Effect of Flavonoids in Hawthorn and Vitamin C Prevents Hypertension in Rats Induced by Heat Exposure.

BACKGROUND: Excessive oxidative stress is associated with hypertension in professional high-temperature working conditions. Polyphenols exhibit a cardioprotective effect. Hawthorn contains high amounts of flavonoids, though its effect on hypertension protection has yet to be studied. This study aims to investigate this effect of extract of hawthorn (EH) or its combination with vitamin C (Vit. C) in rats induced by working under a hot environment. METHODS: Forty-two male rats were randomly divided into a control group under normal temperature and six treatment groups exposed at 33 ± 1 °C along with 1 h of daily treadmill running. They were orally provided with water, Vit. C (14mg/kg), EH (125, 250, and 500 mg/kg), and EH500 + Vit. C, once a day for four weeks. RESULTS: Both EH and Vit. C alone reduced the systolic and diastolic blood pressure of rats exposed to the heat environment; however, their joint supplementation completely maintained their blood pressure to the normal level throughout the experimental period. No morphological changes were found on the intima of aorta. Moreover, the co-supplementation of EH and Vit. C prevented the changes of heat exposure in inducing oxidative stress markers, such as glutathione peroxidase, catalase, total antioxidant capacity, and nitric oxide; the synergistic action was more effective than either individual treatment of EH and Vit. C. Furthermore, the administration of EH had more potent effects on increasing superoxide dismutase, IL-2, the 70 kilodalton heat shock proteins and high sensitivity C reactive protein, and decreasing serum malondialdehyde and lipofuscin in vascular tissue than those in Vit. C group. CONCLUSIONS: A strong synergistic effect of EH and Vit. C on the prevention of hypertension under heat exposure was established, as they inhibited the oxidative stress state. This study also sets up a novel intervention strategy in animal models for investigation on the early phases of hypertension induced by heat exposure.

A hypothalamomedullary network for physiological responses to environmental stresses.

Various environmental stressors, such as extreme temperatures (hot and cold), pathogens, predators and insufficient food, can threaten life. Remarkable progress has recently been made in understanding the central circuit mechanisms of physiological responses to such stressors. A hypothalamomedullary neural pathway from the dorsomedial hypothalamus (DMH) to the rostral medullary raphe region (rMR) regulates sympathetic outflows to effector organs for homeostasis. Thermal and infection stress inputs to the preoptic area dynamically alter the DMH → rMR transmission to elicit thermoregulatory, febrile and cardiovascular responses. Psychological stress signalling from a ventromedial prefrontal cortical area to the DMH drives sympathetic and behavioural responses for stress coping, representing a psychosomatic connection from the corticolimbic emotion circuit to the autonomic and somatic motor systems. Under starvation stress, medullary reticular neurons activated by hunger signalling from the hypothalamus suppress thermogenic drive from the rMR for energy saving and prime mastication to promote food intake. This Perspective presents a combined neural network for environmental stress responses, providing insights into the central circuit mechanism for the integrative regulation of systemic organs.

Dietary supplementation of acetate-conjugated tryptophan alters feed intake, milk yield and composition, blood profile, physiological variables, and heat shock protein gene expression in heat-stressed dairy cows.

The purpose of this study was to investigate the effects of dietary supplementation of rumen-protected tryptophan (RPT) at four levels on milk yield, milk composition, blood profile, physiological variables, and heat shock protein gene expression in dairy cows under conditions of moderate-severe heat stress (MSHS, THI = 80~89). Sixteen early-lactating dairy cows (body weight = 719 ± 66.4 kg, days in milk = 74.3 ± 7.1, milk yield = 33.55 ± 3.74 kg, means ± SEM) were randomly assigned in a factorial arrangement to one of the four treatments: control group (n = 4, no RPT supplementation), 15 g/d RPT (n = 4), 30 g/d RPT (n = 4), or 60 g/d RPT group per cow (n = 4) supplemented to the TMR. A higher dry matter intake (DMI) and milk yield were found in the 30 g RPT group compared with the other groups, and the 3.5% fat-corrected milk yield, energy-corrected milk yield, milk fat, protein, ß-casein, mono-unsaturated fatty acid, and poly-unsaturated fatty acid contents, and serum glucose content were observed in the 30 g RPT group (p < 0.05). The milk lactose concentration was significantly higher in the 30 g RPT group compared with the control and 60 g RPT groups (p < 0.05). The plasma cortisol level was lower, while the serotonin and melatonin concentrations were higher in the 30 g group compared with the other groups (p < 0.05). Heat shock protein (HSP) 70 expression was downregulated in the control and 15 g RPT groups, whereas the expression of HSP90 and HSPB1 remained unchanged among the groups. In particular, the 30 g RPT group was considered to have an improved DMI, milk yield, and lactose concentration, as well as anti-heat stress effects due to the simulation of serotonin and melatonin during MSHS.

