Increase In Core Body Temperature Research Articles

Role of monoaminergic systems and ambient temperature in bath salts constituent 3,4-methylenedioxypyrovalerone (MDPV)-elicited hyperthermia and locomotor stimulation in mice

3,4-Methylenedioxypyrovalerone (MDPV) is a common constituent of illicit bath salts products, and in vitro studies implicate monoamine transporters as mediators of its pharmacological effects. Locomotor and thermoregulatory effects of MDPV depend on ambient temperature, so the current studies aimed to gauge the involvement of dopamine (DA), norepinephrine (NE), and serotonin (5-HT) in MDPV-induced locomotor stimulation and hyperthermia in the mouse at different ambient temperatures. Mice were pretreated with the selective 5-HT-reuptake inhibitor fluoxetine (3 mg/kg), the NE-reuptake inhibitor desipramine (3 mg/kg), the DA-reuptake inhibitor bupropion (10 mg/kg), or saline, followed by 10 mg/kg MDPV while thermoregulation and locomotor activity were monitored via radiotelemetry. In other studies, mice were pretreated for three days with saline, 100 mg/kg of the tryptophan hydroxylase inhibitor para-chlorophenylalanine (p-CPA), or 100 mg/kg of the tyrosine hydroxylase inhibitor α-methyl-para-tyrosine (α-MPT) before receiving 10 mg/kg MDPV on the fourth day. All manipulations were conducted at both 20 °C and 28 °C ambient temperatures. MDPV increased locomotor activity under both ambient conditions and modestly increased core body temperature at 20 °C; however, neither pretreatment with monoamine reuptake inhibitors nor monoamine synthesis inhibitors significantly altered these effects. At 28 °C, MDPV induced a more pronounced hyperthermic effect which was attenuated by bupropion, desipramine, or fluoxetine pretreatment, but not by the monoamine synthesis inhibitors. These results suggest that MDPV may have a more complex pharmacological profile than suggested by in vitro studies, perhaps extending beyond interactions with monoamine transporters. A more thorough binding profile of MDPV at various brain recognition sites should be developed.This article is part of the Special Issue entitled ‘Designer Drugs and Legal Highs.’

Swimming Three Ice Miles within Fifteen Hours.

Ice Mile swimming (1608 m in water of below 5 °Celsius) is becoming increasingly popular. This case study aimed to identify body core temperature and selected haematological and biochemical parameters before and after repeated Ice Miles. An experienced ice swimmer completed three consecutive Ice Miles within 15 h. Swim times, body core temperatures, and selected urinary and haematological parameters were recorded. Body core temperature reached its maximum between 5, 8 and 15 min after immersion (37.7°C, 38.1°C, and 38.0°C, respectively). The swimmer suffered hypothermia during the first Ice Mile (35.4°C) and body core temperature dropped furthermore to 34.5°C during recovery after the first Ice Mile. He developed a metabolic acidosis in both the first and the last Ice Mile (pH 7.31 and pH 7.34, respectively). We observed hyperkalaemia ([K⁺] > 5.5 mM) after the second Ice Mile (6.9 mM). This was followed by a drop in [K⁺] to3.7 mM after the third Ice Mile. Anticipatory thermogenesis (i.e. an initial increase of body core temperature after immersion in ice cold water) seems to be a physiological response in a trained athlete. The results suggest that swimming in ice-cold water leads to a metabolic acidosis, which the swimmer compensates with hyperventilation (i.e. leading to respiratory alkalosis). The shift of serum [K⁺] could increase the risk of a cardiac arrhythmia. Further studies addressing the physiology and potential risks of Ice Mile swimming are required to substantiate this finding.

Opportunities and Challenges for Personal Heat Exposure Research.

