A common measurement of body temperature during exercise in a hot, humid environment is mean skin temperature collected from 3-12 sites on the body. However, such an approach fails to demonstrate localized differences in skin temperature that are likely to exist as a function of gender. The purpose of this study was to examine potential differences in skin temperature between men and women at 17 different locations on the body. Young women (21 ± 1 y; n = 11) and men (23 ± 3; n = 10) were recruited to complete a 60-min walk/jog interval protocol in a hot (34 ± 1 °C), humid (64 ± 8%) environment while skin temperature was measured. Data was analyzed using a repeated-measures ANOVA (p < 0.05) and location of interaction effects determined using a Fisher’s least squares difference test. We observed a higher change (p < 0.05) from baseline skin temperatures (ΔTsk) for women in three locations: left upper back (women: avg. ΔTsk = 4.12 ± 0.20 °C; men: avg. ΔTsk = 2.70 ± 0.10 °C), right upper back (women: avg. ΔTsk = 4.19 ± 0.07 °C; men: avg. ΔTsk = 2.92 ± 0.05 °C), and right mid-back (women: avg. ΔTsk = 4.62 ± 0.14 °C; men: avg. ΔTsk =3.55 ± 0.09 °C). Individual time differences between genders occurred after 7- (left upper back) and 15-min (right upper back, right mid-back) of exercise and were maintained until the end of exercise. Women have a greater increase in skin temperature at three locations on the back following the onset of exercise in a hot, humid environment. This report provides important information regarding the implications of women exercising in a hot, humid environment.

Technological advances in clinical thermometers have resulted in a variety of minimally invasive devices that give rapid results but may not have the accuracy necessary for use in acutely ill adults. Inaccurate temperatures can result in missed opportunities for the early identification and treatment of infection and sepsis. Following the methodology outlined by Whittemore and Knafl, the purpose of this project was to conduct an integrative review of the research on the accuracy of clinical thermometers used for acutely ill adults. The evidence was categorized using the Hierarchy of Evidence for Interventional Studies, and the quality of the studies was appraised using the indicators described by Hooper and Andrews. Forty-seven studies met the inclusion criteria; the findings on device accuracy were contradictory. Device accuracy was found in 10 (n = 27) studies on the tympanic (TM), 2 (n = 8) on the chemical dot (CH), 7 (n = 19) on the temporal artery (TAT), and 3 (n = 13) on the axillary (AX) thermometers. Two of 2 studies found the no-touch (NT) device clinically inaccurate. Diagnostic accuracy was found in 3 (n = 8) and 0 (n = 5) studies on the TM and TAT, respectively. Only 22 studies had an acceptable quality grade of A or B, limiting the validity of the evidence. The evidence did not support the use of the NT and TAT thermometers or the AX route for acutely ill adults. The CH device should be use with caution, and abnormal temperatures should be validated with a more reliable device. For thermometers in use, appropriate training and technique are essential for the most accurate results. Closing the knowledge-to-practice gap on clinical thermometers can change the culture of nursing practice, improve early sepsis identification, and increase the quality of patient care.

Indiana University-Purdue University Indianapolis (IUPUI) / Brain responds to an array of diverse challenges that are defined as either exteroceptive stress, involving cognitive processing of sensory information from the external environment and or interoceptive stress, detected through sensory neural or chemical cues from the internal environment. The physiological response to most stresses consists of autonomic responses that are essential for animal survival in the face of a threatening circumstance. However, it is known that exposition to continuous situations of stress is involved in the development of a series of diseases such as hypertension, myocardial infarction and panic syndrome. Several studies have shown that cells in a specific area of the brain, the dorsomedial hypothalamus (DMH), are involved in the response produced during emotional stress. However, the role of glutamatergic transmission in the DMH in the increase in body temperature induced by experimental stress has not been examined. Research findings thus far indicate that neurons in the DMH play a role in thermoregulation and that local glutamate receptors may be involved. The hypothesis of this thesis is that activity at ionotropic glutamate receptors in the DMH is necessary for the thermogenic response induced by experimental stress. In the present work, microinjections of kynurenate, an excitatory amino acid antagonist, NBQX (2, 3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione), an AMPA/kainate receptor antagonist, DL-2-amino-5-phosphonovaleric acid (APV), an NMDA receptor antagonist, and a mixture of NBQX and APV, were delivered to the DMH before exposure to experimental stress. The stress paradigms used include models for exteroceptive stress and interoceptive stress. The results show that inhibition of both NMDA and non-NMDA receptors is necessary to abolish the thermogenic response produced by all stress paradigms tested. Furthermore, there appears to be a difference in the degree of attenuation of the thermogenic response produced by either inhibition of NMDA receptors or non-NMDA receptors. Together these results support a definite role for ionotropic glutamate receptors within DMH region in the thermogenic response to stress. These results also finally show that the DMH is involved in all the major physiological stress responses including increase in plasma ACTH, increase in heart rate, blood pressure and now temperature as well.

