Restoration of thermoregulation after exercise

2017 ◽  
Vol 122 (4) ◽  
pp. 933-944 ◽  
Author(s):  
Glen P. Kenny ◽  
Ryan McGinn
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Current Knowledge ◽  
Thermal Control ◽  
The Body ◽  
Body Core Temperature ◽  
Whole Body ◽  
Temperature Sensitive ◽  
Internal Core ◽  
Body Core

Performing exercise, especially in 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 (e.g., diabetes). The influence of these factors extends 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 manifest 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.

Control of respiratory evaporative heat loss in exercising goats

1979 ◽  
Vol 46 (5) ◽  
pp. 978-983 ◽  
Author(s):  
J. B. Mercer ◽  
C. Jessen
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Heat Exchangers ◽  
The Body ◽  
Body Core Temperature ◽  
Evaporative Heat Loss ◽  
Hypothalamic Temperature ◽  
Body Core ◽  
Total Body ◽  
Rest And Exercise

Investigations were carried out to determine whether a nonthermal input is involved in the control of respiratory evaporative heat loss (REHL) in exercising goats. Two goats were implanted with hypothalamic perfusion thermodes and three goats were implanted with intravascular heat exchangers to clamp hypothalamic temperature and total body core temperature, respectively. At 30 degrees C air temperature REHL was measured while the animals were resting or walking on a treadmill (3 km.h-1, 5 degrees gradient). When the hypothalamic temperature was clamped between 33.0 and 43.0 degrees C the slopes of the responses relating increased REHL to hypothalamic temperature were similar during rest and exercise. However, the threshold hypothalamic temperatures for the increased REHL responses were lower during exercise than at rest, presumably due to higher extrahypothalamic temperatures. When the body core temperature was clamped between 37.0 and 40.4 degrees C the slopes of the responses relating increased REHL to total body core temperature during exercise showed only minor differences compared to those at rest, none of them conclusively indicating nonthermal influences.

scholarly journals Modeling of Differences Between Body Core and Forehead Temperatures Measured by Infrared Thermometers

2017 ◽  
Author(s):  
Oleg Vesnovsky ◽  
Yiyong Li ◽  
L. D. Timmie Topoleski ◽  
Liang Zhu
Keyword(s):  
Heat Transfer ◽  
Core Temperature ◽  
Ebola Virus ◽  
Thermal Environment ◽  
Surface Condition ◽  
The United States ◽  
The Body ◽  
Body Core Temperature ◽  
Whole Body ◽  
Body Core

In recent years, outbreaks of highly contagious diseases, like the Ebola virus, have motivated vigorous efforts to screen travelers entering the United States, especially at airports. Screening involves monitoring the body temperature of entering travelers, and blocking entry of those showing a fever, indicating a potential infection. Typically, screening is performed using commercially available non-contact infrared thermometers (NCITs). These thermometers require specific use protocols (e.g., working distances) to provide accurate results, which may not be followed by inspectors reluctant to approach potentially contagious travelers. Furthermore, the NCITs’ accuracy is based on an assumption that the NCIT readings from a forehead will predict the body core temperatures using a simple common one-size-fits-all correction offset. Unfortunately, the temperature detected on the forehead surface by an NCIT may not represent the true body core temperature, due to the changing conditions of the external environment and/or surface conditions of the forehead skin. It is not clear whether the correction factor is able to adjust to the thermal environment, or whether the surface condition of the forehead, including sweat and skin tone, affects the NCIT readings. Before a clinical study is conducted to understand the differences between the forehead temperatures and the body core temperatures, a computational model to simulate temperature distribution inside and on the surface of the body is a cost-effective way to identify factors that influence the temperatures and to study the reasons for their deviations. The objectives of this study were to 1) develop a numerical whole-body model and perform computational heat transfer simulations of different body geometries and 2) perform parametric studies to evaluate the effect of environmental factors, such as air temperature and heat transfer coefficient, on the differences between the forehead temperature and body core temperature. This data can be used to evaluate correction factors or needed to use the measured forehead temperature to predict the body core temperature.