Background:Environmental heat exposure is a public health concern. The impacts of environmental heat on mortality and morbidity at the population scale are well documented, but little is known about specific exposures that individuals experience.Objectives:The first objective of this work was to catalyze discussion of the role of personal heat exposure information in research and risk assessment. The second objective was to provide guidance regarding the operationalization of personal heat exposure research methods.Discussion:We define personal heat exposure as realized contact between a person and an indoor or outdoor environment that poses a risk of increases in body core temperature and/or perceived discomfort. Personal heat exposure can be measured directly with wearable monitors or estimated indirectly through the combination of time–activity and meteorological data sets. Complementary information to understand individual-scale drivers of behavior, susceptibility, and health and comfort outcomes can be collected from additional monitors, surveys, interviews, ethnographic approaches, and additional social and health data sets. Personal exposure research can help reveal the extent of exposure misclassification that occurs when individual exposure to heat is estimated using ambient temperature measured at fixed sites and can provide insights for epidemiological risk assessment concerning extreme heat.Conclusions:Personal heat exposure research provides more valid and precise insights into how often people encounter heat conditions and when, where, to whom, and why these encounters occur. Published literature on personal heat exposure is limited to date, but existing studies point to opportunities to inform public health practice regarding extreme heat, particularly where fine-scale precision is needed to reduce health consequences of heat exposure. https://doi.org/10.1289/EHP556

Body temperature responses to handling stress in wintering Black-capped Chickadees (Poecile atricapillus L.)

Body temperature variation in response to acute stress is typically characterized by peripheral vasoconstriction and a concomitant increase in core body temperature (stress-induced hyperthermia). It is poorly understood how this response differs between species and within individuals of the same species, and how it is affected by the environment. We therefore investigated stress-induced body temperature changes in a non-model species, the Black-capped Chickadee, in two environmental conditions: outdoors in low ambient temperature (mean: −6.6°C), and indoors, in milder ambient temperature close to thermoneutrality (mean: 18.7°C). Our results show that the change in body temperature in response to the same handling stressor differs in these conditions. In cold environments, we noted a significant decrease in core body temperature (−2.9°C), whereas the response in mild indoor conditions was weak and non-significant (−0.6°C). Heat loss in outdoor birds was exacerbated when birds were handled for longer time. This may highlight the role of behavioral thermoregulation and heat substitution from activity to body temperature maintenance in harsh condition. Importantly, our work also indicates that changes in the physical properties of the bird during handling (conductive cooling from cold hands, decreased insulation from compression of plumage and prevention of ptiloerection) may have large consequences for thermoregulation. This might explain why females, the smaller sex, lost more heat than males in the experiment. Because physiological and physical changes during handling may carry over to affect predation risk and maintenance of energy balance during short winter days, we advice caution when designing experimental protocols entailing prolonged handling of small birds in cold conditions.

Mild Heat Pretreatment and Serum From Sedentary Humans Subjected to Passive Heat Therapy Protect Endothelial Cells Against Stress from Hypoxia‐Reoxygenation