Tang Chi-wing, Wendy = 飲品味道對炎熱中運動的華籍男女小童之體液平衡及體温調節之影響 / 鄧稚穎. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 74-86). / Text in English; abstracts in English and Chinese. / Tang Chi-wing, Wendy = Yin pin wei dao dui yan re zhong yun dong de hua ji nan nü xiao tong zhi ti ye ping heng ji ti wen diao jie zhi ying xiang / Deng Zhiying. / Dedication --- p.i / Acknowledgements --- p.ii / Abstract --- p.iii / Table of Contents --- p.vi / List of Tables --- p.viii / List of Figure --- p.ix / Chapter CHAPTER ONE --- INTRODUCTION --- p.1 / Chapter 1.1 --- Background --- p.1 / Chapter 1.2 --- Purpose of the Study --- p.4 / Chapter 1.3 --- Hypotheses --- p.5 / Chapter 1.4 --- Definition of Terms --- p.6 / Chapter 1.5 --- Assumptions --- p.7 / Chapter 1.6 --- Delimitations --- p.7 / Chapter 1.7 --- Limitations --- p.8 / Chapter 1.8 --- Significance of Study --- p.8 / Chapter CHAPTER TWO --- REVIEW OF LITERATURE --- p.9 / Chapter 2.1 --- Water Balance during Exercise --- p.9 / Chapter 2.2 --- Effect of Dehydration on Human Body during Exercise --- p.11 / Chapter 2.3 --- Physiological Responses of Dehydration for Children when Exercising in the Heat --- p.17 / Chapter 2.4 --- Effect of Fluid Ingestion during Exercise --- p.20 / Chapter 2.5 --- Drivers of Fluid Replacement --- p.23 / Chapter CHAPTER THREE --- METHODOLOGY --- p.30 / Chapter 3.1 --- Participants --- p.30 / Chapter 3.2 --- Equipment and Instrumentation --- p.31 / Chapter 3.3 --- Preliminary Measurement --- p.31 / Chapter 3.4 --- Study Design and Procedures --- p.35 / Chapter 3.5 --- Collection and Analysis of Blood Samples --- p.44 / Chapter 3.6 --- Statistical Analysis --- p.44 / Chapter CHAPTER FOUR --- RESULTS --- p.46 / Chapter 4.1 --- Exercise Intensity --- p.46 / Chapter 4.2 --- Body Fluid Balance --- p.50 / Chapter 4.3 --- Thermoregulatory Responses --- p.61 / Chapter 4.4 --- Taste Perception Analysis --- p.62 / Chapter 4.5 --- Summary of the Results --- p.66 / Chapter CHAPTER FIVE --- DISCUSSION --- p.67 / Recommendations and Applications --- p.73 / REFERENCES --- p.74 / APPENDIXES --- p.87

The primary purpose of this doctoral dissertation was to investigate the effect of body temperature responses at physiologically relevant sites during an incremental exercise test on the phenomenon of exercise-induced hypoxemia (EIH). This phenomenon has been considered as an important limitation to physical performance with a prevalence of ~50 % in trained male athletes, but described in both sexes, across the range of both age and physical fitness in more recent literature. Previously this phenomenon has been described as a decrement in both arterial oxygen partial pressure (PaO₂) and oxy-haemoglobin saturation (SaO₂or SpO₂) with, particularly important for PaO₂, a lack of or inappropriate correction made for the change in body temperature during intense exercise. The initial study of this thesis determined the thermal response within the body at physiologically relevant sites measured simultaneously during an incremental exercise test. The results demonstrated the inadequacy of rectal temperature as an indicator of the acute temperature changes occurring during an incremental exercise test due to its slow response rate and relative thermal inertia. Radial arterial blood and oesophageal temperatures were shown to behave almost identically during the exercise test, albeit with an offset of approximately 1.3ºC, and were considered much more appropriate and relevant indicators of thermal changes during exercise. As an extension of the initial work active muscle temperature (vastus lateralis) was measured during the exercise test, demonstrating a significantly lower resting temperature than the oft-reported “core” temperatures (rectal and oesophageal) as well as a significantly greater increase in temperature in comparison to all other