Reduction In Core Body Temperature Research Articles

0015 Manipulating Body Temperature: Effects on Sleep in Postmenopausal Women

Abstract Introduction A decline in sleep quality and reduction in slow wave sleep (SWS) and slow wave activity (SWA) are common in older adults. Prior studies have shown that manipulating body temperature during sleep can increase SWS/SWA. The aim of this study was to determine the effects of manipulation of body temperatures during sleep, using a high heat capacity mattress, on SWS/SWA and heart rate variability in post-menopausal women. Methods Twenty-four healthy postmenopausal women between 40–75 years of age (mean age 62.4 ± 8.2 years, mean BMI 25.4 ± 3.5 kg/m2) were randomized in a single-blind, counterbalanced, cross-over manner to sleep on either a high heat capacity mattress (HHCM) or a low heat capacity mattress(LHCM) a week apart. Sleep was recorded using polysomnography during an 8-hour sleep opportunity. Core and peripheral temperatures were recorded using Equivital and ibutton respectively. Results In comparison to the LHCM, sleep on HHCM exhibited a selective increase in SWS (average increase in Stage N3 of 9.6 minutes (2.1%), p = 0.04) and in slow oscillatory activity (0.5-1Hz) in the first NREM/REM cycle (p=0.04). In addition, the HHCM induced a greater reduction in core body temperature (p=0.002), and delayed the increase in mattress surface temperature (maximal difference LHCM-HHCM: 4.66±0.17°C). Average heart rate was 2.7 beats/minute lower across the night on the HHCM compared to the LHCM (p=0.001). Conclusion The results of this study indicate that manipulation of body temperature during sleep may be a useful approach to enhance SWS sleep and cardiovascular function in postmenopausal women. Support Technogel

Protective effects of the phytogenic feed additive “comfort” on growth performance via modulation of hypothalamic feeding- and drinking-related neuropeptides in cyclic heat-stressed broilers

Identification of alternatives to antibiotics in livestock and poultry is necessary. Fueled by consumer preferences, phytogenic feed additives are increasingly used in the food system; however, their mode of action is not well defined. Here, we used broiler chickens, in which appetite and feeding behavior regulation are controlled by complex mechanisms, to determine the effect of the phytogenic feed additive “comfort” (PFA-C) as well as its underlying molecular mechanisms on growth performance in heat-stressed broiler chickens. Heat stress significantly increased birds' core body temperature, water intake, and the hypothalamic expression of heat shock protein (HSP) 70, whereas it decreased feed intake, BW, and woody breast incidence. Phytogenic feed additive “comfort” supplementation downregulated the hypothalamic expression of HSP70, reduced core body temperature, increased feed and water intake, and improved BW in HS broilers. At molecular levels, the effect of PFA-C on growth performance seemed to be mediated by modulation of hypothalamic expression of melanocortin receptor 2, arginine vasopressin, aquaporin 2, and sodium and potassium-transporting ATPase subunit beta 1 polypeptides. In summary, PFA-C supplementation ameliorates heat stress productivity losses via a potential cytoprotective effect, reduction of hypothalamic intracellular stress, and modulation of hypothalamic feeding- and drinking-related polypeptide expression.

Leptin receptor-expressing neuron Sh2b1 supports sympathetic nervous system and protects against obesity and metabolic disease

Leptin stimulates the sympathetic nervous system (SNS), energy expenditure, and weight loss; however, the underlying molecular mechanism remains elusive. Here, we uncover Sh2b1 in leptin receptor (LepR) neurons as a critical component of a SNS/brown adipose tissue (BAT)/thermogenesis axis. LepR neuron-specific deletion of Sh2b1 abrogates leptin-stimulated sympathetic nerve activation and impairs BAT thermogenic programs, leading to reduced core body temperature and cold intolerance. The adipose SNS degenerates progressively in mutant mice after 8 weeks of age. Adult-onset ablation of Sh2b1 in the mediobasal hypothalamus also impairs the SNS/BAT/thermogenesis axis; conversely, hypothalamic overexpression of human SH2B1 has the opposite effects. Mice with either LepR neuron-specific or adult-onset, hypothalamus-specific ablation of Sh2b1 develop obesity, insulin resistance, and liver steatosis. In contrast, hypothalamic overexpression of SH2B1 protects against high fat diet-induced obesity and metabolic syndromes. Our results unravel an unrecognized LepR neuron Sh2b1/SNS/BAT/thermogenesis axis that combats obesity and metabolic disease.