Dietary taurine supplementation ameliorates muscle loss in chronic heat stressed broilers via suppressing the perk signaling and reversing endoplasmic reticulum-stress-induced apoptosis.

BACKGROUND: Heat stress seriously affects animal health and induces enormous financial losses in poultry production. Exploring the appropriate means for ameliorating unfavorable effects caused by heat stress is essential. We investigated whether taurine supplementation could attenuate breast muscle loss in chronic heat-stressed broilers, as well as its mechanism. We designed three groups: a normal control group (22 °C), a heat stress group (32 °C) and a taurine treatment group (32 °C, basal diet + 5 g·kg-1 taurine). RESULTS: We found that taurine significantly moderated the decreases of breast muscle mass and yield, as well as the increases of serum aspartate aminotransferase activity and serum urine acid level in chronic heat-stressed broilers. Additionally, supplementary taurine significantly alleviated elevations of the cytoplasm Ca2+ concentration, protein expressions of GRP78 and p-PERK, mRNA expressions of Ca2+ channels (RyR1, IP3R3) and endoplasmic reticulum (ER) stress factors (GRP78, GRP94, PERK, EIF2α, ATF4, IRE1, XBP1, ATF6 and CHOP), apoptosis (Caspase-3 and TUNEL), protein catabolism, and the reduction of taurine transporter (TauT) mRNA expression in the breast muscle induced by chronic heat stress. CONCLUSION: Supplementary taurine could attenuate chronic heat stress-induced breast muscle loss via reversing ER stress-induced apoptosis and suppressing protein catabolism. © 2020 Society of Chemical Industry.

Impact of passive heat acclimation on markers of kidney function during heat stress.

NEW FINDINGS: What is the central question of this study? Does passive heat acclimation alter glomerular filtration rate and urine-concentrating ability in response to passive heat stress? What is the main finding and its importance? Glomerular filtration rate remained unchanged after passive heat stress, and heat acclimation did not alter this response. However, heat acclimation mitigated the reduction in urine-concentrating ability and reduced the incidence of albuminuria in young healthy adults after passive heat stress. Collectively, these results suggest that passive heat acclimation might improve structural integrity and reduce glomerular permeability during passive heat stress. ABSTRACT: Little is known about the effect of heat acclimation on kidney function during heat stress. The purpose of this study was to determine the impact of passive heat stress and subsequent passive heat acclimation on markers of kidney function. Twelve healthy adults (seven men and five women; 26 ± 5 years of age; 72.7 ± 8.6 kg; 172.4 ± 7.5 cm) underwent passive heat stress before and after a 7 day controlled hyperthermia heat acclimation protocol. The impact of passive heat exposure on urine and serum markers of kidney function was evaluated before and after heat acclimation. Glomerular filtration rate, determined from creatinine clearance, was unchanged with passive heat stress before (pre, 133 ± 41 ml min-1 ; post, 127 ± 51 ml min-1 ; P = 0.99) and after (pre, 129 ± 46 ml min-1 ; post, 130 ± 36 ml min-1 ; P = 0.99) heat acclimation. The urine-to-serum osmolality ratio was reduced after passive heating (P < 0.01), but heat acclimation did not alter this response. In comparison to baseline, free water clearance was greater after passive heating before (pre, -0.86 ± 0.67 ml min-1 ; post, 0.40 ± 1.01 ml min-1 ; P < 0.01) but not after (pre, -0.16 ± 0.57 ml min-1 ; post, 0.76 ± 1.2 ml min-1 ; P = 0.11) heat acclimation. Furthermore, passive heating increased the fractional excretion rate of potassium (P < 0.03) but not sodium (P = 0.13) or chloride (P = 0.20). Lastly, heat acclimation reduced the fractional incidence of albuminuria after passive heating (before, 58 ± 51%; after, 8 ± 29%; P = 0.03). Collectively, these results demonstrate that passive heat stress does not alter the glomerular filtration rate. However, heat acclimation might improve urine-concentrating ability and filtration within the glomerulus.

