Concept: Normal human body temperature
Effects of lowering body temperature via hyperhydration, with and without glycerol ingestion and practical precooling on cycling time trial performance in hot and humid conditions
- Journal of the International Society of Sports Nutrition
- Published over 5 years ago
BACKGROUND: Hypohydration and hyperthermia are factors that may contribute to fatigue and impairment of endurance performance. The purpose of this study was to investigate the effectiveness of combining glycerol hyperhydration and an established precooling technique on cycling time trial performance in hot environmental conditions. METHODS: Twelve well-trained male cyclists performed three 46.4-km laboratory-based cycling trials that included two climbs, under hot and humid environmental conditions (33.3 +/- 1.1[degree sign]C; 50 +/- 6% r.h.). Subjects were required to hyperhydrate with 25 g.kg-1 body mass (BM) of a 4[degree sign]C beverage containing 6% carbohydrate (CON) 2.5 h prior to the time trial. On two occasions, subjects were also exposed to an established precooling technique (PC) 60 min prior to the time trial, involving 14 g.kg-1 BM ice slurry ingestion and applied iced towels over 30 min. During one PC trial, 1.2 g.kg-1 BM glycerol was added to the hyperhydration beverage in a double-blind fashion (PC+G). Statistics used in this study involve the combination of traditional probability statistics and a magnitude-based inference approach. RESULTS: Hyperhydration resulted in large reductions (-0.6 to -0.7[degree sign]C) in rectal temperature. The addition of glycerol to this solution also lowered urine output (330 ml, 10%). Precooling induced further small (-0.3[degree sign]C) to moderate (-0.4[degree sign]C) reductions in rectal temperature with PC and PC+G treatments, respectively, when compared with CON (0.0[degree sign]C, P<0.05). Overall, PC+G failed to achieve a clear change in cycling performance over CON, but PC showed a possible 2% (30 s, P=0.02) improvement in performance time on climb 2 compared to CON. This improvement was attributed to subjects' lower perception of effort reported over the first 10 km of the trial, despite no clear performance change during this time. No differences were detected in any other physiological measurements throughout the time trial. CONCLUSIONS: Despite increasing fluid intake and reducing core temperature, performance and thermoregulatory benefits of a hyperhydration strategy with and without the addition of glycerol, plus practical precooling, were not superior to hyperhydration alone. Further research is warranted to further refine preparation strategies for athletes competing in thermally stressful events to optimize health and maximize performance outcomes.
Humans' core body temperature (CBT) is strictly controlled within a narrow range. Various studies dealt with the impact of physical activity, clothing, and environmental factors on CBT regulation under terrestrial conditions. However, the effects of weightlessness on human thermoregulation are not well understood. Specifically, studies, investigating the effects of long-duration spaceflight on CBT at rest and during exercise are clearly lacking. We here show that during exercise CBT rises higher and faster in space than on Earth. Moreover, we observed for the first time a sustained increased astronauts' CBT also under resting conditions. This increase of about 1 °C developed gradually over 2.5 months and was associated with augmented concentrations of interleukin-1 receptor antagonist, a key anti-inflammatory protein. Since even minor increases in CBT can impair physical and cognitive performance, both findings have a considerable impact on astronauts' health and well-being during future long-term spaceflights. Moreover, our findings also pinpoint crucial physiological challenges for spacefaring civilizations, and raise questions about the assumption of a thermoregulatory set point in humans, and our evolutionary ability to adapt to climate changes on Earth.
Introduction Responses to physical activity while wearing personal protective equipment in hot laboratory conditions are well documented. However less is known of medical professionals responding to an emergency in hot field conditions in standard attire. Therefore, the purpose of this study was to assess the physiological responses of medical responders to a simulated field emergency in tropical conditions. METHODS: Ten subjects, all of whom were chronically heat-acclimatized health care workers, volunteered to participate in this investigation. Participants were the medical response team of a simulated field emergency conducted at the Northern Territory Emergency Services training grounds, Yarrawonga, NT, Australia. The exercise consisted of setting up a field hospital, transporting patients by stretcher to the hospital, triaging and treating the patients while dressed in standard medical response uniforms in field conditions (mean ambient temperature of 29.3°C and relative humidity of 50.3%, apparent temperature of 27.9°C) for a duration of 150 minutes. Gastrointestinal temperature was transmitted from an ingestible sensor and used as the index of core temperature. An integrated physiological monitoring device worn by each participant measured and logged heart rate, chest temperature and gastrointestinal temperature throughout the exercise. Hydration status was assessed by monitoring the change between pre- and post-exercise body mass and urine specific gravity (USG). RESULTS: Mean core body temperature rose from 37.5°C at the commencement of the exercise to peak at 37.8°C after 75 minutes. The individual peak core body temperature was 38.5°C, with three subjects exceeding 38.0°C. Subjects sweated 0.54 L per hour and consumed 0.36 L of fluid per hour, resulting in overall dehydration of 0.7% of body mass at the cessation of exercise. Physiological strain index was indicative of little to low strain. CONCLUSIONS: The combination of the unseasonably mild environmental conditions and moderate work rates resulted in minimal heat storage during the simulated exercise. As a result, low sweat rates manifested in minimal dehydration. When provided with access to fluids in mild environmental conditions, chronically heat-acclimatized medical responders can meet their hydration requirements through ad libitum fluid consumption. Whether such an observation is replicated under a harsher thermal load remains to be investigated. Brearley MB , Heaney MF , Norton IN . Physiological responses of medical team members to a simulated emergency in tropical field conditions. Prehosp Disaster Med. 2013;28(2):1-6 .