Impaired stress resistance is a hallmark of disease and dysfunction in many clinical populations, including primary aging and cardiovascular diseases. Repeated exposure to passive heat stress (‘heat therapy’) has widespread physiological benefits, including cellular protection against novel stressors. Both increased heat shock protein (HSP) expression as a direct effect of increases in body core temperature and upregulation of circulating factors may impart this protection.PurposeWe tested the ability of both mild heat pre‐treatment and serum from human subjects who had undergone 8 weeks of heat therapy to protect against cellular stress following hypoxia‐reoxygenation (H/R), a model of ischemic events, in cultured endothelial cells.MethodsSerum was collected from 10 young, sedentary subjects before (0wk) and after 8 weeks of passive heat therapy (immersion in 40.5°C bath 4–5× per week to increase rectal temperature to 38.5–39.0°C for 60 min per session). Purchased human umbilical vein endothelial cells were incubated for 24h at 37°C (control), 39°C (heat pre‐treatment), or at 37°C with 10% serum from heat therapy subjects. Cells were collected before and after incubation at 1% O2 for 16h (hypoxia), followed by 20% O2 for 4h (reoxygenation) and assessed for markers of cell stress. Data are presented as mean±S.E. % change from basal conditions (before H/R).ResultsIn control cells, H/R increased nuclear NFkB p65 protein (i.e. activation) by +106±38%, increased IL‐6 release into the supernatant by +37±8% (normalized to total protein), and increased superoxide production by +272±45% (cell permeable fluorescent stain). Heat pre‐treatment prevented H/R‐induced NFkB activation (−3±12%, p=0.04 vs. control) and attenuated superoxide production (+141±11%, p=0.01), but had no effect on IL‐6 production (+40±14%, p=0.85). Exposure to sera from human subjects who had undergone heat therapy prevented H/R‐induced NFkB activation (0wk: +301±125% vs. 8wk: +13±31%, p=0.045) and attenuated IL‐6 release (0wk: 172±57 pg/mg total protein vs. 8wk: 110±40 pg/mg, p=0.048), but had no effect on superoxide production (0wk: +47±14% vs. 8wk: +124±70%, p=0.24). H/R also decreased cytoplasmic hemeoxygenase‐1 (HO‐1) protein by −25±8%, a heat shock protein (Hsp32) that can suppress NFkB activation. Interestingly, HO‐1 protein increased following H/R in cells pre‐treated with heat (+45±27%, p=0.02) or exposed to heat therapy sera (0wk: −11±15% vs. 8wk: +38±24%, p=0.06).ConclusionsMarkers of cellular oxidative and inflammatory stress associated with H/R were attenuated by both increases in temperature (to levels similar to core temperature increases observed in humans undergoing heat therapy) and heat therapy‐induced changes in circulating factors. These data suggest heat therapy is capable of imparting stress resistance via both direct heat (presumably via HSPs) and humoral factors.Support or Funding InformationSupported by AHA Grant #14PRE20380300 and the Eugene and Clarissa Evonuk Memorial Foundation

Using heat as a therapeutic tool for the aging vascular tree.

Healthy aging in humans is associated with progressive deterioration of various organ systems, the cardiovascular system being one of the most notable. Young arteries have a pronounced ability to dilate and constrict to mediate changes in blood flow in response to various stimuli (e.g. exposure to a cold or hot environment). With increasing age, complex structural and functional changes to the blood vessels occur which are further exacerbated by common comorbidities including hypertension, diabetes mellitus and hypercholesterolemia. These changes in both the endothelial and smooth muscular layers of the vasculature are mediated through impaired dilator signalling pathways (e.g. nitric oxide signaling and endothelium-derived hyperpolarizing factor) along with augmented contractile pathways (e.g. renin-angiotensin system and endothelin-1). These age-related changes along with the intimal accumulation of lipids (i.e., atherosclerosis, which can strongly impede dilator function) are thought to span the entire arterial tree. In older adults, the impairments in cardiovascular function are most evident during passive heat stress and/or exercise. Recent reports have indicated that passive exposure to heat that elicits a marked increase in body core temperature, and therefore dilation of the arterial tree, may improve macro- and microvascular dilator function in young adults. Given that older adults exhibit a greater capacity for improvement in dilator function, it is possible that chronic heat exposure, or heat therapy, could improve dilator function of the arterial tree which may have multiple health benefits.

On the potential for RF heating in MRI to affect metabolic rates and 18 FDG signal in PET/MR: simulations of long-duration, maximum normal mode heating.

To examine the possibility that MR-induced RF power deposition (SAR) and the resulting effects on temperature-dependent metabolic rates or perfusion rates might affect observed 18FDG signal in PET/MR. Using numerical simulations of the SAR, consequent temperature increase, effect on rates of metabolism or perfusion, and [18FDG] throughout the body, we simulated the potential effect of maximum-allowable whole-body SAR for the entire duration of an hour-long PET/MR scan on observed PET signal for two different 18FDG injection times: one hour before onset of imaging and concurrent with the beginning of imaging. This was all repeated three times with the head, the heart, and the abdomen (kidneys) at the center of the RF coil. Qualitatively, little effect of MR-induced heating is observed on simulated PET images. Maximum relative increases in PET signal (26% and 31% increase, respectively, for the uptake models based on metabolism and the perfusion) occur in regions of low baseline metabolic rate (also associated with low perfusion and, thus, greater potential temperature increase due to high local SAR), such that PET signal in these areas remains comparatively low. Maximum relative increases in regions of high metabolic rate (and also high perfusion: heart, thyroid, brain, etc.) are affected mostly by the relatively small increase in core body temperature and thus are not affected greatly (10% maximum increase). Even for worst-case heating, little effect of MR-induced heating is expected on 18FDG PET images during PET/MR for many clinically relevant applications. For quantitative, dynamic MR/PET studies requiring high SAR for extended periods, it is hoped that methods like those introduced here can help account for such potential effects in design of a given study, including selection of reference locations that should not experience notable increase in temperature.