[Changes in selected physiological indicators and thermal stress assessment under the influence of baths in a dry and wet sauna in young healthy women]. / Zmiany wybranych wskazników fizjologicznych oraz ocena stresu cieplnego pod wplywem kapieli w saunie suchej i mokrej u mlodych zdrowych kobiet.

BACKGROUND: There are differences between dry and wet sauna baths because of the heat load and human body's reactions. High humidity in a wet sauna makes evaporation of sweat from the skin surface more difficult. In addition, the dynamics of sweating is different in men and women. The aim of the study was to assess changes in physiological indicators and to compare the impact of dry and wet saunas on the thermal comfort feeling, which was assessed using the Bedford thermal scale, and the physiological strain index (PSI) and the cumulative heat stress index (CHSI) in young healthy women. MATERIAL AND METHODS: Ten women aged 22-24 years took part in the study. A session in each sauna lasted 60 min and consisted of 3 thermal 15-min exposures, in 5-min intervals for rest and cooling with water. The temperature in the dry sauna was 91±1.2°C and in the wet sauna 59±1.3°C, while the humidity was 18±0.7% and 60.5±0.8%, respectively. Body weight, systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), rectal temperature (Tre) and the thermal sensation (Bedford scale) were also measured. The PSI and CHSI values were both calculated. RESULTS: The average weight loss after a dry sauna bath was significantly higher than after a wet sauna bath. Significantly higher increases in Tre, as well as in HR were observed after treatment in the wet sauna, compared to the dry sauna. Both treatments resulted in an increase in SBP and a decrease in DBP. The arduousness of thermal discomfort and the levels of PSI and CHSI were skurgreater in the wet sauna bathing than in the dry sauna. CONCLUSIONS: Heat exposure in the wet sauna creates a greater burden for young women's bodies than the same dry sauna treatment, and the changes observed in the examined traits were higher than in men subjected to similar thermal loads. Med Pr. 2019;70(6):701-10.

Effect of heat stress on vascular outcomes in humans.

In addition to its role as an environmental stressor, scientists have recently demonstrated the potential for heat to be a therapy for improving or mitigating declines in arterial health. Many studies at both ends of the scientific controls spectrum (tightly controlled, experimental vs. practical) have demonstrated the beneficial effects of heating on microvascular function (e.g., reactive hyperemia, cutaneous vascular conductance); endothelial function (e.g., flow-mediated dilation); and arterial stiffness (e.g., pulse-wave velocity, compliance, ß-stiffness index). It is important to note that findings of beneficial effects are not unanimous, likely owing to the varied methodology in both heating protocols and assessments of outcome measures. Mechanisms of action for the effects of both acute and chronic heating are also understudied. Heat science is a very promising area of human physiology research, as it has the potential to contribute to approaches addressing the global cardiovascular disease burden, particularly in aging and at risk populations, and those for whom exercise is not feasible or recommended.

Hemostatic responses to exercise, dehydration, and simulated bleeding in heat-stressed humans.