measurement sites. Overall, the results of this first study indicated that the physiologically relevant temperatures measured at the oesophageal and muscle sites differed markedly to the outdated rectal temperature measurement site and should be used as measures of thermal response when evaluating oxygen loading (oesophageal) or unloading (active muscle). Utilising the definition of EIH as a decrease in PaO₂ of ≥ 10 mmHg, the effect of temperature correcting PaO₂ was evaluated in the second study. Arterial blood gases measured simultaneously to the temperature measurements during the incremental exercise test were adjusted for the temperature changes at each site (every 1ºC increase in temperature will increase a PaO₂ value by ~5 mmHg). Whilst uncorrected PaO₂ values indicated an almost 100% prevalence of EIH in this group, oesophageal temperature corrected PaO₂ values decreased this prevalence to ~50% while muscle temperature corrections resolved all cases of EIH and demonstrated an HYPEROXAEMIA (i.e. the reverse of the well-established phenomenon) in the majority of subjects. Further investigation of arterial oxygen content during the exercise test indicates that there is no disruption in the delivery of oxygen to the active muscles and therefore any performance decrement should be attributed to another mechanism. Whilst the phenomenon of EIH is determined by the definition applied and the use of temperature corrections in the case of PaO₂, its reproducibility in a test-retest situation had not previously been determined. Utilising a subset of previously tested subjects, the reproducibility of both temperature and PaO₂ were determined with results indicating that the blood gas response was highly reproducible, especially the minimum PaO₂ value noted during each exercise test. However, comparing a more statistically relevant definition of a change in PaO₂ of ± 2 standard deviations from the mean resting PaO₂ to the previous delimiter of 10 mmHg indicated a lesser reproducibility of the prevalence of EIH. In summary, this thesis exposes the inadequacies of previous research into EIH with regard to the expected reproducibility of the phenomenon and the need to correctly adjust PaO₂ values for exercise-induce hyperthermia as well as demonstrating the difference in thermal responses to acute exercise in physiologically significant areas of the body. Furthermore, previously described correlations between the change in PaO₂ and VO₂ max were not evident in the subjects tested within this thesis, nor was there any indication of a diffusion limitation based on reduced pulmonary capillary transit time (by association with VO₂ max) or pulmonary oedema (rebuked by a rapid return of PaO₂ to above resting levels following exercise cessation). / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1320633 / Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2008

The negative consequence of recent climate change on the Earth’s biodiversity has become more evident in recent years. Some animals, due to insularity or habitat fragmentation, are unable to shift their ranges altitudinally and latitudinally. Vulnerable species need to rely on behavioural and, more importantly, physiological responses in order to persist through present climatic changes. It has therefore become more obvious that physiological responses of individuals need to be incorporated into predictive models of the responses of mammals to accelerated climate change. The primary purpose of this study was to test the ‘Hyperthermic Daily Torpor’ hypothesis proposed recently by Lovegrove et al., (in press). The hypothesis suggests that, based on albeit limited evidence, some small mammals may be capable of hyperthermia induced hypometabolism equivalent to that experienced during torpor and hibernation in response to cold temperatures. These authors