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PurposeTo determine if 7d of New Zealand blackcurrant (NZBC) extract alters the heat shock, inflammatory and apoptotic response during prolonged exertional-heat stress.MethodsTen men (Age: 29 ± 2 years, Stature: 1.82 ± 0.02 m, Mass: 80.3 ± 2.7 kg, V̇O2max: 56 ± 2 mL·kg−1·min−1) ingested two capsules of CurraNZ™ (NZBC extract: 210 mg anthocyanins·day−1) or PLACEBO for 7d prior to 1 h treadmill run (65% V̇O2max) in hot ambient conditions (34 °C/40% RH). Blood samples were collected before (Pre), immediately after (Post), 1 h after (1-Post), and 4 h after (4-Post) exercise. Heat shock proteins (HSP90, HSP70, HSP32) were measured in plasma. HSP and protein markers of inflammatory capacity (TLR4, NF-κB) and apoptosis (BAX/BCL-2, Caspase 9) were measured in peripheral blood mononuclear cells (PBMC).ResultseHSP32 was elevated at baseline in NZBC(+ 31%; p < 0.001). In PLACEBO HSP32 content in PBMC was elevated at 4-Post(+ 98%; p = 0.002), whereas in NZBC it fell at Post(− 45%; p = 0.030) and 1-Post(− 48%; p = 0.026). eHSP70 was increased at Post in PLACEBO(+ 55.6%, p = 0.001) and NZBC (+ 50.7%, p = 0.010). eHSP90 was increased at Post(+ 77.9%, p < 0.001) and 1-Post(+ 73.2%, p < 0.001) in PLACEBO, with similar increases being shown in NZBC (+ 49.0%, p = 0.006 and + 66.2%, p = 0.001; respectively). TLR4 and NF-κB were both elevated in NZBC at PRE(+ 54%, p = 0.003 and + 57%, p = 0.004; respectively). Main effects of study condition were also shown for BAX/BCL-2(p = 0.025) and Caspase 9 (p = 0.043); both were higher in NZBC.Conclusion7d of NZBC extract supplementation increased eHSP32 and PBMC HSP32 content. It also increased inflammatory and apoptotic markers in PBMC, suggesting that NZBC supports the putative inflammatory response that accompanies exertional-heat stress.

Climate change impact has disturbed the rainfall pattern worsening the problems of water availability in the aquatic ecosystem of India and other parts of the world. Arsenic pollution, mainly through excessive use of groundwater and other anthropogenic activities, is aggravating in many parts of the world, particularly in South Asia. We evaluated the efficacy of selenium nanoparticles (Se-NPs) and riboflavin (RF) to ameliorate the adverse impacts of elevated temperature and arsenic pollution on growth, anti-oxidative status and immuno-modulation in Pangasianodon hypophthalmus . Se-NPs were synthesized using fish gill employing green synthesis method. Four diets i.e., Se-NPs (0 mg kg −1 ) + RF (0 mg kg −1 ); Se-NPs (0.5 mg kg −1 ) + RF (5 mg kg −1 ); Se-NPs (0.5 mg kg −1 ) + RF (10 mg kg −1 ); and Se-NPs (0.5 mg kg −1 ) + RF (15 mg kg −1 ) were given in triplicate in a completely randomized block design. The fish were treated in arsenic (1/10th of LC 50 , 2.68 mg L −1 ) and high temperature (34 °C). Supplementation of the Se-NPs and RF in the diets significantly (p < 0.01) enhanced growth performance (weight gain, feed efficiency ratio, protein efficiency ratio, and specific growth rate), anti-oxidative status and immunity of the fish. Nitroblue tetrazolium (NBT), total immunoglobulin, myeloperoxidase and globulin enhanced (p < 0.01) with supplementation (Se-NPs + RF) whereas, albumin and albumin globulin (A:G) ratio (p < 0.01) reduced. Stress biomarkers such as lipid peroxidation in the liver, gill and kidney, blood glucose, heat shock protein 70 in gill and liver as well as serum cortisol reduced (p < 0.01) with supplementation of Se-NPs and RF, whereas, acetylcholine esterase and vitamin C level in both brain and muscle significantly enhanced (p < 0.01) in compared to control and stressors group (As + T) fed with control diet. The fish were treated with pathogenic bacteria after 90 days of experimental trial to observe cumulative mortality and relative survival for a week. The arsenic concentration in experimental water and bioaccumulation in fish tissues was also determined, which indicated that supplementation of Se-NPs and RF significantly reduced (p < 0.01) bioaccumulation. The study concluded that a combination of Se-NPs and RF has the potential to mitigate the stresses of high temperature and As pollution in P. hypophthalmus .