Heat stress followed by an accompanying hemorrhagic challenge may influence hemostasis. We tested the hypothesis that hemostatic responses would be increased by passive heat stress, as well as exercise-induced heat stress, each with accompanying central hypovolemia to simulate a hemorrhagic insult. In aim 1, subjects were exposed to passive heating or normothermic time control, each followed by progressive lower-body negative pressure (LBNP) to presyncope. In aim 2 subjects exercised in hyperthermic environmental conditions, with and without accompanying dehydration, each also followed by progressive LBNP to presyncope. At baseline, pre-LBNP, and post-LBNP (<1, 30, and 60 min), hemostatic activity of venous blood was evaluated by plasma markers of hemostasis and thrombelastography. For aim 1, both hyperthermic and normothermic LBNP (H-LBNP and N-LBNP, respectively) resulted in higher levels of factor V, factor VIII, and von Willebrand factor antigen compared with the time control trial (all P < 0.05), but these responses were temperature independent. Hyperthermia increased fibrinolysis [clot lysis 30 min after the maximal amplitude reflecting clot strength (LY30)] to 5.1% post-LBNP compared with 1.5% (time control) and 2.7% in N-LBNP ( P = 0.05 for main effect). Hyperthermia also potentiated increased platelet counts post-LBNP as follows: 274 K/µl for H-LBNP, 246 K/µl for N-LBNP, and 196 K/µl for time control ( P < 0.05 for the interaction). For aim 2, hydration status associated with exercise in the heat did not affect the hemostatic activity, but fibrinolysis (LY30) was increased to 6-10% when subjects were dehydrated compared with an increase to 2-4% when hydrated ( P = 0.05 for treatment). Central hypovolemia via LBNP is a primary driver of hemostasis compared with hyperthermia and dehydration effects. However, hyperthermia does induce significant thrombocytosis and by itself causes an increase in clot lysis. Dehydration associated with exercise-induced heat stress increases clot lysis but does not affect exercise-activated or subsequent hypovolemia-activated hemostasis in hyperthermic humans. Clinical implications of these findings are that quickly restoring a hemorrhaging hypovolemic trauma patient with cold noncoagulant fluids (crystalloids) can have serious deleterious effects on the body's innate ability to form essential clots, and several factors can increase clot lysis, which should therefore be closely monitored.

Effects of pre-lambing maternal energy supplementation on post-weaning productive performance and thermoregulatory capacity of heat-stressed male lambs.

Nutritional requirements of sheep during late gestation increase as a consequence of high fetal growth, mammary tissue development and colostrum synthesis. While prepartum energy supplementation is a nutritional strategy to improve lamb postnatal performance in thermoneutral environments, this has not been studied under heat stress. This study aimed to evaluate effects of maternal energy supplementation during the last third of pregnancy on post-weaning feedlot performance and thermoregulation capacity of heat-stressed male lambs born from multiple births. Twenty Dorper x Pelibuey entire male lambs with initial body weight of 18.2 ±â€¯0.4 kg, aged 2.7 mo (weaned) and born in multiple pregnancies were used in a 32 d feeding study. Treatments were based in the prenatal origin of the lambs: 1) ewes fed 100 (n = 10, Control) and 2) 125% (n = 10, Supplemented) of metabolizable energy requirements from day 100 of gestation to lambing. Lambs were housed outdoor in individual pens under summer environment conditions in an arid region (temperature = 36 ±â€¯4.4 °C and temperature-humidity index = 81 ±â€¯3.9 units). Overall feedlot performance was not affected by pre-partum maternal feeding, although lower (P = 0.04) growth rate and feed efficiency occurred during the last 8 d of the study in lambs born from supplemented ewes. Rectal temperature, respiratory rate and hair coat temperature during daytime were unaffected by prepartum supplementation. Serum concentrations of glucose, cholesterol, urea, total protein and thyroid hormones were similar between lambs born from control and supplemented ewes. It is concluded that, in hair sheep breeds, prepartum energy supplementation did not alter overall post-weaning productive performance and thermoregulation capacity of heat-stressed male lambs that were born in multiple pregnancies.

Folic acid supplementation improves vascular endothelial function, yet not skin blood flow during exercise in the heat, in patients with heart failure.

Heart failure (HF) patients are susceptible to heat strain during exercise, secondary to blunted skin blood flow (SkBF) responses, which may be explained by impaired nitric oxide (NO)-dependent vasodilation. Folic acid improves vascular endothelial function and SkBF through NO-dependent mechanisms in healthy older individuals and patients with cardiovascular disease. We examined the effect of folic acid supplementation (5 mg/day for 6 wk) on vascular function [brachial artery flow-mediated dilation (FMD)] and SkBF responses [cutaneous vascular conductance (CVC)] during 60 min of exercise at a fixed metabolic heat production (300 WHprod) in a 30°C environment in 10 patients with HF (New York Heart Association Class I-II) and 10 healthy controls (CON). Serum folic acid concentration increased in HF [preintervention (pre): 1.4 ± 0.2; postintervention (post): 8.9 ± 6.7 ng/ml, P = 0.01] and CON (pre: 1.3 ± 0.6; post: 5.2 ± 4.9 ng/ml, P = 0.03). FMD improved by 2.1 ± 1.3% in HF ( P < 0.01), but no change was observed in CON postintervention ( P = 0.20). During exercise, the external workload performed on the cycle ergometer to attain the fixed level of heat production for exercise was similar between groups (HF: 60 ± 13; CON: 65 ± 20 external workload, P = 0.52). Increases in CVC during exercise were similar in HF (pre: 0.89 ± 0.43; post: 0.83 ± 0.45 au/mmHg, P = 0.80) and CON (pre: 2.01 ± 0.79; post: 2.03 ± 0.72 au/mmHg, P = 0.73), although the values were consistently lower in HF for both pre- and postintervention measurement intervals ( P < 0.05). These findings demonstrate that folic acid improves vascular endothelial function in patients with HF but does not enhance SkBF during exercise at a fixed metabolic heat production in a warm environment.