Use of water spray fan for heat injury management in military personnel exercising in Belize

### Key messages With the heat injuries that have deranged physiology,[1][1] we present an effective method to cool the patients as the primary goal is to reduce core body temperature...

Artepillin C, a Key Component of Brazilian Propolis, Induces Thermogenesis in Inguinal White Adipose Tissue of Mice through a Creatine-Metabolism-Related Thermogenic Pathway.

Induction of beige adipocytes in white adipose tissue (WAT) is a potential therapeutic target for the treatment of obesity because beige adipocytes release excess energy via uncoupling-protein-1-associated thermogenesis. In this study, we investigated how artepillin C (ArtC) promotes thermogenesis in vivo. We demonstrated that 28 day administration of ArtC (10 mg/kg of body weight) to mice significantly induced thermogenesis in beige adipocytes in inguinal WAT (iWAT) and suppressed reductions in core body temperature induced by cold exposure at 4 °C. Moreover, ArtC-induced thermogenesis in iWAT was significantly inhibited by treatment with a creatine metabolism inhibitor, and ArtC significantly upregulated the expression of creatine-metabolism-related enzymes in the thermogenic pathway. These results indicate that ArtC induces thermogenesis in beige adipocytes in iWAT, and the observed ArtC-induced thermogenesis is associated with the creatine-metabolism-related thermogenic pathway, which is characteristically observed in beige adipocytes.

Phytogenic feed- and water-additives improve feed efficiency in broilers via modulation of (an)orexigenic hypothalamic neuropeptide expression

Fueled by consumer preference for natural and antibiotic-free products, phytogenics have become the fastest growing segment of the animal feed additives. Yet, their modes of action are not fully understood. This study was undertaken to determine the effect of 5 phytogenics (3 feed- and 2 water-supplements) on the growth performance of commercial broilers, and their potential underlying molecular mechanisms. Day-old male Cobb 500 chicks (n = 576) were randomly assigned into 48 pens consisting of 6 treatments (Control; AVHGP; SCP; BHGP; AVSSL; SG) in a complete randomized design (12 birds/pen, 8 pens/treatment, 96 birds/treatment). Chicks had ad libitum access to feed and water. Individual body weight (BW) was recorded weekly and feed intake was measured daily. Core body temperatures were continuously recorded using thermo-loggers. At d 35, hypothalamic tissues were excised from the thermo-logger-equipped chickens (n = 8 birds/treatment) to determine the expression of feeding-related neuropeptides.Both feed (AVHGP, SCP, BHGP) and water-supplemented (AVSSL, SG) phytogenics significantly improved feed efficiency (FE) compared to the control birds. This higher FE was achieved via a reduction in core body temperature and improvement of market BW, without changes in feed intake in broilers supplemented with phytogenic water additives as compared to the control group. Broilers fed dietary phytogenics, however, attained higher feed efficiency via a reduction in feed intake while maintaining similar BW as the control group. At the molecular levels, the effects of the phytogenic water additives seemed to be mediated by the activation of the hypothalamic AgRP-ORX-mTOR-S6k1 and inhibition of CRH pathways. The effect of the phytogenic feed additives appeared to be exerted through the activation of AdipoQ, STAT3, AMPK, and MC1R pathways.This is the first report describing the likely central mechanisms through which phytogenic additives improve the growth performance and feed efficiency in broilers.

Effects of sleep on a high-heat capacity mattress on sleep stages, EEG power spectra, cardiac interbeat intervals and body temperatures in healthy middle-aged men‡.

This study deals with the question whether a slow (non-disturbing) reduction of core body temperature (CBT) during sleep increases sleep stage N3 and EEG slow wave energy (SWE) and leads to a slowing of heart rate in humans. Thirty-two healthy male subjects with a mean ± SD age 46 ± 4 years and body mass index 25.2 ± 1.8 kg/m2. A high-heat capacity mattress (HM) was used to lower body temperatures in sleep and was compared to a conventional low-heat capacity mattress (LM) in a double-blinded fashion. Polysomnography was performed accompanied by measurements of skin-, core body- and mattress surface-temperatures, and heart rate. EEG power spectral analyses were carried out using Fast Fourier Transform. Interbeat intervals were derived from the electrocardiogram. The HM led to a larger decline in CBT, mediated through higher heat conduction from the core via the proximal back skin onto the mattress together with reduced heart rate. These effects occurred together with a significant increase in sleep stage N3 and standardized slow wave energy (sSWE, 0.791-4.297 Hz) accumulated in NREM sleep. In the 2nd half of the night sSWE increase was significantly correlated with body temperature changes, for example with CBT decline in the same phase. A HM subtly decreases CBT, leading to an increased amount of sleep stage N3 and of sSWE, as well as a slowing of heart rate.