Afferent neural transmission of temperature sensation from skin thermoreceptors to the central thermoregulatory system is important for the defense of body temperature against environmental thermal challenges. Here, we report a thermosensory pathway that triggers physiological heat-defense responses to elevated environmental temperature. Using in vivo electrophysiological and anatomical approaches in the rat, we found that neurons in the dorsal part of the lateral parabrachial nucleus (LPBd) glutamatergically transmit cutaneous warm signals from spinal somatosensory neurons directly to the thermoregulatory command center, the preoptic area (POA). Intriguingly, these LPBd neurons are located adjacent to another group of neurons that mediate cutaneous cool signaling to the POA. Functional experiments revealed that this LPBd-POA warm sensory pathway is required to elicit autonomic heat-defense responses, such as cutaneous vasodilation, to skin-warming challenges. These findings provide a fundamental framework for understanding the neural circuitry maintaining thermal homeostasis, which is critical to survive severe environmental temperatures.

On many dairy farms cows are kept indoors. Providing outdoor access is often considered desirable, but housing can protect animals from aversive climatic conditions. For example, by providing shade and fans, indoor housing can protect cows from heat stress they might otherwise experience on open pasture. This study tested how public attitudes to cattle rearing varied when participants were experimentally assigned to different scenarios using a 2 x 2 factorial design varying pasture versus indoor housing with or without heat stress. Participants (n = 581) were randomly assigned to a single scenario, and attitudes in response to the scenario were measured using a Likert scale (1 = \"strongly disagree\" to 5 = \"strongly agree\"). We also asked open-ended questions allowing participants to explain their responses. Participants responded most positively to the scenario that provided both pasture access and protection from heat stress (Likert 4.1±0.08), and least positively to scenario with indoor housing and heat stress (Likert 2.2±0.08). However, when the different animal welfare attributes were in conflict (i.e. naturalness as provided by pasture, and biological functioning/affective state as associated with protection from heat stress), participants placed priority on the latter: they were more supportive of the scenario providing indoor housing that protected cows from heat stress (Likert 3.5±0.08), than they were of a pasture rearing system that exposed cows to heat stress (Likert 2.4±0.08). Open-ended responses indicated that participants viewed the lack of protection from heat stress as a failure in the farmer's duty of care towards the cow. We conclude that participants valued both access to pasture and protection from heat stress for dairy cows, but prioritized protecting animal from heat stress when these features were in conflict.

Purpose It is usually stated that glycogen is stored in human muscle bound to water in a proportion of 1:3 g. We investigated this proportion in biopsy samples during recovery from prolonged exercise. Methods On two occasions, nine aerobically trained subjects ( V ˙ O 2 max  = 54.4 ± 1.05 mL kg −1  min −1 ; mean ± SD) dehydrated 4.6 ± 0.2 % by cycling 150 min at 65 % V ˙ O 2 max in a hot-dry environment (33 ± 4 °C). One hour after exercise subjects ingested 250 g of carbohydrates in 400 mL of water (REH LOW ) or the same syrup plus water to match fluid losses (i.e., 3170 ± 190 mL; REH FULL ). Muscle biopsies were obtained before, 1 and 4 h after exercise. Results In both trials muscle water decreased from pre-exercise similarly by 13 ± 6 % and muscle glycogen by 44 ± 10 % ( P  < 0.05). After recovery, glycogen levels were similar in both trials (79 ± 15 and 87 ± 18 g kg −1 dry muscle; P  = 0.20) while muscle water content was higher in REH FULL than in REH LOW (3814 ± 222 vs. 3459 ± 324 g kg −1  dm, respectively; P  < 0.05; ES = 1.06). Despite the insufficient water provided during REH LOW , per each gram of glycogen, 3 g of water was stored in muscle (recovery ratio 1:3) while during REH FULL this ratio was higher (1:17). Conclusions Our findings agree with the long held notion that each gram of glycogen is stored in human muscle with at least 3 g of water. Higher ratios are possible (e.g., during REH FULL ) likely due to water storage not bound to glycogen.