Coptidis Rhizoma Prevents Heat Stress-Induced Brain Damage and Cognitive Impairment in Mice.

Heat stress conditions lead to neuroinflammation, neuronal death, and memory loss in animals. Coptidis Rhizoma (CR) exhibits potent fever-reducing effects and has been used as an important traditional medicinal herb for treating fever. However, to date, the effects of antipyretic CR on heat-induced brain damages have not been investigated. In this study, CR significantly reduced the elevation of ear and rectal temperatures after exposure to heat in mice. Additionally, CR attenuated hyperthermia-induced stress responses, such as release of cortisol into the blood, and upregulation of heat shock protein and c-Fos in the hypothalamus and hippocampus of mice. The administration of CR inhibited gliosis and neuronal loss induced by thermal stress in the hippocampal CA3 region. Treatment with CR also reduced the heat stress-induced expression of nuclear factor kappa ß, tumor necrosis factor-α, and interleukin-1ß (IL-1ß) in the hippocampus. Moreover, CR significantly decreased proinflammatory mediators such as IL-9 and IL-13 in the heat-stressed hypothalamus. Furthermore, CR attenuated cognitive dysfunction triggered by thermal stress. These results indicate that CR protects the brain against heat stress-mediated brain damage via amelioration of hyperthermia and neuroinflammation in mice, suggesting that fever-reducing CR can attenuate thermal stress-induced neuropathology.

Supplementing an immunomodulatory feed ingredient to modulate thermoregulation, physiologic, and production responses in lactating dairy cows under heat stress conditions.

This study compared vaginal temperature, physiologic, and productive parameters in lactating dairy cows supplemented or not with Omnigen-AF (Phibro Animal Health, Teaneck, NJ) during the summer months in a tropical environment. Thirty-two lactating, primiparous (n = 16) and multiparous (n = 16) pregnant Holstein × Gir cows were ranked by parity, days in milk, body weight, and body condition score (BCS), and assigned to receive (SUPP; n = 16) or not (CON; n = 16) Omnigen-AF (Phibro Animal Health, Teaneck, NJ) at 56 g/cow daily (as-fed basis). During the experimental period (d -6 to 56), cows were maintained in a single drylot pen with ad libitum access to water and a total mixed ration, and milked twice daily. Cows received Omnigen-AF mixed with 200 g of corn (as-fed basis) after the daily morning milking through self-locking head gates, whereas CON cows concurrently received 56 g of kaolin mixed with 200 g of corn. For feed intake evaluation, cows from both treatments were randomly divided in 4 groups of 8 cows each, and allocated to 8 individual feeding stations for 3 d. Intake was evaluated 4 times per group from d 1 to 56. From d -6 to 0, d 15 to 28, and d 43 to 56, cow vaginal temperature was recorded hourly. Environmental temperature-humidity index (THI) was also recorded hourly from d 15 to 28 and d 43 to 56. Cows were evaluated for body weight and BCS on d -6 and 56, individual milk production was recorded daily from d -6 to 56, and milk samples were collected on d -6, 0, 7, 14, 21, 28, 35, 42, 49, and 56 for analyses of somatic cell count and milk components. Blood samples were collected on d -6, -3, 0, 9, 15, 18, 21, 24, 27, 36, 45, 48, 51, 54, and 56. Results from samples or observations collected from d -6 to 0 were included as an independent covariate in each respective analysis. Environmental THI was 74.2 ± 0.5 and cows were exposed to THI >68 for 633 h within a total of 672 h of evaluation. Cows assigned to CON had greater vaginal temperature on d 28, 43, 45, and from d 48 to 55 (by 0.38 to 0.52%), as well as greater mean somatic cell count (by 97%) and serum haptoglobin concentrations (by 89%) compared with SUPP cows. Cows assigned to SUPP had greater mean dry matter intake (by 7%), BCS on d 56 (by 11%), and mean serum insulin concentrations (by 35%) compared with CON cows. Hence, SUPP ameliorated hyperthermia, improved nutritional status, and modulated systemic and mammary gland immune parameters in lactating dairy cows exposed to heat stress conditions.

