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

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.

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Control of respiratory evaporative heat loss in exercising goats

Journal of Applied Physiology ◽

10.1152/jappl.1979.46.5.978 ◽

1979 ◽

Vol 46 (5) ◽

pp. 978-983 ◽

Cited By ~ 10

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.

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Modulation of carbohydrate and fat utilization by diet, exercise and environment

Biochemical Society Transactions ◽

10.1042/bst0311270 ◽

2003 ◽

Vol 31 (6) ◽

pp. 1270-1273 ◽

Cited By ~ 76

Author(s):

A.E. Jeukendrup

Keyword(s):

Carbohydrate Metabolism ◽

Environmental Conditions ◽

Fat Metabolism ◽

Body Core Temperature ◽

Moderate Intensity ◽

Moderate Intensity Exercise ◽

Substrate Use ◽

Ambient Temperatures ◽

Relative Contribution ◽

Body Core

At rest and during exercise carbohydrate and fat are the predominant substrates. They are oxidized simultaneously but the relative contribution of these two substrates is dependent on a variety of factors including the exercise intensity and duration, diet, environmental conditions and training status. Changes in carbohydrate metabolism during the transition from rest to exercise and from low- to high-intensity exercise are mainly due to allosteric regulation. The factors that up-regulate fat metabolism in the transition to moderate-intensity exercise and the factors that result in a down-regulation of fat metabolism at higher intensities are incompletely understood. Substrate use is further modulated by the endocrine milieu (e.g. catecholamines, insulin, cortisol) and possibly cytokines (e.g. interleukin-6). With increasing duration of exercise there are marked increases in fat metabolism and decreases in carbohydrate metabolism and this has been ascribed mainly to substrate availability. Both acute food intake and chronic diets also have profound effects on substrate utilization. An increase in carbohydrate intake will rapidly suppress fat metabolism and increase carbohydrate metabolism whereas such an adaptation to a high-fat diet may take several days. The environmental conditions can also alter substrate use; high ambient temperatures can increase glycogen breakdown as a result of increased body core temperature and increased circulation catecholamines. Low temperatures can also increase carbohydrate metabolism, especially when shivering. In addition to these factors adaptation to training, in particular endurance training, will reduce the reliance on carbohydrate metabolism and increase fat oxidation, especially from intramuscular triacylglycerol stores.

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Faculty Opinions recommendation of Circadian disruption of body core temperature and rest-activity rhythms after general (propofol) anesthesia in rats.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1162503.624034 ◽

2009 ◽

Author(s):

Misha Perouansky

Keyword(s):

Core Temperature ◽

Circadian Disruption ◽

Body Core Temperature ◽

Activity Rhythms ◽

Body Core ◽

Rest Activity

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The recommended Threshold Limit Values for heat exposure fail to maintain body core temperature within safe limits in older working adults

Journal of Occupational and Environmental Hygiene ◽

10.1080/15459624.2017.1321844 ◽

2017 ◽

Vol 14 (9) ◽

pp. 703-711 ◽

Cited By ~ 13

Author(s):

Dallon T. Lamarche ◽

Robert D. Meade ◽

Andrew W. D'Souza ◽

Andreas D. Flouris ◽

Stephen G. Hardcastle ◽

...

Keyword(s):

Core Temperature ◽

Heat Exposure ◽

Body Core Temperature ◽

Limit Values ◽

Threshold Limit Values ◽

Working Adults ◽

Threshold Limit ◽

Body Core ◽

Safe Limits

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Hypothalamic paraventricular nucleus is critical for renal vasoconstriction elicited by elevations in body temperature

AJP Renal Physiology ◽

10.1152/ajprenal.00488.2007 ◽

2008 ◽

Vol 294 (2) ◽

pp. F309-F315 ◽

Cited By ~ 12

Author(s):

Joo Lee Cham ◽

Emilio Badoer

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Blood Flow ◽

Renal Blood Flow ◽

Core Temperature ◽

Paraventricular Nucleus ◽

Hypothalamic Paraventricular Nucleus ◽

Body Core Temperature ◽

Control Group ◽

Body Core

Redistribution of blood from the viscera to the peripheral vasculature is the major cardiovascular response designed to restore thermoregulatory homeostasis after an elevation in body core temperature. In this study, we investigated the role of the hypothalamic paraventricular nucleus (PVN) in the reflex decrease in renal blood flow that is induced by hyperthermia, as this brain region is known to play a key role in renal function and may contribute to the central pathways underlying thermoregulatory responses. In anesthetized rats, blood pressure, heart rate, renal blood flow, and tail skin temperature were recorded in response to elevating body core temperature. In the control group, saline was microinjected bilaterally into the PVN; in the second group, muscimol (1 nmol in 100 nl per side) was microinjected to inhibit neuronal activity in the PVN; and in a third group, muscimol was microinjected outside the PVN. Compared with control, microinjection of muscimol into the PVN did not significantly affect the blood pressure or heart rate responses. However, the normal reflex reduction in renal blood flow observed in response to hyperthermia in the control group (∼70% from a resting level of 11.5 ml/min) was abolished by the microinjection of muscimol into the PVN (maximum reduction of 8% from a resting of 9.1 ml/min). This effect was specific to the PVN since microinjection of muscimol outside the PVN did not prevent the normal renal blood flow response. The data suggest that the PVN plays an essential role in the reflex decrease in renal blood flow elicited by hyperthermia.

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MK801 impairs thermoregulation in the heat

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y02-055 ◽

2002 ◽

Vol 80 (3) ◽

pp. 226-232 ◽

Cited By ~ 5

Author(s):

Frédéric Canini ◽

Nadine Simler ◽

Lionel Bourdon

Keyword(s):

Locomotor Activity ◽

Nmda Receptor ◽

Receptor Antagonist ◽

Core Temperature ◽

Exposure Duration ◽

Heat Exposure ◽

Nmda Receptor Antagonist ◽

Dopamine Metabolism ◽

Body Core Temperature ◽

Body Core

The effects of MK801 (dizocilpine), a glutamate NMDA receptor antagonist, on thermoregulation in the heat were studied in awake rats exposed to 40°C ambient temperature until their body core temperature reached 43°C. Under these conditions, MK801-treated rats exhibited enhanced locomotor activity and a steady rise in body core temperature, which reduced the heat exposure duration required to reach 43°C. Since MK801-treated rats also showed increased striatal dopaminergic metabolism at thermoneutrality, the role of dopamine in the MK801-induced impairment of thermoregulation in the heat was determined using co-treatment with SCH23390, a dopamine D1 receptor antagonist. SCH23390 normalized the locomotor activity in the heat without any effect on the heat exposure duration. These results suggest that the MK801-induced impairment of thermoregulation in the heat is related to neither a dopamine metabolism alteration nor a locomotor activity enhancement.Key words: heatstroke, NMDA receptor, thermoregulation, dopamine, locomotion.

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