Injections of Galanin-Like Peptide directly into the nucleus of the tractus solitarius (NTS) reduces food intake and body weight but increases metabolic rate and plasma leptin

Galanin-Like Peptide (GALP) is a hypothalamic neuromediator of metabolism and reproduction. GALP is known to stimulate reproduction and alter food intake and body weight in multiple species. The regulation of body weight involves control of both energy intake and energy expenditure. Since GALP is known to alter food intake - possibly via the autonomic nervous system - we first hypothesized that GALP would increase metabolic rate. First, male Sprague-Dawley rats were implanted with intracerebroventricular (ICV) cannulae and abdominal radiotelemetry temperature transmitters. Following ICV injection with either 5nmol GALP or vehicle, the oxygen consumption of each rat was monitored for 8h. Food intake, core temperature, and general motor activity were monitored for 24h. GALP significantly increased oxygen consumption, an indirect estimator of metabolic rate, without having any significant effect on motor activity. Compared to controls, GALP increased core body temperature during the photophase and reduced food intake over the 24h period following injection. ICV GALP also increased plasma levels of luteinizing hormone (LH). A second group of male Sprague-Dawley rats were implanted with abdominal transmitters and given injections of GALP directly into the nucleus of the tractus solitarius (NTS). These injections resulted in a significant reduction in food intake, and a significant increase in both oxygen consumption and core body temperature compared to vehicle injections. Direct injections of GALP into the NTS compared to vehicle also resulted in a significant increase in plasma leptin levels, but not LH levels. GALP appears to increase energy expenditure in addition to decreasing energy input by actions within the NTS and thus may play an important role in the hypothalamic regulation of body weight.

Validation of an intramuscularly-implanted microchip and a surface infrared thermometer to estimate core body temperature in broiler chickens exposed to heat stress

Heat stress in poultry is associated with an increased core body temperature (CBT) which can be fatal. Methods of estimating CBT range from the minimally invasive method of inserting a digital thermometer into the cloaca of the bird, to the implantation of a temperature recording device (e.g. a data logger) in the peritoneal cavity, a method which gives the most accurate measure of CBT but may be considered invasive. To validate the use of less invasive alternatives to assess CBT in broiler (meat type) chickens using injectable devices, 12 birds were subject to surgery to implant a data logger deep in the body cavity and a microchip in the breast muscle. The birds were then placed in floor pens with an additional 36 birds and subsequently subjected to one of four simulated heat stress conditions over a 3-day period. Measurements of body temperature were collected at intervals from the data logger and microchip (CBT and IM-chip, respectively) along with taken under the wing, feet, comb and cloaca using an infrared thermometer. Changes in body temperature were calculated as the ΔT between pre heat stress and end of 3h heat stress each day. There was no relationship between CBT and IM-chip, but there was a significant correlation between ΔCBT and ΔIM-chip (R=0.71, P<0.05) during the heat stress. SBT measured under the wing correlated with CBT (R=0.71, P<0.05). Collectively these data confirm the suitability of intramuscularly-implanted microchip and strategically-positioned infrared thermometers to monitor CBT in birds exposed to heat stress, thereby replacing the invasive surgery and associated side-effects of deep body-implanted data loggers for the benefit of animal welfare.