Pectinase-treated Panax ginseng protects heat stress-induced testicular damage in rats.

Testicular hyperthermia is well studied to cause impaired spermatogenesis. In the present study, the protective effect of enzymatically modified (pectinase-treated) Panax ginseng (GINST) against intermittent sub-chronic heat stress-induced testicular damage in rats was investigated. Male Sprague-Dawley rats were divided into four groups: normal control (NC), heat-stressed control (HC), heat-stressed plus GINST-100 mg/kg/day (HG100) and heat-stressed plus GINST-200 mg/kg/day (HG200) treatment groups. GINST (100 and 200 mg/kg/day) was mixed separately with a regular pellet diet and was administered orally for 8 weeks starting from 1 week before heat exposure. Parameters such as organ weight, blood chemistry, sperm kinetic values, expression of antioxidant enzymes, spermatogenesis molecules and sex hormone receptors levels were measured. Data revealed that kidney and epididymis weight were significantly (P < 0.05) decreased with heat stress and recovered by GINST treatment. Further, the altered levels of blood chemistry panels and sperm kinetic values in heat stress-induced rats were attenuated when GINST was administered (P < 0.05). Furthermore, the expression levels of antioxidant-related enzymes (GSTM5 and GPX4), spermatogenesis-related proteins (CREB1 and INHA) and sex hormone receptors (androgen receptor, luteinizing hormone receptor and follicle-stimulating hormone receptor) were reduced by heat stress; however, GINST treatment effectively ameliorated these changes. In conclusion, GINST was effective in reducing heat-induced damage in various male fertility factors in vivo and has considerable potential to be developed as a useful supplement in improving male fertility.

Effects of face/head and whole body cooling during passive heat stress on human somatosensory processing.

We herein investigated the effects of face/head and whole body cooling during passive heat stress on human somatosensory processing recorded by somatosensory-evoked potentials (SEPs) at C4' and Fz electrodes. Fourteen healthy subjects received a median nerve stimulation at the left wrist. SEPs were recorded at normothermic baseline (Rest), when esophageal temperature had increased by ~1.2°C (heat stress: HS) during passive heating, face/head cooling during passive heating (face/head cooling: FHC), and after HS (whole body cooling: WBC). The latencies and amplitudes of P14, N20, P25, N35, P45, and N60 at C4' and P14, N18, P22, and N30 at Fz were evaluated. Latency indicated speed of the subcortical and cortical somatosensory processing, while amplitude reflected the strength of neural activity. Blood flow in the internal and common carotid arteries (ICA and CCA, respectively) and psychological comfort were recorded in each session. Increases in esophageal temperature due to HS significantly decreased the amplitude of N60, psychological comfort, and ICA blood flow in the HS session, and also shortened the latencies of SEPs (all, P < 0.05). While esophageal temperature remained elevated, FHC recovered the peak amplitude of N60, psychological comfort, and ICA blood flow toward preheat baseline levels as well as WBC. However, the latencies of SEPs did not recover in the FHC and WBC sessions. These results suggest that impaired neural activity in cortical somatosensory processing during passive HS was recovered by FHC, whereas conduction velocity in the ascending somatosensory input was accelerated by increases in body temperature.

Muscle sympathetic nerve activity response to heat stress is attenuated in chronic heart failure patients.