CTTP Reflects the Severity and Prognosis of Heat Stroke

Background: Temperature control plays a pivotal role in patients with heat stroke (HS), but little work has been done sufficiently on the use of temperature control to reflect disease progression. Here, we defined and analyzed the concrete role of effective controlling time for core temperature to physiological level (CTTP), in order to explore a potential index to guide the diagnosis and treatment of HS. Method: According to Chinese physical characteristics and the consensus of chinese experts, we defined CTTP as time interval of HS onset to stabilization of core temperature (rectal temperature) below 37.7℃. From 2010.01 to 2018.06 in our hospital, we collected a total of 28 HS cases with clinical diagnosis and treatment records for analyzing the correlation between CTTP and organ injuries, prognosis, APACHE II score and other indices. Results: There was a significant growth of exertional HS cases year by year, whereas the hospital mortality remained steady over the years, with an overall mortality rate being 17.85%. After analyzing the basic characteristics of CTTP, we found that it didn't obey normal distribution (P 0.05). Moreover, CTTP length determined the number of damaged organs (r=0.494, P=0.008). The top five of damaged organs in HS patients were central nervous system disorder (100%), liver injury (78.57%), renal injury (67.86%), myocardial injury (57.14%) and blood coagulation disorder (53.57%). Furthermore, some patients with organ injuries, such as renal function impairment, myocardial damage, pulmonary infection, had both higher mean and median of CTTP than the couterpart (P 0.05). Most importantly, CTTP was closely correlated with APACHE II score (r=0.888, P<0.001). Conclusion To reduce core body temperature early and rapidly with preventive measures against rebound lays the foundation for HS treatment. CTTP is an efficient indicator for assessing the severity and prognosis of HS. The injury in some organs (such as heart, lung and kidney) is in a CTTP-dependent manner, and these patients can benefit remarkably from CTTP control. Funding Statement: This work was supported by grants from the Science Fund for Distinguished Young Scholars of Sichuan Province (No.2017JQ0012), National Science Funds of China (No.81500208), China Postdoctoral Science Foundation (No.2017M613429), Youth Programme for PLA (17QNP047). Declaration of Interests: No competing financial interests exist. Ethics Approval Statement: The Institutional Review Board of Chengdu Military General Hospital approved this study and waived the requirement of informed consent, and we confirmed that all analyses followed the relevant guidelines and regulations.

Health Risks and Interventions in Exertional Heat Stress.

With climate change, heat waves are expected to become more frequent in the near future. Already, on average more than 25 000 "heat deaths" are estimated to occur in Europe every year. However, heat stress and heat illnesses arise not just when ambient temperatures are high. Physical exertion increases heat production within the organism many times over; if not enough heat is lost, there is a risk of exertional heat stress. This review article discusses contributing factors, at-risk groups, and the diagnosis and treatment of heat illnesses. A selective literature search was carried out on PubMed. Current guidelines and expert recommendations were also included. Apart from muscular heat production (>70% of converted energy), there are other factors that singly or in combination can give rise to heat stress: clothing, climate/acclimatization, and individual factors. Through its insulating properties, clothing reduces the evaporation of sweat (the most effective physiological cooling mechanism). A sudden heat wave, or changing the climate zone (as with air travel), increases the risk of a heat-related health event. Overweight, low fitness level, acute infections, illness, dehydration, and other factors also reduce heat tolerance. In addition to children, older people are particularly at risk because of their reduced physiological adaptability, (multi-)morbidity, and intake of prescription drugs. A heat illness can progress suddenly to life-threatening heat stroke. Successful treatment depends on rapid diagnosis and cooling the body down as quickly as possible. The aim is to reduce core body temperature to <40 °C within 30 minutes. Immediately effective cooling interventions are the only causal treatment for heat stroke. Time once lost cannot be made up. Prevention (acclimatization, reduced exposure, etc.) and terminating the heat stress in good time (e.g., stopping work) are better than any cure.

Ghrelin receptor in agouti-related peptide neurones regulates metabolic adaptation to calorie restriction.