Body Fatness, Body Core Temperature, and Heat Loss During Moderate-Intensity Exercise

2013 ◽  
Vol 84 (11) ◽  
pp. 1153-1158 ◽  
Author(s):  
Jayme D. Limbaugh ◽  
Gregory S. Wimer ◽  
Lynn H. Long ◽  
William H. Baird
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Body Core Temperature ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Body Fatness ◽  
Body Core

scholarly journals Canine hyperthermia with cerebral protection

1976 ◽  
Vol 40 (4) ◽  
pp. 543-548 ◽  
Author(s):  
R. W. Carithers ◽  
R. C. Seagrave
Keyword(s):  
Core Temperature ◽  
Cold Water ◽  
Brain Temperature ◽  
Body Core Temperature ◽  
Whole Body ◽  
Similar Time ◽  
Data Points ◽  
Body Core ◽  
Heat Transfer System ◽  
The Brain

Extreme whole-body hyperthermia was achieved without lasting side effects in canines by elevating body core temperature to 42 degrees C, using a warm water bath. Cold water irrigation of the nasal alar fold permitted an additional core temperature elevation of 0.5–1.0 degrees C above brain temperature for periods up to 1.5 h. The brain-core temperature differential was maintained by a physiological arteriovenous heat exchanger located at the base of the brain. The maximum tolerable core temperature for the 21 nonirrigated dogs was 42 degrees C for 60–90 min, whereas that for the 28 irrigated dogs was 42.5–43 degrees C for similar time intervals. A mathematical model of the total heat transfer system described the observed dynamic temperature responses. It was the solution of a differential equation which fit the normalized experimental data points and predicted reasonable values for known and unknown experimental parameters.

Thermal control of respiratory evaporative heat loss in exercising dogs

1980 ◽  
Vol 49 (6) ◽  
pp. 979-984 ◽  
Author(s):  
J. B. Mercer ◽  
C. Jessen
Keyword(s):  
Heat Loss ◽  
Thermal Control ◽  
Body Core Temperature ◽  
Threshold Temperature ◽  
Evaporative Heat Loss ◽  
Hypothalamic Temperature ◽  
Body Core ◽  
Hypothalamic Thermosensitivity ◽  
Total Body ◽  
Heat Exchanges

Experiments were carried out to determine whether respiratory evaporative heat loss (REHL) in exercising dogs is entirely under thermal control or whether a nonthermal input is additionally involved. To determine body core thermosensitivity, hypothalamic perfusion thermodes and intravascular heat exchanges were chronically implanted in the animals. This allowed the temperature of these two areas to be independently manipulated. At 30 degrees C air temperature, REHL was measured in three dogs during rest or while running on a treadmill (6 km . h-1, 0 degree gradient). During exercise, the threshold temperature was lowered by 9 degrees C, and the slope of the heat-loss response was reduced to one-third as compared with rest when hypothalamic temperature alone was clamped at various levels between 30 degrees and 42 degrees C. However, when extrahypothalamic body core temperature was additionally clamped, the decrease in threshold during exercise was reduced to 0.43 degrees C, while the slope of the response was identical to that during rest. The results suggest that by taking account of total body core thermosensitivity, instead of hypothalamic thermosensitivity, the alleged role of a nonthermal input is greatly reduced. In addition, the results showed that the major pat of central thermosensitivity must be attributed to the extrahypothalamic body core.

Computational model for calculating body-core temperature elevation in rabbits due to whole-body exposure at 2.45 GHz

2008 ◽  
Vol 53 (12) ◽  
pp. 3391-3404 ◽  
Author(s):  
Akimasa Hirata ◽  
Hironori Sugiyama ◽  
Masami Kojima ◽  
Hiroki Kawai ◽  
Yoko Yamashiro ◽  
...  
Keyword(s):  
Computational Model ◽  
Core Temperature ◽  
Body Core Temperature ◽  
Whole Body ◽  
Temperature Elevation ◽  
Body Core

Thermal regulatory dysfunction of growth hormone in classical heat stroke?