Heat stress evokes significant increases in muscle sympathetic nerve activity (MSNA) in healthy individuals. The MSNA response to heat stress in chronic heart failure (CHF) is unknown. We hypothesized that the MSNA response to heat stress is attenuated in CHF. Passive whole body heating was applied with water-perfused suits in 13 patients (61 ± 2 yr) with stable class II-III CHF, 12 age-matched (62 ± 2 yr) healthy subjects, and 14 young (24 ± 1 yr) healthy subjects. Mild heating (i.e., increases in skin temperature ΔTsk ~2-4°C, internal temperature ΔTcore <0.3°C) significantly decreased MSNA in CHF patients; however, it did not significantly alter the MSNA in the age-matched and young healthy subjects. Heat stress (i.e., ΔTsk ~4°C and ΔTcore ~0.6°C) raised MSNA in the age-matched (32.9 ± 3.2 to 45.6 ± 4.2 bursts/min; P < 0.001) and young (14.3 ± 1.7 to 26.3 ± 2.4 bursts/min; P < 0.001) controls, but not in CHF (46.2 ± 5.3 to 50.5 ± 5.3 bursts/min; P = 0.06). The MSNA increase by the heat stress in CHF (Δ4.2 ± 2.0 bursts/min) was significantly less than those seen in the age-matched (Δ12.8 ± 1.7 bursts/min, P < 0.05) and young (Δ12.0 ± 2.7 bursts/min, P < 0.05) control groups. These data suggest that the MSNA response to heat stress is attenuated in CHF patients. We speculate that the attenuated MSNA response to heat stress may contribute to impaired cardiovascular adjustments in CHF in a hot environment.

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

NEW FINDINGS: 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 ± 151 mmHg min) and core hyperthermia trials (563 ± 194 mmHg min) relative to control conditions (1010 ± 246 mmHg min; 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 ± 106 mmHg min; 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.

Temperature and blood flow distribution in the human leg during passive heat stress.

The influence of temperature on the hemodynamic adjustments to direct passive heat stress within the leg's major arterial and venous vessels and compartments remains unclear. Fifteen healthy young males were tested during exposure to either passive whole body heat stress to levels approaching thermal tolerance [core temperature (Tc) + 2°C; study 1; n = 8] or single leg heat stress (Tc + 0°C; study 2; n = 7). Whole body heat stress increased perfusion and decreased oscillatory shear index in relation to the rise in leg temperature (Tleg) in all three major arteries supplying the leg, plateauing in the common and superficial femoral arteries before reaching severe heat stress levels. Isolated leg heat stress increased arterial blood flows and shear patterns to a level similar to that obtained during moderate core hyperthermia (Tc + 1°C). Despite modest increases in great saphenous venous (GSV) blood flow (0.2 l/min), the deep venous system accounted for the majority of returning flow (common femoral vein 0.7 l/min) during intense to severe levels of heat stress. Rapid cooling of a single leg during severe whole body heat stress resulted in an equivalent blood flow reduction in the major artery supplying the thigh deep tissues only, suggesting central temperature-sensitive mechanisms contribute to skin blood flow alone. These findings further our knowledge of leg hemodynamic responses during direct heat stress and provide evidence of potentially beneficial vascular alterations during isolated limb heat stress that are equivalent to those experienced during exposure to moderate levels of whole body hyperthermia.

Carcass and meat quality traits of chickens fed diets concurrently supplemented with vitamins C and E under constant heat stress.