Ghrelin is a gut hormone that signals to the hypothalamus to stimulate growth hormone release, increase food intake and promote fat deposition. The ghrelin receptor, also known as growth hormone secretagogue receptor (GHS-R), is highly expressed in the brain, with the highest expression in agouti-related peptide (AgRP) neurones in the hypothalamus. Compelling evidence indicates that ghrelin serves as a survival hormone with respect to maintaining blood glucose and body weight during nutritional deficiencies. Recent studies have demonstrated that AgRP neurones are involved in metabolic and behavioural adaptation to an energy deficit to improve survival. In the present study, we used a neuronal subtype-specific GHS-R knockout mouse (AgRP-Cre;Ghsrf/f ) to investigate the role of GHS-R in hypothalamic AgRP neurones in metabolic and behavioural adaptation to hypocaloric restricted feeding. We subjected the mice to a restricted feeding regimen of 40% mild calorie restriction (CR), with one-quarter of food allotment given in the beginning of the light cycle and three-quarters given at the beginning of the dark cycle, to mimic normal mouse intake pattern. The CR-fed AgRP-Cre;Ghsrf/f mice exhibited reductions in body weight, fat mass and blood glucose. Metabolic profiling of these CR-fed AgRP-Cre;Ghsrf/f mice showed a trend toward reduced basal metabolic rate, significantly reduced core body temperature and a decreased expression of thermogenic genes in brown adipose tissue. This suggests a metabolic reset to a lower threshold. Significantly increased physical activity, a trend toward increased food anticipatory behaviour and altered fuel preferences were also observed in these mice. In addition, these CR-fed AgRP-Cre;Ghsrf/f mice exhibited a decreased counter-regulatory response, showing impaired hepatic glucose production. Lastly, hypothalamic gene expression in AgRP-Cre;Ghsrf/f mice revealed increased AgRP expression and a decreased expression of genes in β-oxidation pathways. In summary, our data suggest that GHS-R in AgRP neurones is a key component of the neurocircuitry involved in metabolic adaptation to calorie restriction.

Mice keep their cool.

Ptgds-expressing neurons in the preoptic area of anterior hypothalamus detect increases in brain temperature and reduce core body temperature via increased production of prostaglandin D2.

Feasibility and Safety of Transnasal High Flow Air to Reduce Core Body Temperature in Febrile Neurocritical Care Patients: A Pilot Study.

Fever is an important determinant of prognosis following acute brain injury. Current non-pharmacologic techniques to reduce fever are limited and induce a shivering response. We investigated the safety and efficacy of a novel transnasal unidirectional high flow air device in reducing core body temperature in the neurocritical care unit (NCCU) setting. This pilot study included seven consecutive patients in the NCCU who were febrile (> 37.5°C) for > 24h despite standard non-pharmacologic and first-line antipyretic agents. Medical grade high flow air was delivered transnasally using a standard continuous positive airway pressure machine with a positive pressure of 20cmH2O for 2h. Core esophageal and tympanic temperature were continuously monitored. Mean age was 40 ± 14yo, and 72% (5/7 patients) were men. Five patients had intracerebral or intraventricular hemorrhage, one subject had transverse myelitis, and the remaining patient had anoxic brain injury due to a cardiac arrest. After 2h of cooling, core temperature was significantly lower than the baseline pre-cooling temperature (37.3 ± 0.5°C vs. 38.4 ± 0.6°C; p < 0.002). Mean transnasal airflow rate was 57.5 ± 6.5 liters per minute. Five of the seven subjects were normothermic at the end of the 2-h period. One subject with severe hyperthermia (39.7°C) and the other with multiple interruptions to therapy due to technical reasons did not cool. The core temperature within 30min of cessation of airflow increased and was similar to the pre-cooling baseline temperature (38.3 ± 0.4°C vs. 38.4 ± 0.6°C, p = NS). Rate of core cooling was 0.6 ± 0.15°C per hour at this flow rate. No shivering response was observed. No protocol-related adverse events occurred. High flow transnasal air in a unidirectional fashion lowers core body temperature in febrile patients in the NCCU setting. No adverse events were seen, and the process showed no signs of shivering or any other serious side effects during short-term exposure. This pilot study should inform further investigation.