Antithrombotic therapy with oral aspirin or clopidogrel (Plavix®) is associated with an attenuated skin vasodilator response and a greater rate of rise in core temperature in healthy, middle-aged individuals during passive heating in a water perfused suit. PURPOSE: The present double-blind, crossover study examined the functional consequences of 7 days of low-dose aspirin (ASA, 81 mg/day) vs.clopidogrel (CLO, 75 mg/day) treatment in 14 healthy, middle-aged (50-65 yrs) men and women during passive heating in air (40 min at 30°C, 40% rh) followed by exercise (60% O2peak). METHODS: Oral temperature (Tor) was measured in the antechamber (23.0 ± 0.1°C) before entering a warm environmental chamber. After 40 minutes of rest subjects cycled on a recumbent cycle ergometer for up to 120 minutes. Esophageal temperature (Tes) and laser Doppler flux were measured continuously, and the latter was normalized to maximal cutaneous vascular conductance (%CVCmax). RESULTS: Prior to entry into the environmental chamber there were no differences in Tor among treatments; however, after 40 minutes of rest in the heat, Tes was significantly higher for ASA and CLO vs. placebo (37.2±0.1°C, 37.3±0.1°C, vs. 37.0±0.1°C, both P<0.001), a difference that persisted throughout exercise (P<0.001 vs. placebo). The mean body temperature thresholds for the onset of cutaneous vasodilation were shifted to the right for both ASA and CLO during exercise (P<0.05). CONCLUSION: ASA and CLO resulted in elevated core temperatures during passive heat stress and shifted the onset of peripheral thermoeffector mechanisms toward higher body temperatures during exercise heat stress.
Physical resilience is the ability of an organism to respond to stressors that acutely disrupt normal physiological homeostasis. By definition, resilience decreases with increasing age, while frailty, defined as a decline in tissue function, increases with increasing age. Assessment of resilience could therefore be an informative early paradigm to predict healthy aging compared to frailty, which measures late life dysfunction. Parameters for resilience in the laboratory mouse are not yet well defined, and no single standardized stress test exists. Since aging involves multiple genetic pathways, integrative responses involving multiple tissues, organs, and activities need to be measured to reveal the overall resilience status, suggesting a battery of stress tests, rather than a single all-encompassing one, would be most informative. Three simple, reliable, and inexpensive stressors are described in this review that could be used as a panel to determine levels of resilience. Brief cold water immersion allows a recovery time to normothermia as an indicator of resilience to hypothermia, i.e. the quicker the return to normal body temperature, the more robust the resilience. Sleep deprivation (SD) impairs remote memory in aged mice, and has detrimental effects on glucose metabolism. Cyclophosphamide (CYP) targets white blood cells, especially myeloid cells resulting in neutropenia with a rebound neutrophilia in an age-dependent manner. Thus a strong neutrophilic response indicates resilience. In conclusion, resilience promises to be an especially useful measurement of biological age, i.e. how fast a particular organ or tissue ages. The three stressors, cold, SD, and CYP, are applicable to human medicine and aging because they represent clinically relevant stress conditions that have effects in an age-dependent manner. They are thus an attractive perturbation for resilience testing in mice to measure the effectiveness of interventions that target basic aging processes.
Thermoregulation is the maintenance of a relatively constant core body temperature. Humans normally maintain a body temperature at 37°C, and maintenance of this relatively high temperature is critical to human survival. This concept is so important that control of thermoregulation is often the principal example cited when teaching physiological homeostasis. A basic understanding of the processes underpinning temperature regulation is necessary for all undergraduate students studying biology and biology-related disciplines, and a thorough understanding is necessary for those students in clinical training. Our aim in this review is to broadly present the thermoregulatory process taking into account current advances in this area. First, we summarize the basic concepts of thermoregulation and subsequently assess the physiological responses to heat and cold stress, including vasodilation and vasoconstriction, sweating, nonshivering thermogenesis, piloerection, shivering, and altered behavior. Current research is presented concerning the body’s detection of thermal challenge, peripheral and central thermoregulatory control mechanisms, including brown adipose tissue in adult humans and temperature transduction by the relatively recently discovered transient receptor potential channels. Finally, we present an updated understanding of the neuroanatomic circuitry supporting thermoregulation.