The objective of this study was to determine if a diet supplemented simultaneously with vitamins C and E would alleviate the negative effects of heat stress, applied between 28 and 42 days of age, on performance, carcass and meat quality traits of broiler chickens. A total of 384 male broiler chickens were assigned to a completely randomized design, with a 2×3 factorial arrangement (diet with or without vitamin supplementation and two ambient temperatures plus a pair-feeding group) and 16 replicates. Chickens were kept in thermoneutral conditions up to 28 days of age. They were then housed in groups of four per cage, in three environmentally controlled chambers: two thermoneutral (22.5 and 22.6°C) and one for heat stress (32°C). Half the chickens were fed a diet supplemented with vitamins C (257 to 288 mg/kg) and E (93 to 109 mg/kg). In the thermoneutral chambers, half of the chickens were pair-fed to heat stressed chickens, receiving each day the average feed intake recorded in the heat stress chamber in the previous day. Meat physical quality analyses were performed on the pectoralis major muscle. No ambient temperature×diet supplementation interaction effects were detected on performance, carcass, or meat quality traits. The supplemented diet resulted in lower growth performance, attributed either to a carry-over effect of the lower initial BW, or to a possible catabolic effect of vitamins C and E when supplemented simultaneously at high levels. Heat stress reduced slaughter and carcass weights, average daily gain and feed intake, and increased feed conversion. Growth performance of pair-fed chickens was similar to that of heat stressed chickens. Exposure to heat stress increased carcass and abdominal fat percentages, but reduced breast, liver and heart percentages. Pair-fed chickens showed the lowest fat percentage and their breast percentage was similar to controls. Heat stress increased meat pH and negatively affected meat color and cooking loss. In pair-fed chickens, meat color was similar to the heat stressed group. Shear force was not influenced by heat stress, but pair-fed chickens showed the tenderest meat. In conclusion, reduction in growth performance and negative changes in meat color in heat stressed chickens were attributed to depression in feed intake, whereas negative changes in body composition, higher meat pH and cooking loss were credited to high ambient temperature per se. Diet supplementation with vitamins C and E as antioxidants did not mitigate any of these negative effects.

Effects of passive heat stress on human somatosensory processing.

Herein, we investigated the effects of passive heat stress on human somatosensory processing recorded by somatosensory-evoked potentials (SEPs). Fifteen healthy subjects received a median nerve stimulation at the left wrist under two thermal conditions: Heat Stress and normothermic Time Control. The latencies and amplitudes of P14, N20, P25, N35, P45, and N60 at C4' and P14, N18, P22, and N30 at Fz were evaluated. Under the Heat Stress condition, SEPs were recorded at normothermic baseline (1st), early in heat stress (2nd), when esophageal temperature had increased by ~1.0°C (3rd) and ~2.0°C (4th), and after heat stress (5th). In the Time Control condition, SEPs were measured at the same time intervals as those in the Heat Stress condition. The peak latencies and amplitudes of SEPs did not change early in heat stress. However, the latencies of P14, N20, and N60 at C4' and P14, N18, and P22 at Fz were significantly shorter in the 4th session than in the 1st session. Furthermore, the peak amplitudes of P25 and N60 at C4', and P22 and N30 at Fz decreased with increases in body temperature. On the other hand, under the Time Control condition, no significant differences were observed in the amplitudes or latencies of any component of SEPs. These results suggested that the conduction velocity of the ascending somatosensory input was accelerated by increases in body temperature, and hyperthermia impaired the neural activity of cortical somatosensory processing.

Effects of selenium and vitamin E on performance, physiological response, and selenium balance in heat-stressed sheep.

Forty-two 7-mo-old Australian Merino wethers were used in a 50-d trial to investigate the effects of Se and vitamin E on the performance and physiological responses of heat-stressed sheep. Sheep were exposed to thermoneutral conditions (maximum = 24°C and minimum = 20°C) for 28 d followed by heat (maximum = 38°C and minimum = 28°C) for 22 d. Hot conditions were imposed between 0700 and 1800 h. Sheep were randomly allocated to diets containing 0.8 mg/kg Se (Sel-Plex), 150 mg/kg vitamin E, or 0.8 mg/kg Se and 150 mg/kg vitamin E for either the duration of the study (50 d) or from d 1 of the hot period until the end of the study. A control group that received no supplemental Se and vitamin E for the duration of the study was included. Feed intake was measured daily and sheep were weighed weekly. Blood samples were collected from all sheep before feeding on d 1, 21, and 49 for measurement of biochemical and enzymatic variables. The concentration of Se was determined in offered and refused feed, feces, urine, water, plasma, liver, and kidneys. Exposure to heat reduced ( < 0.05) DMI by 11.9%, ADG by 198 g, serum concentration of urea nitrogen and Se by 17.8%, and plasma total antioxidant status by 26.4%. During hot conditions, sheep receiving Se and vitamin E supplements for 50 d had reduced ( < 0.05) BW loss and elevated G:F compared to control sheep. Serum Se concentration and the plasma total antioxidant status were greatest in sheep receiving Se and vitamin E supplements for 50 d ( < 0.05). These results indicate that dietary supplementation with Se and vitamin E reduces the adverse effects of a high heat load. Additional studies are warranted to elucidate the mechanisms responsible for these effects.