The cardiopulmonary effects of sodium fluoroacetate (1080) in Sprague-Dawley rats

Sodium fluoroacetate (1080) is a highly toxic metabolic poison that has the potential because of its lack of defined color, odor, and taste and its high water solubility to be intentionally or unintentionally ingested through food adulteration. Although the mechanism of action for 1080 has been known since the 1950's, no known antidote exists. In an effort to better understand the cardiopulmonary impacts of 1080, we utilized whole-body plethysmography and telemeterized Sprague-Dawley rats which allowed for the real-time measurement of respiratory and cardiac parameters following exposure using a non-invasive assisted-drinking method. Overall, the animals showed marked depression of respiratory parameters over the course of 24 hours post-exposure and the development of hemorrhage in the lung tissue. Tidal volume was reduced by 30% in males and 60% in females at 24 hours post-exposure, and respiratory frequency was significantly depressed as well. In telemeterized female rats, we observed severe cardiac abnormalities, highlighted by a 50% reduction in heart rate, 75% reduction in systolic blood pressure, and a 3.5-fold lengthening of the QRS interval over the course of 24 hours. We also observed a reduction in core body temperature of nearly 15°C. Our study was able to describe the severe and pronounced effects of sodium fluoroacetate poisoning on cardiopulmonary function, the results of which indicate that both tissue specific and systemic deficits contribute to the toxicological progression of 1080 intoxication and will need to be accounted for when developing any potential countermeasure for 1080 poisoning.

Hypothermia and cardiac electrophysiology: a systematic review of clinical and experimental data.

Moderate therapeutic hypothermia procedures are used in post-cardiac arrest care, while in surgical procedures, lower core temperatures are often utilized to provide cerebral protection. Involuntary reduction of core body temperature takes place in accidental hypothermia and ventricular arrhythmias are recognized as a principal cause for a high mortality rate in these patients. We assessed both clinical and experimental literature through a systematic literature search in the PubMed database, to review the effect of hypothermia on cardiac electrophysiology. From included studies, there is common experimental and clinical evidence that progressive cooling will induce changes in cardiac electrophysiology. The QT interval is prolonged and appears more sensitive to decreases in temperature than the QRS interval. Severe hypothermia is associated with more pronounced changes, some of which are proarrhythmic. This is supported clinically where severe accidental hypothermia is commonly associated with ventricular fibrillation or asystole. J-waves in human electrocardiogram recordings are regularly but not always observed in hypothermia. Its relation to ventricular repolarization and arrhythmias is not obvious. Little clinical data exist on efficacy of anti-arrhythmic drugs in hypothermia, while experimental data show the potential of some agents, such as the class III antiarrhythmic bretylium. It is apparent that QT-prolonging drugs should be avoided.

Effect of high flow transnasal dry air on core body temperature in intubated human subjects

PurposeEarly initiation of hypothermia is recommended in the setting of cardiac arrest. Current hypothermia methods are invasive and expensive and not applicable in ambulatory settings. We investigated the evaporative cooling effect of high flow transnasal dry air on core esophageal temperature in human volunteers. Methods & resultsA total of 32 subjects (mean age 53.2 ± 9.3 yrs., mean weight 90 ± 17 kg) presenting for elective electrophysiological procedures were enrolled for the study. Half of the subjects were men. Following general anesthesia induction, high flow (30 LPM) medical grade ambient dry air with a relative humidity ∼20% was administered through a nasal mask for 60 min. Core temperature was monitored at the distal esophagus. Half of the subjects (16/32) were subject to high flow air and the remainder served as controls. Over a 1-h period, mean esophageal temperature decreased from 36.1 ± 0.3 °C to 35.5 ± 0.1 °C in the test subjects (p < 0.05). No significant change in temperature was observed in the control subjects (36.3 ± 0.3 °C to 36.2 ± 0.2 °C, p = NS). No adverse events occurred. ConclusionTransnasal high flow dry air through the nasopharynx reduces core body temperature. This mechanism can be harnessed to induce hypothermia in patients where clinically indicated without any deleteriouseffects in a short time exposure.