Aerobic exercise and thermal stress instigate robust challenges to the immune system. Various attempts to modify or supplement the diet have been proposed to bolster the immune system responses. The purpose of this study was to identify the impact of yeast beta-glucan (Saccharomyces cerevisiae) supplementation on exercise-induced muscle damage and inflammation. Healthy, active men (29.6 ± 6.7 years, 178.1 ± 7.2 cm, 83.2 ± 11.2 kg, 49.6 ± 5.1 mL/kg/min, n = 16) and women (30.1 ± 8.9 years, 165.6 ± 4.1 cm, 66.7 ± 10.0 kg, 38.7 ± 5.8 mL/kg/min, n = 15) were randomly assigned in a double-blind and cross-over fashion to supplement for 13 days with either 250 mg/day of yeast beta-glucan (YBG) or a maltodextrin placebo (PLA). Participants arrived fasted and completed a bout of treadmill exercise at 55% peak aerobic capacity (VO2Peak) in a hot (37.2 ± 1.8 °C) and humid (45.2 ± 8.8%) environment. Prior to and 0, 2, and 72 h after completing exercise, changes in white blood cell counts, pro- and anti-inflammatory cytokines, markers of muscle damage, markers of muscle function, soreness, and profile of mood states (POMS) were assessed. In response to exercise and heat, both groups experienced significant increases in white blood cell counts, plasma creatine kinase and myoglobin, and soreness along with reductions in peak torque and total work with no between-group differences. Concentrations of serum pro-inflammatory cytokines in YBG were lower than PLA for macrophage inflammatory protein 1β (MIP-1β) (p = 0.044) and tended to be lower for interleukin 8 (IL-8) (p = 0.079), monocyte chemoattractment protein 1 (MCP-1) (p = 0.095), and tumor necrosis factor α (TNF-α) (p = 0.085). Paired samples t-tests using delta values between baseline and 72 h post-exercise revealed significant differences between groups for IL-8 (p = 0.044, 95% Confidence Interval (CI): (0.013, 0.938, d = −0.34), MCP-1 (p = 0.038, 95% CI: 0.087, 2.942, d = −0.33), and MIP-1β (p = 0.010, 95% CI: 0.13, 0.85, d = −0.33). POMS outcomes changed across time with anger scores in PLA exhibiting a sharper decline than YBG (p = 0.04). Vigor scores (p = 0.04) in YBG remained stable while scores in PLA were significantly reduced 72 h after exercise. In conclusion, a 13-day prophylactic period of supplementation with 250 mg of yeast-derived beta-glucans invoked favorable changes in cytokine markers of inflammation after completing a prolonged bout of heated treadmill exercise.

PurposeTo determine the impact of altering dietary sodium intake for 3 days preceding exercise on sweat sodium concentration [Na+], and cardiovascular and thermoregulatory variables.MethodsFifteen male endurance athletes (runners n = 8, cyclists n = 7) consumed a low (LNa, 15 mg kg−1 day−1) or high (HNa, 100 mg kg−1 day−1) sodium diet, or their usual free-living diet [UDiet, 46 (37–56) mg kg−1 day−1] for 3 days in a double-blind, randomized cross-over design, collecting excreted urine (UNa) and refraining from exercise. On day 4, they completed 2 h running at 55% \\[\\dot{V}\\]O2max or cycling at 55% maximum aerobic power in Tamb 35 °C. Pre- and post-exercise blood samples were collected, and sweat from five sites using absorbent patches along the exercise protocol.ResultsUNa on days 2–3 pre-exercise [mean (95% CI) LNa 16 (12–19) mg kg−1 day−1, UDiet 46 (37–56) mg kg−1 day−1, HNa 79 (72–85) mg kg−1 day−1; p < 0.001] and pre-exercise aldosterone [LNa 240 (193–286) mg kg−1 day−1, UDiet 170 (116–224) mg kg−1 day−1, HNa 141 (111–171) mg kg−1 day−1; p = 0.001] reflected sodium intake as expected. Pre-exercise total body water was greater following HNa compared to LNa (p < 0.05), but not UDiet. Estimated whole-body sweat [Na+] following UDiet was 10–11% higher than LNa and 10–12% lower than HNa (p < 0.001), and correlated with pre-exercise aldosterone (1st h r =  − 0.568, 2nd h r =  − 0.675; p < 0.01). Rectal temperature rose more quickly in LNa vs HNa (40–70 min; p < 0.05), but was similar at the conclusion of exercise, and no significant differences in heart rate or perceived exertion were observed.ConclusionsThree day altered sodium intake influenced urinary sodium excretion and sweat [Na+], and the rise in rectal temperature, but had no effect on perceived exertion during moderate-intensity exercise in hot ambient conditions.