The sympathetic nervous system is controlled by transient receptor potential vanilloid 1 in the regulation of body temperature
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology
- Published almost 3 years ago
Transient receptor potential vanilloid 1 (TRPV1) is involved in sensory nerve nociceptive signaling. Recently, it has been discovered that TRPV1 receptors also regulate basal body temperature in multiple species from mice to humans. In the present study, we investigated whether TRPV1 modulates basal sympathetic nervous system (SNS) activity. C57BL6/J wild-type (WT) mice and TRPV1 knockout (KO) mice were implanted with radio-telemetry probes for measurement of core body temperature. AMG9810 (50 mg/kg) or vehicle (2% DMSO/5% Tween 80/10 ml/kg saline) was injected intraperitoneally. Adrenoceptor antagonists or vehicle (5 ml/kg saline) was injected s.c. In WT mice, the TRPV1 antagonist, AMG9810, caused significant hyperthermia, associated with increased noradrenaline concentrations in brown adipose tissue. The hyperthermia was significantly attenuated by the β-adrenoceptor antagonist propranolol, the mixed α-/β-adrenoceptor antagonist labetalol, and the α1-adrenoceptor antagonist prazosin. TRPV1 KO mice have a normal basal body temperature, indicative of developmental compensation. d-Amphetamine (potent sympathomimetic) caused hyperthermia in WT mice, which was reduced in TRPV1 KO mice, suggesting a decreased sympathetic drive in KOs. This study provides new evidence that TRPV1 controls thermoregulation upstream of the SNS, providing a potential therapeutic target for sympathetic hyperactivity thermoregulatory disorders.-Alawi, K. M., Aubdool, A. A., Liang, L., Wilde, E., Vepa, A., Psefteli, M.-P., Brain, S. D., Keeble, J. E. The sympathetic nervous system is controlled by transient receptor potential vanilloid 1 in the regulation of body temperature.
The perceptual strain index (PeSI) has been shown to overcome the limitations associated with the assessment of the physiological strain index (PSI), primarily the need to obtain a core body temperature measurement. The PeSI uses the subjective scales of thermal sensation and perceived exertion (RPE) to provide surrogate measures of core temperature and heart rate, respectively. Unfortunately, thermal sensation has shown large variability in providing an estimation of core body temperature. Therefore, the primary aim of this study was to determine if thermal comfort improved the ability of the PeSI to predict the PSI during exertional-heat stress.
- Journal of applied physiology (Bethesda, Md. : 1985)
- Published over 1 year ago
Performing exercise, especially in the hot conditions, can heat the body causing significant increases in internal body temperature. To offset this increase, powerful and highly developed autonomic thermoregulatory responses (i.e., skin blood flow and sweating) are activated to enhance whole-body heat loss; a response mediated by temperature sensitive receptors in both the skin and the internal core regions of the body. Independent of thermal control of heat loss, nonthermal factors can have profound consequences on the body’s ability to dissipate heat during exercise. These include the activation of the body’s sensory receptors (i.e., baroreceptors, metaboreceptors, mechanoreceptors, etc.) as well as phenotypic factors such as age, sex, acclimation, fitness, and chronic diseases such as diabetes. The influence of these factors extend into recovery such that marked impairments in thermoregulatory function occur leading to prolonged and sustained elevations in body core temperature. Irrespective of the level of hyperthermia, there is a time-dependent suppression of the body’s physiological ability to dissipate heat. This delay in the restoration of postexercise thermoregulation has been associated with disturbances in cardiovascular function which manifests most commonly as postexercise hypotension. This review examines the current knowledge regarding the restoration of thermoregulation postexercise. In addition, the factors that are thought to accelerate or delay the return of body core temperature to resting levels are highlighted with a particular emphasis on strategies to manage heat stress in athletic and/or occupational settings.
To the Editor: In the Permissive Hyperthermia through Avoidance of Acetaminophen in Known or Suspected Infection in the Intensive Care Unit (HEAT) trial, Young et al. (Dec. 3 issue)(1) report that early administration of acetaminophen to treat fever due to probable infection in critically ill patients did not affect outcomes. There may be two contributing factors that should raise caution in accepting the null hypothesis. First, in healthy persons, normal body temperature is considered to be 37°C (98.6°F) and varies by 0.5 to 1.0°C. A temperature of 38.3°C or higher (≥101°F) generally defines fever in the intensive care unit (ICU). . . .