ENERGY EXPENDITURE DURING TARGETED TEMPERATURE MANAGEMENT: A PROSPECTIVE COHORT STUDY

SESSION TITLE: Miscellaneous Critical Care SESSION TYPE: Original Investigations PRESENTED ON: 10/10/2018 07:30 AM - 08:30 AM PURPOSE: To measure and quantify the relationship between core body temperature and metabolic consumption during targeted temperature management. METHODS: Ten patients (mean age 39.7, range 24 to 65, 7 males, 3 females) undergoing targeted temperature management after cardiac arrest at 32OC to 33OC were included in this prospective cohort study.Mild therapeutic hypothermia was induced by active cooling using temperature controlled intravenous filters (Zoll Thermoguard XP). A triple lumen catheter was inserted into a femoral vein. Core body temperature was continuously monitored.After ROSC external passive and internal active cooling was started immediately in order to expedite the reduction of body temperature, once the thermometer reached 32O to 33OC the external cooling was stopped and internal active cooling was used to maintain the temperature over a period of 48 hours.The rewarming phase was undertaken over a period of 24 hours (1OC/3 hours).Indirect calorimetry was determined by computerized respiratory gas exchange (Deltatrac II, Datex-Ohmeda). Oxygen consumption and carbon dioxide production were measured every hour during induction, the 48 hours of hypothermia and 24 hours of rewarming. The basal metabolic rate (kilocalories/day) was calculated using the Harris-Benedict equation: RESULTS: Cooling was started within 15±7 minutes after ROSC. The core body target temperature was achieved after 95±30 minutes of initiating cooling. The average drop in temperature compared to the target temperature (32OC- 33OC) was 2.7OC per hour. During the stage of steady state of targeted temperature management, core body temperature was 31.5±0.9OC.The oxygen consumption compared with baseline temperature was reduced by 82 mL/min (95% CI 59 to 107 mL/min; p=0.003).The basal metabolic rate was decreased by 35.6% (95% CI 26.9 to 52.3%; p=0.004) during the stage of steady state targeted temperature management.Future analysis and calculations will compute correlation between temperature, time and energy expenditure as well as estimations of fat and protein oxidation rates by means of mathematical equations. CONCLUSIONS: The main finding of an immediate reduction in oxygen consumption achieved by targeted temperature management was directly proportional to the reduction in core body temperature. Other studies by Bruder, Tokutomi, and Saur have shown similar measured values and results.Some of the limitations of this study are the small number of patients leading to big differences in measurements. Ideally, a similar study with a larger number of patients should be conducted to confirm our results. Another limitation was the use of different core body thermometers for which differences were not calculated. CLINICAL IMPLICATIONS: From a clinical perspective, it would seem reasonable to reduce the caloric intake during targeted temperature management since the basal metabolic rate was decreased by 35.6%. DISCLOSURES: Speaker/Speaker's Bureau relationship with Sunovian Please note: $5001 - $20000 Added 11/20/2017 by Salim Surani, source=Web Response, value=Honoraria Advisory Committee Member relationship with Astra Zeneca Please note: $5001 - $20000 Added 11/20/2017 by Salim Surani, source=Web Response, value=Consulting fee No relevant relationships by Emmanuel Urquieta, source=Web Response No relevant relationships by Joseph Varon, source=Web Response

A Neural Circuit Underlying the Generation of Hot Flushes

Hot flushes are a sudden feeling of warmth commonly associated with the decline of gonadal hormones at menopause. Neurons in the arcuate nucleus of the hypothalamus that express kisspeptin and neurokinin B (Kiss1ARH neurons) are candidates for mediating hot flushes because they are negatively regulated by sex hormones. We used a combination of genetic and viral technologies in mice to demonstrate that artificial activation of Kiss1ARH neurons evokes a heat-dissipation response resulting in vasodilation (flushing) and a corresponding reduction of core-body temperature in both females and males. This response is sensitized by ovariectomy. Brief activation of Kiss1ARH axon terminals in the preoptic area of the hypothalamus recapitulates this response, while pharmacological blockade of neurokinin B (NkB) receptors in the same brain region abolishes it. We conclude that transient activation of Kiss1ARH neurons following sex-hormone withdrawal contributes to the occurrence of hot flushes via NkB release in the rostral preoptic area.