1996 ◽  
Vol 134 (6) ◽  
pp. 727-730
Author(s):  
Abdulaziz Alzeer ◽  
Abdullah Al Arifi ◽  
Mohsen El-Hazmi ◽  
Arjumand S Warsy ◽  
Eric S Nylen
Keyword(s):  
Growth Hormone ◽  
Core Temperature ◽  
Heat Stroke ◽  
The Body ◽  
Body Core Temperature ◽  
Treatment Unit ◽  
Gh Secretion ◽  
Body Core ◽  
Time Of Admission ◽  
Regulatory Dysfunction

Alzeer A, Al Arifi A, El-Hazmi M, Warsy AS, Nylen ES. Thermal regulatory dysfunction of growth hormone in classical heat stroke? Eur J Endocrinol 1996;134:727–30. ISSN 0804–4643 Growth hormone (GH) secretion associated with classical (non-exertional) heat stroke (HS) was evaluated in 26 HS victims and 10 control (non heat-exhausted) subjects during the annual Hajj in Makkah, Saudi Arabia. On admission to the HS treatment unit, the GH level was 1.54 ± 0.14 ng/ml (approximately 3.5-fold higher in the HS victims compared to controls; p = 0.005). The GH levels subsequently declined by 78% by 24 h. The categorized GH response was significantly associated with survival for those subjects with a GH level of < 5.53 ng/ml by 6 h (chi-squared test; p = 0.06). In those patients who died (N = 6), there was a continued increase in GH levels from the time of admission, which peaked at 6 h. In those patients who survived, the GH levels peaked at the time of admission and declined rapidly thereafter. There was a direct correlation of age and GH level upon admission (p = 0.02), as well as to peak GH (p = 0.041). However, there was no relationship of GH level to either body core temperature or the cooling time. In summary, HS induced significant GH secretion. The degree of GH response was not related to the body core temperature and was more pronounced in older individuals and in those that died. Although patients with GH deficiency and HS are characterized by anhidrosis/hypohidrosis, there does not appear to be dysfunction of GH response to heat stress-associated HS. In contrast, a vigorous GH response at 6 h suggested a worse outcome. ES Nylen, Rm GE 246, VAMC, 50 Irving St, NW Washington, DC 20422, USA

Heat loss responses in rats acclimated to heat loaded intermittently

1990 ◽  
Vol 68 (1) ◽  
pp. 66-70 ◽  
Author(s):  
O. Shido ◽  
T. Nagasaka
Keyword(s):  
Skin Temperature ◽  
Heat Loss ◽  
Core Temperature ◽  
Thermal Conductance ◽  
Heat Acclimation ◽  
The Body ◽  
Body Core Temperature ◽  
Acclimation Temperature ◽  
Hypothalamic Temperature ◽  
Direct Body

The present study examined the heat loss response of heat-acclimated rats to direct body heating with an intraperitoneal heater or to indirect warming by elevating the ambient temperature (Ta). The heat acclimation of the rats was attained through exposure to Ta of 33 or 36 degrees C for 5 h daily during 15 consecutive days. Control rats were kept at Ta of 24 degrees C for the same acclimation period. Heat acclimation lowered the body core temperature at Ta of 24 degrees C, and the core temperature level was lowered as acclimation temperature increased. When heat was applied by direct body heating, the threshold hypothalamic temperature (Thy) for the tail skin vasodilation was also lower in heat-acclimated rats than in the control rats. However, the amount of increase in Thy from the resting level to the threshold was the same in all three groups. When heat was applied by indirect warming, threshold Thy was slightly higher in heat-acclimated than in control rats. The amount of increase in Thy from the resting level to the threshold was significantly greater in heat-acclimated rats. In addition, Ta and the skin temperature at the onset of skin vasodilation were significantly higher in heat-acclimated rats. The results indicate that heat-acclimated rats were less sensitive to the increase in skin temperature in terms of threshold Thy. The gain constant of nonevaporative heat loss response was assessed by plotting total thermal conductance against Thy.(ABSTRACT TRUNCATED AT 250 WORDS)

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