small but statistically significant reduction of peak work capacity was observed in the heat stress versus temperate conditions (253 ± 30 and 259 ± 30 W, respectively, p = 0.02). Mean dot{V}{text{O}}_{ 2hbox{max} } was not statistically different in the two conditions (p = 0.16) but values were 3.4% lower in the heat, and 9 of 12 participants demonstrated lower values in the heat stress trial. No differences in responses of heart rate, cardiac output, stroke volume, core temperature, hydration status, or myocardial systolic or diastolic function were observed between the two conditions, but perceived body temperature was higher in the heat.ConclusionsThe small, negative impact of heat on exercise performance and dot{V}{text{O}}_{ 2hbox{max} } could not be explained by disturbances in myocardial functional responses to exercise in young adult males.

Cognitive and perceptual responses during passive heat stress in younger and older adults.

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

Novel Application of Chemical Cold Packs for Treatment of Exercise-Induced Hyperthermia: A Randomized Controlled Trial

Heat-related illness is a common disease with significant morbidity and mortality. Despite no proven efficacy, application of chemical cold packs (CCP) to the skin overlying the large vessels of the neck, groin, and axillae is a traditional recommended cooling modality. The study objective was to compare the cooling rates of CCP applied to these traditional areas vs the glabrous skin surfaces of the cheeks, palms, and soles in exercise-induced hyperthermia. Ten healthy adult male volunteers walked on a treadmill in a heated room (40°±0.5°C) while wearing insulated military overgarments until their esophageal temperatures (Tes) reached 39.2°C. Each participant had three heat stress trials on separate days: no treatment followed by randomly ordered traditional (neck, groin, and axillae) cooling and glabrous skin cooling. With no treatment, Tes remained stable after the first 5 minutes of the heat trial (ΔTes=0.12°±0.07°C/10 min). Traditional cooling followed a linear decline (ΔTes=0.17°±0.04°C/10 min; P<.001). Glabrous cooling enhanced the treatment effect by a steeper decline (ΔTes=0.30°±0.06°C/10 min; P<.001), significantly different from traditional cooling by 2-way analysis of variance (P<.001). Application of CCP to glabrous skin surfaces was more effective for treating exercise-induced heat stress than the traditional CCP cooling intervention. This novel cooling technique may be beneficial as an adjunctive treatment for heat-related illness in the prehospital environment.

Seasonal heat acclimatization in wildland firefighters

The purpose of this study was to determine changes in physiological markers of heat acclimatization across a 4-month wildland fire season. Wildland firefighters (WLFF) (n=12) and non-WLFF (n=14) were assessed pre- and post-season for body mass, percent body fat, and peak V.O2. Both groups completed a 60-min heat stress trial (walking at 50% of peak V.O2) in a climate controlled chamber (43.3°C, 33% RH) pre and post-fire season (May through September). During the trials, core (Tc) and skin (Tsk) temperatures, heart rate (HR), physiological strain index (PSI), and rating of perceived exertion (RPE) were measured. There were no differences pre or post-season between the WLFF and non-WLFF groups in body mass, percent body fat, or peak V.O2. During the 73 days where the WLFF were involved in direct wildland fire suppression, daily high temperature for the WLFF was higher compared to the non-WLFF, 30.6±5.4°C and 26.9±6.1°C, respectively, p<0.05. Tc was lower at post-season compared to pre-season (p<0.05) for the WLFF at 30, 45, and 60min (pre 30, 45, and 60: 37.9±0.3, 38.3±0.3 and 38.5±0.3°C, respectively; post 30, 45, and 60: 37.8±0.3, 38.1±0.3 and 38.2±0.4°C, respectively). For WLFF, PSI was lower (p<0.05) at 15, 30, 45, and 60min at post-season compared to pre-season (4.2±0.7, 5.6±0.9, 6.5±0.9, and 7.1±1.1 for 15, 30, 45, and 60min pre-season, respectively; 3.6±0.8, 4.9±1.0, 5.7±1.2, 6.3±1.3 for 15, 30, 45, and 60min post-season, respectively). For WLFF, RPE was lower during the post-season trial at 30, 45, and 60min (pre 30, 45, and 60: 11.7±1.4, 12.3±1.2, and 13.5±1.4, respectively; post 30, 45, and 60: 10.7±1.2, 11.3±1.3, and 11.9±1.5, respectively), p<0.05. There were no differences between pre and post-season for the non-WLFF for Tc and PSI, but RPE was lower at 15min during the pre-season trial. WLFFs demonstrated significant decreases in Tc, PSI, and RPE during controlled heat stress after the season. Since an age and fitness-matched control group experienced no indication of heat acclimatization, it is suggested that the long-term occupational heat exposure accrued by the WLFFs was adequate to incur heat acclimatization.