태권도 선수들의 심부온도를 낮추기 위한 전략으로서의 차가운 물 섭취에 대한 효과 검증

Cold-water ingestion is an effective pre-cooling method and this method reduce core body temperature and improve performance. However, A practical and effective method of precooling for application at high-intensity interval events like as Taekwondo Kyorugi venues has not been demonstrated. Therefore aim of this study is to determine whether recovery benefits of pre-cooling before Taekwondo Kyoruki in the real competition environment (temperature=16℃; humidity=28%). Ten healthy, fit, collegiate taekwondo players (ten male; mean (SD) age 19.7 (0.5) years; weight 68.63 (5.7) kg; height 175.82 (2.9) cm) completed 6 minute taekwondo specific a trial match on separate 1hour twice (randomised, crossover design). Participants ingested 1000 mL of cold (2℃) or normal (24℃) water in 4×250-mL aliquots over 30 and 10minutes of pre-exercise rest. During a 1st trial match and recovery, there was no interaction(core: F=0.38, P.05, lactate: F=0.68, P.05), only time main effect (core: F=37.16, P.05, lactate: F=141.43, P.05). During a 2nd trial match and recovery, it also no interaction (core: F=1.86, P.05), only time main effect(core: F=75.41, P.05) however, there was interaction in lactate(F=3.09, P.05). We demonstrated that pre-exercise ingestion of cold water is not effective precooling method suitable for taekwondo-based application but pre-exercise ingestion of cold water may effect recovery when have a one after another match

Cows exposed to heat stress during fetal life exhibit improved thermal tolerance.

Maternal heat stress during late gestation affects calf function during postnatal life. The objective of the present study was to evaluate whether calves that experience heat stress in utero have altered thermoregulatory responses to acute heat stress later in life. Specifically, the hypothesis was that heat stress in utero would improve the response to acute heat stress at maturity. Females were born to dams exposed to heat stress or cooled during late gestation preceding their birth. All animals were raised postnatally under identical management. Twelve lactating Holstein cows that were exposed to in utero heat stress (HT) and 12 that were exposed to in utero control (CON) were used. A heat stress challenge was conducted in 3 blocks using 4 HT and 4 CON cows matched according to milk yield, stage of lactation, and parity. Each challenge consisted of transfer from a barn with shade and evaporative cooling to one with shade but no additional cooling for 48 h. The challenge was replicated twice for each block. Sweating rate, respiration rate, rectal temperature (RT), and skin temperature were measured on each cow at 0900, 1100, 1300, 1500, and 1700 h for 2 consecutive days. Mean ambient temperature across 6 challenge days was 26.15 ± 4.75°C. Tendencies for differences at 1700 h were observed between treatments for RT (HT: 39.5 ± 0.1; CON: 39.6 ± 0.1°C; = 0.065), however, there was no difference in respiration rate (HT: 77.6 ± 1.6; CON: 79.5 ± 1.6 bpm; = 0.85). Sweating rate for shaved skin (HT: 29.4 ± 2.0; CON: 36.0 ± 2.0 g/mh; = 0.057) and for non-shaved skin (HT: 22.5 ± 1.5; CON: 29.2 ± 1.2 g/mh; = 0.01) differed between groups. However, there was no effect on skin temperature at the shaved location (HT: 36.2 ± 0.2; CON: 36.0 ± 0.2°C; = 0.81), but there was a tendency for differences for the non-shaved area (HT: 35.4 ± 0.2; CON: 34.9 ± 0.2°C; = 0.097). Cows that underwent in utero heat stress had greater skin temperature at 1700 h vs. in utero control cows, which may be because HT cows increased skin perfusion, and consequently greater cooling via conduction. In utero HT cows would then have higher heat loss and reduced core body temperature, which results in lower rectal temperature and lower sweating rate when exposed to heat stress. These results support the hypothesis that heat stress in utero in late gestation increases heat tolerance at maturity by increasing capacity to dissipate heat to maintain core body temperature.

A cross-species translational pharmacokinetic-pharmacodynamic evaluation of core body temperature reduction by the TRPM8 blocker PF-05105679

PF-05105679 is a moderately potent TRPM8 blocker which has been evaluated for the treatment of cold pain sensitivity. The TRPM8 channel is responsible for the sensation of cold environmental temperatures and has been implicated in regulation of core body temperature. Consequently, blockade of TRPM8 has been suggested to result in lowering of core body temperature. As part of the progression to human studies, the effect of PF-05105679 on core body temperature has been investigated in animals. Safety pharmacology studies showed that PF-05105679 reduced core body temperature in a manner that was inversely related to body weight of the species tested (greater exposure to PF-05105679 was required to lower temperature by 1°C in higher species). Based on an allometric (body weight) relationship, it was hypothesized that PF-05105679 would not lower core body temperature in humans at exposures that could exhibit pharmacological effects on cold pain sensation. On administration to humans, PF-05105679 was indeed effective at reversing the cold pain sensation associated with the cold pressor test in the absence of effects on core body temperature.