Visual function and retinal vessel diameters during hyperthermia in man.

To assess the effect of elevated core body temperature on temporal and spatial contrast sensitivity and retinal vessel diameters. The study included 13 healthy volunteers aged 20-37years. Core body temperature elevation (target +1.1°C) was induced by wrapping the participants in cling film, tinfoil and warming blankets. Subsequent cooling was achieved by undressing. Flicker sensitivity (critical flicker fusion frequency) was chosen to assess temporal resolution, while the Freiburg Vision Test was used to determine spatial contrast sensitivity at 1.5 cycles per degree. Scanning laser ophthalmoscopy was used to measure retinal trunk vessel diameters. Assessment was made at baseline, during hyperthermia and after cooling. The induction of a mean increase in core body temperature of 1.02°C was associated with a 7.15-mmHg mean reduction in systolic blood pressure (p<0.01), a 10.6-mmHg mean reduction in diastolic blood pressure (p<0.01), a mean increase in pulse rate of 36.3bpm (p<0.0001), a 2.66% improvement in flicker sensitivity (CI95 1.37-3.94, p<0.001), a 2.80% increase in retinal artery diameters (CI95 1.09-4.51, p<0.01) and a 2.95% increase in retinal vein diameters (CI95 0.96-4.94, p<0.01). There was no detectable effect of temperature on spatial contrast sensitivity. All ocular test parameters returned to baseline levels after cooling. Increased core body temperature was accompanied by improved temporal visual resolution and retinal trunk vessel dilation. The results suggest that hyperthermia is associated with enhanced retinal function and increased retinal metabolism.

Association Between Exercise-Induced Hyperthermia and Intestinal Permeability: A Systematic Review.

Prolonged and strenuous physical exercise increases intestinal permeability, allowing luminal endotoxins to translocate through the intestinal barrier and reach the bloodstream. When recognized by the immune system, these endotoxins trigger a systemic inflammatory response that may affect physical performance and, in severe cases, induce heat stroke. However, it remains to be elucidated whether there is a relationship between the magnitude of exercise-induced hyperthermia and changes in intestinal permeability. In this systematic review, we evaluated whether an exercise-induced increase in core body temperature (T Core) is associated with an exercise-induced increase in intestinal permeability. The present systematic review screened the MEDLINE/PubMed and Web of Science databases in September 2016, without any date restrictions. Sixteen studies that were performed in healthy participants, presented original data, and measured both the exercise-induced changes in T Core and intestinal permeability were selected. These studies assessed intestinal permeability through the measurement of sugar levels in the urine and measurement of intestinal fatty acid binding protein or lipopolysaccharide levels in the blood. Exercise increased both T Core and intestinal permeability in most of the 16 studies. In addition, a positive and strong correlation was observed between the two parameters (r = 0.793; p < 0.001), and a T Core exceeding 39 °C was always associated with augmented permeability. The magnitude of exercise-induced hyperthermia is directly associated with the increase in intestinal permeability.

Altered cytokine profile, pain sensitivity, and stress responsivity in mice with co-disruption of the developmental genes Neuregulin-1 × DISC1

The complex genetic origins of many human disorders suggest that epistatic (gene×gene) interactions may contribute to a significant proportion of their heritability estimates and phenotypic heterogeneity. Simultaneous disruption of the developmental genes and schizophrenia risk factors Neuregulin-1 (NRG1) and Disrupted-in-schizophrenia 1 (DISC1) in mice has been shown to produce disease-relevant and domain-specific phenotypic profiles different from that observed following disruption of either gene alone. In the current study, anxiety and stress responsivity phenotypes in male and female mutant mice with simultaneous disruption of DISC1 and NRG1 were examined. NRG1×DISC1 mutant mice were generated and adult mice from each genotype were assessed for pain sensitivity (hot plate and tail flick tests), anxiety (light-dark box), and stress-induced hypothermia. Serum samples were assayed to measure circulating levels of pro-inflammatory cytokines. Mice with the NRG1 mutation, irrespective of DISC1 mutation, spent significantly more time in the light chamber, displayed increased core body temperature following acute stress, and decreased pain sensitivity. Basal serum levels of cytokines IL8, IL1β and IL10 were decreased in NRG1 mutants. Mutation of DISC1, in the absence of epistatic interaction with NRG1, was associated with increased serum levels of IL1β. Epistatic effects were evident for IL6, IL12 and TNFα. NRG1 mutation alters stress and pain responsivity, anxiety, and is associated with changes in basal cytokine levels. Epistasis resulting from synergistic NRG1 and DISC1 gene mutations altered pro-inflammatory cytokine levels relative to the effects of each of these genes individually, highlighting the importance of epistatic mechanisms in immune-related pathology.