argue that such hyperthermic hypometabolism should reduce the risk of entry into pathological hyperthermia and also reduce the rate of water loss driven by heat-induced evaporative cooling. The reaction norms of desert mammals have been selected to be adaptive over a wide range of climatic conditions due to the unpredictability of their habitat. Thus, they are good models for testing the reaction norms that may be expressed in response to accelerated climate change. We therefore tested our hypothesis using two presumably heat-adapted desert rodents; the Namaqua rock mouse, Aethomys namaquensis, and the pygmy rock mouse, Petromyscus collinus, as model species. We used indirect respirometry to measure metabolic rate at high ambient temperatures. We progressively exposed the animals to high temperatures to induce thermal tolerance and thus minimize the risks of lethal hyperthermia. We also measured subcutaneous and core temperatures, using temperature-sensitive PIT tags (BioTherm Identipet) and modified iButtons (Maxim Integrated), respectively. A. namaquensis displayed the capacity for hyperthermia-induced hypometabolism (Q10 79 = 1.27 ± 1.61) whereas the P. collinus did not (Q10 = 2.45 ± 1.41). The implications of such a physiological response in A. namaquensis are crucial in terms of its capacity to minimize the risks of lethal, pathological hyperthermia. Recent models of endothermic responses to global warming based on ectothermic models predict a dichotomy in the thermoregulatory responses of mammals to high temperatures. This study, to our knowledge, provides some of the first data on these interspecific variations in the thermoregulatory responses of mammals to high temperatures. However, the different physiological responses to hyperthermia between these two species cannot be meaningfully interpreted without phylogenetically independent comparisons with other species, that is, a more expansive interspecific analysis. Nonetheless, we provide some autecological sketches to assist in future multivariate interspecific analyses. Physiological differences between captive or captive-bred and free-ranging mammals preclude the extrapolation of our findings to free-ranging mammals. It is almost impossible to collect MR data in the field, although a few authors have successfully done so, and it is often not feasible to collect Tb data in small free-ranging mammals. Most studies have therefore made use of externally-mounted temperature-sensitive data loggers in order to collect Tskin data as a proxy for Tcore data in free-ranging mammals. However, misleading gradients between Tskin and Tcore can occur if data loggers are placed too close to major-heat producing tissues and the effects of the external environment on these data loggers may result in large Tskin – Tcore gradients. The second objective of this thesis therefore was to test the validity of using subcutaneous temperatures (Tsub) from subcutaneously injected temperature-sensitive PIT tags as a proxy for Tcore using the Namaqua rock mouse, Aethomys namaquensis. We found that the difference between Tcore and Tsub was minimal (~ 0.34˚C) within the thermoneutral zone (TNZ) with slight, non-significant, differences outside the TNZ. There was a tendency for Tsub to underestimate Tcore below thermoneutrality and overestimate it above thermoneutrality. We attributed these differences to the various heat loss and heat gain mechanisms activated in response to heat and cold stress in order to maintain a setpoint Tb. Nevertheless, we found that the Tcore – Tskin differential never exceeded 1.59˚C above the wide 108 range of Tas (5˚ – 41˚C) measured. Thus, we can conclude that subcutaneous temperatures provide a reasonably reliable proxy for core temperature in small mammals. / Thesis (M.Sc.)-University of KwaZulu-Natal, Pietermaritzburg, 2012.