Background Fructose intake, mainly as table sugar or high fructose corn syrup, has increased in recent decades and is associated with increased risk for kidney stones. We hypothesized that fructose intake alters serum and urinary components involved in stone formation. Methods We analyzed a previously published randomized controlled study that included 33 healthy male adults (40–65 years of age) who ingested 200 g of fructose (supplied in a 2-L volume of 10% fructose in water) daily for 2 weeks. Participants were evaluated at the Unit of Nephrology of the Mateo Orfila Hospital in Menorca. Changes in serum levels of magnesium, calcium, uric acid, phosphorus, vitamin D, and intact PTH levels were evaluated. Urine magnesium, calcium, uric acid, phosphorus, citrate, oxalate, sodium, potassium, as well as urinary pH, were measured. Results Ingestion of fructose was associated with an increased serum level of uric acid ( p  < 0.001), a decrease in serum ionized calcium ( p  = 0.003) with a mild increase in PTH ( p  < 0.05) and a drop in urinary pH ( p  = 0.02), an increase in urine oxalate ( p  = 0.016) and decrease in urinary magnesium ( p  = 0.003). Conclusions Fructose appears to increase urinary stone formation in part via effects on urate metabolism and urinary pH, and also via effects on oxalate. Fructose may be a contributing factor for the development of kidney stones in subjects with metabolic syndrome and those suffering from heat stress. Trial registration ClinicalTrials.gov NCT00639756 March 20, 2008.

We examined the extent to which peripheral changes affect EMG signal adjustments during repeated sprinting in temperate and hot conditions. Randomised, crossover study. Ten males performed 10×6-s ‘all-out’ cycling sprints (recovery=30s) in either a temperate (24°C/30%rH) or a hot (35°C/40%rH) environment with concomitant surface EMG recordings of the vastus lateralis (VL) and rectus femoris (RF). In addition, peak-to-peak M-wave amplitudes were obtained for each muscle after each sprint (i.e., 15s into recovery). For both the VL and RF muscles RMS decreased across sprint repetitions (P<0.01), while significantly lower values for the VL (P=0.012), but not the RF (P=0.096), occurred in hot vs. temperate conditions. M-wave-normalised RMS for VL muscle decreased across sprint repetitions (P=0.030), with no condition or interaction effects (both P>0.621). M-wave-normalised RMS for the RF muscle was lower in the heat (P<0.034), with no significant sprint or interaction effects (both P>0.240). Controlling for changes in maximal M-wave amplitude of the quadriceps muscles after each bout of a repeated cycling exercise in hot and temperate conditions allows researchers to account for fatigue- and/or heat-induced neural and peripheral adjustments.

PurposeThe aim of this study was to examine the effect of passive heat stress on heart rate variability parameters in healthy children.MethodFifteen children (9.3 ± 1.6 years) of both sexes (eight male) participated in two randomized experimental conditions separated by 5–12 days. Children were seated for 2 h in an environmental chamber for two sessions: neutral (22.4 ± 0.1 °C, 40.4 ± 6.5% RH) and hot (34.9 ± 0.3 °C, 36.6 ± 6.2% RH) conditions. Electrocardiogram, mean skin temperature, tympanic temperature, and blood pressure were recorded. Five min epochs were averaged for analysis of cardiac autonomic function over the 2-h protocol.ResultMean skin and tympanic temperatures and heart rate increased during the hot condition (all p < 0.01) while mean arterial pressure decreased (p < 0.01). During the hot condition, root-mean-square difference of successive normal RR intervals (45 ± 9 to 38 ± 7 ms), and low- (LF, 1536 ± 464 vs. 935 ± 154 ms2) and high-frequency power (HF, 1544 ± 693 vs. 866 ± 355 ms2) decreased, whereas LF/HF ratio increased (1.64 ± 0.24 vs. 2.40 ± 0.23 au); all indices were different from neutral (all p < 0.05). These were all unchanged throughout the neutral condition (all p > 0.05), except for LF/HF ratio which decreased during the neutral condition (p < 0.05).ConclusionMild hyperthermia elicited marked changes in cardiac autonomic control in young children. These data suggest that, in healthy children, vagal withdrawal is responsible for the cardiac autonomic response to hyperthermia.