Three nights of sleep deprivation does not alter thermal strain during exercise in the heat

Individuals exposed to total sleep deprivation may experience an increased risk of impaired thermoregulation and physiological strain during prolonged physical activity in the heat. However, little is known of the impact of more relevant partial sleep deprivation (PSD). This randomized counterbalanced study investigated the effect of PSD on thermal strain during an exercise-heat stress. Ten healthy individuals performed two stress tests (45 min running, 70 % [Formula: see text] 33 °C, 40 % RH). Each trial followed three nights of controlled sleep: normal [479 (SD 2) min sleep night(-1); Norm] and PSD [116 (SD 4) min sleep night(-1)]. Energy balance and hydration state were controlled throughout the trials. Rectal temperatures (T re), mean skin temperature ([Formula: see text]), heart rate (HR), RPE, and thermal sensations (TS) were measured at regular intervals during each heat stress trial. There was a significant main effect of time (P < 0.05) for all of these variables. However, no differences (P > 0.05) were observed between PSD and Norm, respectively, for T re [39.0 (0.5) vs. 39.1 (0.5) °C], [Formula: see text], [36.1 (0.6) vs. 36.0 (0.7) °C] and HR [181 (13) vs. 182 (13) beats min(-1))] at the end of exercise-heat stress. There were no differences (P > 0.05) in [Formula: see text], PSI, RPE, TS and whole-body sweat rate between PSD versus Norm. Since greater physiological strain during exercise-heat stress did not follow three nights of PSD, it appears that sleep loss may have minimal impact upon thermal strain during exercise in the heat, at least as evaluated within this experiment.

Heat stress does not augment ventilatory responses to presyncopal limited lower body negative pressure

Simulated haemorrhage, e.g. lower body negative pressure (LBNP), reduces central blood volume and mean arterial pressure, while ventilation increases. Passive whole-body heat stress likewise increases ventilation. The objective of this project was to test the hypothesis that ventilatory responses to reductions in central blood volume and arterial pressure during simulated haemorrhage are enhanced when individuals are heat stressed rather than normothermic. Eight healthy men (34 ± 9 years old, 176 ± 6 cm tall and 80.2 ± 4.2 kg body weight) underwent a simulated haemorrhagic challenge via LBNP until presyncope on two separate occasions, namely normothermic control and whole-body heat-stress trials. Baseline ventilation and core and mean skin temperatures were not different between trials (all P > 0.05). Prior to LBNP, heat stress increased core (from 36.8 ± 0.2 to 38.2 ± 0.2°C, P < 0.05) and mean skin temperatures (from 33.9 ± 0.5 to 38.1 ± 0.6°C, P < 0.05), as well as minute ventilation (from 8.01 ± 2.63 to 13.68 ± 6.68 l min(-1), P < 0.01). At presyncope, mean arterial pressure and middle cerebral artery blood velocity decreased in both trials (P < 0.05). At presyncope, ventilation increased to 23.22 ± 6.78 (P < 0.01) and 25.88 ± 10.16 l min(-1) (P < 0.01) in the normothermic and hyperthermic trials, respectively; however, neither the increase in ventilation from the pre-LBNP period nor the absolute ventilation was different between normothermic and hyperthermic trials (P > 0.05). These data suggest that the increase in ventilation during simulated haemorrhage induced via LBNP is not altered in heat-stressed humans.

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.