The primary purpose of this doctoral dissertation was to investigate the effect of body temperature responses at physiologically relevant sites during an incremental exercise test on the phenomenon of exercise-induced hypoxemia (EIH). This phenomenon has been considered as an important limitation to physical performance with a prevalence of ~50 % in trained male athletes, but described in both sexes, across the range of both age and physical fitness in more recent literature. Previously this phenomenon has been described as a decrement in both arterial oxygen partial pressure (PaO₂) and oxy-haemoglobin saturation (SaO₂or SpO₂) with, particularly important for PaO₂, a lack of or inappropriate correction made for the change in body temperature during intense exercise. The initial study of this thesis determined the thermal response within the body at physiologically relevant sites measured simultaneously during an incremental exercise test. The results demonstrated the inadequacy of rectal temperature as an indicator of the acute temperature changes occurring during an incremental exercise test due to its slow response rate and relative thermal inertia. Radial arterial blood and oesophageal temperatures were shown to behave almost identically during the exercise test, albeit with an offset of approximately 1.3ºC, and were considered much more appropriate and relevant indicators of thermal changes during exercise. As an extension of the initial work active muscle temperature (vastus lateralis) was measured during the exercise test, demonstrating a significantly lower resting temperature than the oft-reported “core” temperatures (rectal and oesophageal) as well as a significantly greater increase in temperature in comparison to all other measurement sites. Overall, the results of this first study indicated that the physiologically relevant temperatures measured at the oesophageal and muscle sites differed markedly to the outdated rectal temperature measurement site and should be used as measures of thermal response when evaluating oxygen loading (oesophageal) or unloading (active muscle). Utilising the definition of EIH as a decrease in PaO₂ of ≥ 10 mmHg, the effect of temperature correcting PaO₂ was evaluated in the second study. Arterial blood gases measured simultaneously to the temperature measurements during the incremental exercise test were adjusted for the temperature changes at each site (every 1ºC increase in temperature will increase a PaO₂ value by ~5 mmHg). Whilst uncorrected PaO₂ values indicated an almost 100% prevalence of EIH in this group, oesophageal temperature corrected PaO₂ values decreased this prevalence to ~50% while muscle temperature corrections resolved all cases of EIH and demonstrated an HYPEROXAEMIA (i.e. the reverse of the well-established phenomenon) in the majority of subjects. Further investigation of arterial oxygen content during the exercise test indicates that there is no disruption in the delivery of oxygen to the active muscles and therefore any performance decrement should be attributed to another mechanism. Whilst the phenomenon of EIH is determined by the definition applied and the use of temperature corrections in the case of PaO₂, its reproducibility in a test-retest situation had not previously been determined. Utilising a subset of previously tested subjects, the reproducibility of both temperature and PaO₂ were determined with results indicating that the blood gas response was highly reproducible, especially the minimum PaO₂ value noted during each exercise test. However, comparing a more statistically relevant definition of a change in PaO₂ of ± 2 standard deviations from the mean resting PaO₂ to the previous delimiter of 10 mmHg indicated a lesser reproducibility of the prevalence of EIH. In summary, this thesis exposes the inadequacies of previous research into EIH with regard to the expected reproducibility of the phenomenon and the need to correctly adjust PaO₂ values for exercise-induce hyperthermia as well as demonstrating the difference in thermal responses to acute exercise in physiologically significant areas of the body. Furthermore, previously described correlations between the change in PaO₂ and VO₂ max were not evident in the subjects tested within this thesis, nor was there any indication of a diffusion limitation based on reduced pulmonary capillary transit time (by association with VO₂ max) or pulmonary oedema (rebuked by a rapid return of PaO₂ to above resting levels following exercise cessation). / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1320633 / Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2008

During flight missions, fighter pilots are in general exposed to vast amounts of stress including mild hypoxia, vibrations, high accelerations, and thermal discomfort. It is interesting to predict potential risks with a certain mission or flight case due to these stresses to increase safety for fighter pilots. The most predominant risk is typically thermal discomfort which can lead to serious health concerns. Extensive exposure to high or low temperature in combination with a demanding work situation weakens the physical and mental state of the pilot and can eventually lead to life-threatening conditions. One method to estimate the physical and mental state of a person is to measure the body core temperature. The body core temperature cannot be measured continuously during flight and needs to be estimated by using for instance a human thermoregulatory model. In this