Effect of hypohydration on thermoregulatory responses in men with low and high body fat exercising in the heat.

This is the first known investigation to compare thermoregulatory responses to exercise heat stress between men with high and low body fat (BF) in a physiologically uncompensable environment while simultaneously examining the confounding influence of hydration status. Both groups demonstrated similar sweating and cutaneous vasodilatory responses when euhydrated, despite vast differences in rectal temperature. Furthermore, in contrast to low BF, individuals with high BF demonstrated similar increases in core body temperature when either euhydrated or hypohydrated.

Fhf2 gene deletion causes temperature-sensitive cardiac conduction failure.

Fever is a highly conserved systemic response to infection dating back over 600 million years. Although conferring a survival benefit, fever can negatively impact the function of excitable tissues, such as the heart, producing cardiac arrhythmias. Here we show that mice lacking fibroblast growth factor homologous factor 2 (FHF2) have normal cardiac rhythm at baseline, but increasing core body temperature by as little as 3 °C causes coved-type ST elevations and progressive conduction failure that is fully reversible upon return to normothermia. FHF2-deficient cardiomyocytes generate action potentials upon current injection at 25 °C but are unexcitable at 40 °C. The absence of FHF2 accelerates the rate of closed-state and open-state sodium channel inactivation, which synergizes with temperature-dependent enhancement of inactivation rate to severely suppress cardiac sodium currents at elevated temperatures. Our experimental and computational results identify an essential role for FHF2 in dictating myocardial excitability and conduction that safeguards against temperature-sensitive conduction failure.

The Impact of Central and Peripheral Cyclooxygenase Enzyme Inhibition on Exercise-Induced Elevations in Core Body Temperature.

Exercise increases core body temperature (TC) due to metabolic heat production. However, the exercise-induced release of inflammatory cytokines including interleukin-6 (IL-6) may also contribute to the rise in TC by increasing the hypothalamic temperature set point. This study investigated whether the exercise-induced increase in TC is partly caused by an altered hypothalamic temperature set point. Fifteen healthy, active men age 36 ± 14 y were recruited. Subjects performed submaximal treadmill exercise in 3 randomized test conditions: (1) 400 mg ibuprofen and 1000 mg acetaminophen (IBU/APAP), (2) 1000 mg acetaminophen (APAP), and (3) a control condition (CTRL). Acetaminophen and ibuprofen were used to block the effect of IL-6 at a central and peripheral level, respectively. TC, skin temperature, and heart rate were measured continuously during the submaximal exercise tests. Baseline values of TC, skin temperature, and heart rate did not differ across conditions. Serum IL-6 concentrations increased in all 3 conditions. A significantly lower peak TC was observed in IBU/APAP (38.8°C ± 0.4°C) vs CTRL (39.2°C ± 0.5°C, P = .02) but not in APAP (38.9°C ± 0.4°C) vs CTRL. Similarly, a lower ΔTC was observed in IBU/APAP (1.7°C ± 0.3°C) vs CTRL (2.0°C ± 0.5°C, P < .02) but not in APAP (1.7°C ± 0.5°C) vs CTRL. No differences were observed in skin temperature and heart-rate responses across conditions. The combined administration of acetaminophen and ibuprofen resulted in an attenuated increase in TC during exercise compared with a CTRL. This observation suggests that a prostaglandin-E2-induced elevated hypothalamic temperature set point may contribute to the exercise-induced rise in TC.

Obesogenic and Diabetogenic Effects of High-Calorie Nutrition Require Adipocyte BK Channels.

Elevated adipose tissue expression of the Ca2+- and voltage-activated K+ (BK) channel was identified in morbidly obese men carrying a BK gene variant, supporting the hypothesis that K+ channels affect the metabolic responses of fat cells to nutrients. To establish the role of endogenous BKs in fat cell maturation, storage of excess dietary fat, and body weight (BW) gain, we studied a gene-targeted mouse model with global ablation of the BK channel (BKL1/L1) and adipocyte-specific BK-deficient (adipoqBKL1/L2) mice. Global BK deficiency afforded protection from BW gain and excessive fat accumulation induced by a high-fat diet (HFD). Expansion of white adipose tissue-derived epididymal BKL1/L1 preadipocytes and their differentiation to lipid-filled mature adipocytes in vitro, however, were improved. Moreover, BW gain and total fat masses of usually superobese ob/ob mice were significantly attenuated in the absence of BK, together supporting a central or peripheral role for BKs in the regulatory system that controls adipose tissue and weight. Accordingly, HFD-fed adipoqBKL1/L2 mutant mice presented with a reduced total BW and overall body fat mass, smaller adipocytes, and reduced leptin levels. Protection from pathological weight gain in the absence of adipocyte BKs was beneficial for glucose handling and related to an increase in body core temperature as a result of higher levels of uncoupling protein 1 and a low abundance of the proinflammatory interleukin-6, a common risk factor for diabetes and metabolic abnormalities. This suggests that adipocyte BK activity is at least partially responsible for excessive BW gain under high-calorie conditions, suggesting that BK channels are promising drug targets for pharmacotherapy of metabolic disorders and obesity.

Should Cooling Vests Be Used to Treat Exertional Heatstroke? A Critically Appraised Topic.

Are TC cooling rates acceptable (ie, >0.08°C/min) when hyperthermic humans are treated with cooling vests postexercise? No significant differences in TC cooling rates occurred between cooling vests and no cooling vests. Cooling rates across all studies were ≤0.053°C/min. Clinical Bottom Line: Cooling vests do not provide acceptable cooling rates of hyperthermic humans postexercise and should not be used to treat EHS. Instead, EHS patients should be treated with cold-water immersion within 30 min of collapse to avoid central nervous system dysfunction and organ failure. Strength of Recommendation: Strong evidence (eg, level 2 studies with PEDro scores ≥5) suggests that cooling vests do not reduce TC quickly and thus should not be used in EHS scenarios.

A Role for Cyclooxygenase and Nitric Oxide Synthase in Sweating and Skin Blood Flow During Exercise in the Heat in Young Individuals with Type 1 Diabetes