study, a model of the human thermoregulatory system and the cockpit environment is developed. Current thermoregulatory models are not customized for fighter pilots but a model developed by Fiala et al. in 2001, which has previously shown good performance in both cold and warm environments as well as for various activation levels for the studied person, is used as a theoretical foundation. Clothing layers are implemented in the model corresponding to clothes used by pilots in the Swedish air force flying the fighter aircraft Gripen E in warm outside conditions. Cooling garments and air conditioning systems as well as avionics, canopy, and cockpit air are included in the model to get a realistic description of the cockpit environment. Input to the model is a flight case containing data with altitude and velocity of the fighter during a mission. human heat transfer; body temperature regulation; physiological model;cooling garment; cockpit modeling

These studies investigated the impact of intensity and body temperature on performance and cardiovascular regulation during high intensity and prolonged exercise. In study 1, polyphenol antioxidant supplementation proved to have no effect on exercise performance and related variables (gross efficiency, perceived exertion, maximal power) during exercise in the heat. Furthermore, there were no differences between the cardiovascular or thermoregulatory responses between control and antioxidant treatments. Study 2 utilized an integrative approach to investigate a classic topic in exercise physiology, namely, is the cardiac output to oxygen consumption relationship linear across a wide range of exercise intensities? The slope of the CO vs. VO2 relationship was significantly reduced from 70 to 100% of VO2max when compared to the slope from 40 to 70% of VO2max (2.0 ± 0.4 vs. 4.4 ± 0.3 l/min, p = 0.025). This finding, in combination with the plateau and eventual reduction in stroke volume at high intensity exercise compared to moderate intensity exercise (146.0 ± 16.6 vs. 138.5 ± 14.9 ml/beat, p = 0.015), argues in favor of a cardiac limitation to high intensity exercise. This study also showed that the pattern of oxygen extraction at the whole body level (arterial venous O2 difference) and the muscle level (deoxygenated hemoglobin) is not similar and that muscle specific differences exist regarding oxygen extraction. Study 3 determined that hyperthermia (elevation of skin temperature by 4.3°C and core temperature by 0.8°C) did not reduce SV independent of the increase in HR. Even under conditions of moderate hyperthermia the reduction in SV is due to the increase in HR and temporally unrelated to increases in cutaneous blood flow. In summary, antioxidant supplementation had no effect on performance, cardiovascular, or thermoregulatory responses to exercise in the heat in well trained subjects. High intensity exercise is associated with a reduced rate of increase in the CO vs. VO2 relationship. Finally, hyperthermia does not reduce SV during exercise when HR is maintained at normal levels. / text

The purpose of this study was to determine if a relationship existed in healthy older adults between two psychological and physiological variables. The conceptual framework suggested that a relationship of psychological and physiological functions would facilitate positive adjustment to the stressors of aging. Life satisfaction represented psychological functioning; body temperature represented physiological functioning; body temperature represented physiological functioning. Because some evidence exists that normal temperature for older adults is lower than 98.6°F, an additional purpose was to determine if the sample had a normal body temperature lower than 98.6°F. Subjects were 174 healthy Caucasians aged 60-97. None were taking antibiotic, phenotiazine, cortisone, or reserpine containing drugs. Life satisfaction was measured using Neugarten's Life Satisfaction Index A (LSIA); body temperature was measured with an IVAC 821 oral electronic thermometer. Subjects rated perceived health on the Health Status Scale (HSS), and enumerated the past year's stressful life events on a modification of Holmes and Rahe's Social Readjustment Rating Questionnaire (SRRQ). Data were collected in winter and summer to determine if body temperature was different based on season. Statistical significance was p = .05. An ANOVA revealed no significant differences between winter and summer groups. The Pearson product-moment revealed no correlation between LSIA and TEMP. LSIA was significantly correlated with HSS and AGE; that is, subjects who were more satisfied with their lives considered themselves healthier, and were younger than other subjects. TEMP was significantly related only to SEX, indicating that females had higher temperatures than males. The mean temperature for all subjects, 98.24°F, was statistically different from 98.6°F, as were winter (98.32°F) and summer (98.17°F) group means. No difference was found between winter and summer mean temperatures, indicating that season of the year did not affect body temperatures in this sample. It was concluded that no psychophysiological relationship was found because body temperature may index only illness, not health. The mean temperature was not clinically different from 98.6°F most likely because these subjects were not taking drugs known to affect body temperature. A recommendation was that nurses evaluate each older client's temperature against his own normal, versus a universal normal.