Recent studies show that individuals with type 1 diabetes mellitus (T1DM) have impaired heat loss responses. This is evidenced as a decrease in local sweat rate and an increase in core body temperature during exercise in the heat compared to non‐diabetic matches; however, the underlying mechanisms are currently unknown. Previous studies have shown that nitric oxide synthase (NOS) and cyclooxygenase (COX) increase sweating, while NOS, but not COX, contributes to cutaneous vasodilation in young adults exercising in the heat. Thus, the aim of our study was to determine if the impairments in local heat loss responses displayed by individuals with T1DM may be attributed to COX and/or NOS activity. Seven (5 males, 2 females) young (24±3 years) individuals with T1DM were instrumented with four microdialysis fibres in the forearm skin which were perfused with either 1) 10 mM ketorolac (KETO, non‐selective COX inhibitor), 2) 10 mM NG‐nitro‐L‐arginine methyl ester (L‐NAME, non‐selective NOS inhibitor), 3) a combination of L‐NAME and KETO (L‐NAME+KETO), or 4) lactated Ringer (Control). Sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC; laser Doppler perfusion units/mean arterial pressure) were measured continuously throughout the protocol. Participants performed two 30 min bouts of exercise at a fixed rate of heat production of 400 W in the heat (35°C, 20% relative humidity); separated by a 20‐ and 40‐min recovery respectively. During the first and second exercise bouts, we showed that the inhibition of COX (KETO) resulted in an increase in sweat rate relative to Control (average of last 5 min of second exercise; Control: 1.02±0.11 mg min−1 cm−2, KETO: 1.12±0.12 mg min−1 cm−2; P=0.029). However, a decrease in sweat rate was observed when both NOS and COX were inhibited (L‐NAME+KETO: 0.86±0.11 mg min−1 cm−2; P=0.031). Furthermore, inhibition of NOS alone did not significantly modulate sweating (L‐NAME: 0.93±0.11 mg min−1 cm−2; P=0.11). With respect to CVC, the inhibition of NOS (average of last 5 min of second exercise, 45±9%max), as well as NOS and COX (49±4%max) resulted in similar decreases in CVC relative to Control (68±1%max)(both P&lt;0.05). In contrast, the inhibition of COX alone did not modulate CVC (64±4%max; P=0.33). Our results demonstrate that COX attenuates sweating during exercise in the heat in young adults with T1DM, which may occur through NOS‐dependent mechanisms. Finally, we show that individuals with T1DM exhibit NOS‐ but not COX‐dependent cutaneous vasodilation during exercise in the heat.Support or Funding InformationThis study was supported by grants from the Canadian Institutes of Health Research (286363; funds held by Dr. Glen P. Kenny).

Thermogenesis induced by amino acid administration prevents intraoperative hypothermia and reduces postoperative infectious complications after thoracoscopic esophagectomy.

Minimally invasive thoracoscopic esophagectomy has potential advantages in minimizing the impairment of respiratory function and reducing surgical stress. However, thoracoscopic esophagectomy occasionally results in anesthesia-induced hypothermia, particularly in cases involving artificial pneumothorax with CO2. Thermogenesis induced by amino acid administration has been reported during anesthesia. Here, we tested the efficacy of amino acid treatment for the prevention of hypothermia, and we investigated the potential of this treatment to reduce postoperative infectious complications after thoracoscopic esophagectomy. We conducted a randomized trial in patients with esophageal cancer who underwent thoracoscopic esophagectomy in the prone position in two groups and analyzed the incidences of hypothermia and surgical complications. One-hundred and thirty patients were randomized. Administration of amino acids resulted in a significant increase in core body temperature. In the saline (n = 60) and amino acid (n = 70) administration groups, 30% and 14.2% of patients, respectively, experienced infectious surgical complications (P = 0.029), and 21.6% and 22.8% of patients, respectively, experienced noninfectious surgical complications (P = 0.86). Univariate analysis revealed that blood loss and amino acid administration were significant factors for infectious surgical complications. Multivariate analysis revealed that amino acid administration was an independent factor reducing infectious surgical complications (P = 0.025, 95% confidence interval: 0.105-0.864). Administration of amino acids prevents hypothermia and reduces postoperative infectious complications after thoracoscopic esophagectomy.

Effects of vigorous walking exercise on core body temperature and inhibitory control in thermosensitive persons with multiple sclerosis.

Acute, moderate intensity aerobic exercise might improve cognition in multiple sclerosis (MS), but it is unknown if increases in core body temperature (Ctemp) that negates those effects in thermosensitive persons with MS. Fourteen fully ambulatory, thermosensitive persons with MS completed 20-min bouts of vigorous intensity treadmill walking exercise and seated quiet rest in a randomized, counterbalanced order. Ctemp was measured throughout each experimental condition. Inhibitory control (i.e., an executive function) was measured immediately prior to and following each condition. Ctemp was elevated (~0.6 °C) with vigorous exercise versus quiet rest (p < 0.05). There further were pre-to-post improvements in inhibitory control for vigorous exercise versus quiet rest (ηp(2) = 0.29). Exercise-related increases in Ctemp do not nullify the potential acute exercise benefits on inhibitory control in MS.