Ionic Concepts of the Set-Point for Body Temperature

2015 ◽  
pp. 371-390 ◽  
Author(s):  
R. D. Myers
Keyword(s):  
Body Temperature ◽  
Set Point

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

2017 ◽  
Vol 12 (5) ◽  
pp. 662-667 ◽  
Author(s):  
Matthijs T.W. Veltmeijer ◽  
Dineke Veeneman ◽  
Coen C.C.W. Bongers ◽  
Mihai G. Netea ◽  
Jos W. van der Meer ◽  
...  
Keyword(s):  
Heart Rate ◽  
Body Temperature ◽  
Skin Temperature ◽  
Core Body Temperature ◽  
Exercise Tests ◽  
Hypothalamic Temperature ◽  
Set Point ◽  
Exercise Induced ◽  
Core Body ◽  
The Impact

Purpose: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.Methods: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.Results: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.Conclusions: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.

Light masking of circadian rhythms of heat production, heat loss, and body temperature in squirrel monkeys

1999 ◽  
Vol 276 (2) ◽  
pp. R298-R307 ◽  
Author(s):  
Edward L. Robinson ◽  
Charles A. Fuller
Keyword(s):  
Body Temperature ◽  
Heat Loss ◽  
Heat Production ◽  
Whole Body ◽  
Direct Calorimetry ◽  
Set Point ◽  
Subjective Night ◽  
Timing System ◽  
Circadian Timing System ◽  
Body Heat

Whole body heat production (HP) and heat loss (HL) were examined to determine their relative contributions to light masking of the circadian rhythm in body temperature (Tb). Squirrel monkey metabolism ( n = 6) was monitored by both indirect and direct calorimetry, with telemetered measurement of body temperature and activity. Feeding was also measured. Responses to an entraining light-dark (LD) cycle (LD 12:12) and a masking LD cycle (LD 2:2) were compared. HP and HL contributed to both the daily rhythm and the masking changes in Tb. All variables showed phase-dependent masking responses. Masking transients at L or D transitions were generally greater during subjective day; however, L masking resulted in sustained elevation of Tb, HP, and HL during subjective night. Parallel, apparently compensatory, changes of HL and HP suggest action by both the circadian timing system and light masking on Tb set point. Furthermore, transient HL increases during subjective night suggest that gain change may supplement set point regulation of Tb.

Hyperthermia

2018 ◽  
Author(s):  
Matt Wise ◽  
Paul Frost
Keyword(s):  
Body Temperature ◽  
Neuroleptic Malignant Syndrome ◽  
Core Body Temperature ◽  
Heat Stroke ◽  
Drug Induced ◽  
Muscle Cramps ◽  
Set Point ◽  
Heat Exhaustion ◽  
Neurological Signs ◽  
Core Body

An elevation in core body temperature due to thermoregulatory failure with a normal thermoregulatory set point is called hyperthermia. Globally, the most common heat illnesses are heat exhaustion and heat stroke, and these are major causes of morbidity and mortality. These illnesses represent a continuum of disease ranging from mild (heat exhaustion) to total (heat stroke) failure of thermoregulation. Heat exhaustion is characterized by sweating, muscle cramps, fatigue, vomiting, headaches, dizziness, and fainting. These symptoms may also occur in heat stroke but, in addition, neurological signs such as confusion, seizures, and coma predominate. While the diagnosis of these conditions may be straightforward, hyperthermia may complicate a variety of rarer illnesses, including neuroleptic malignant syndrome and drug-induced hyperthermia.

scholarly journals Contribution of thermal and nonthermal factors to the regulation of body temperature in humans

2006 ◽  
Vol 100 (6) ◽  
pp. 2065-2072 ◽  
Author(s):  
Igor B. Mekjavic ◽  
Ola Eiken
Keyword(s):  
Body Temperature ◽  
Temperature Regulation ◽  
Animal Experiments ◽  
Reciprocal Inhibition ◽  
Set Point ◽  
Neurophysiological Studies ◽  
Thermoregulatory System ◽  
Effector Pathways ◽  
Cross Inhibition ◽  
Inhibition Theory

The set point has been used to define the regulated level of body temperature, suggesting that displacements of core temperature from the set point initiate heat production (HP) and heat loss (HL) responses. Human and animal experiments have demonstrated that the responses of sweating and shivering do not coincide at a set point but rather establish a thermoeffector threshold zone. Neurophysiological studies have demonstrated that the sensor-to-effector pathways for HP and HL overlap and, in fact, mutually inhibit each other. This reciprocal inhibition theory, presumably reflecting the manner in which thermal factors contribute to homeothermy in humans, does not incorporate the effect of nonthermal factors on temperature regulation. The present review examines the actions of these nonthermal factors within the context of neuronal models of temperature regulation, suggesting that examination of these factors may provide further insights into the nature of temperature regulation. It is concluded that, although there is no evidence to doubt the existence of the HP and HL pathways reciprocally inhibiting one another, it appears that such a mechanism is of little consequence when comparing the effects of nonthermal factors on the thermoregulatory system, since most of these factors seem to exert their influence in the region after the reciprocal cross-inhibition. At any given moment, both thermal and several nonthermal factors will be acting on the thermoregulatory system. It may, therefore, not be appropriate to dismiss the contribution of either when discussing the regulation of body temperature in humans.

STUDY OF HUMAN THERMOREGULATION: ADAPTIVE OPTIMIZATION CONTROL THEORY ANALYSIS

2008 ◽  
Vol 08 (01) ◽  
pp. 97-108 ◽  
Author(s):  
E. Y. K. NG ◽  
L. W. LIM
Keyword(s):  
Body Temperature ◽  
Control Theory ◽  
Core Body Temperature ◽  
Thermal Control ◽  
General Information ◽  
Point Of View ◽  
Adaptive Optimization ◽  
Set Point ◽  
Laboratory Exercise ◽  
Human Thermoregulation

An example of homeostasis is temperature regulation at a desired level; this physiological process leads to the preservation of a stable biological environment. A control-theory–based model permits a biomedical engineer to understand the complex operation of thermoregulation, by converting general information to knowledge, and can be integrated to see how systemic parameters influence the entire system. The thermal inputs organized in the hypothalamus to activate thermoregulation responses to heat and cold stimuli, with the widely accepted set-point hypothesis for the regulation of body temperature from a control systems point of view, are, however, not entirely known. There are circumstances (e.g. fever) in which the presumed set-point mechanism appears to break down. This paper evaluates a novel set-level adaptive optimal thermal control paradigm inspired by Hebbian covariance synaptic adaptation, previously proposed based on its potential to predict the homeostatic respiratory system. It introduces a Hebbian feedback covariance learning (HFCL) concept in order to align a neuronal network into the analysis of the thermoregulation system. Hebbian theory is concerned with how neurons connect among themselves to become engrams. The passive-active mathematical model for simulating human thermoregulation during exercise was compared in cool, warm, and hot environments, and then was translated into MATLAB to predict thermoregulation. The two-node core and shell model predictions are comparable with observed thermoregulation responses from the existing literature. The thermoregulation changes with respect to proportionality constant and sensitivity of the receptors. A reasonably general agreement with the measured mean group data of earlier performed laboratory exercise studies was obtained for peak temperature, although it tended to overpredict the core body temperature.

Hypothalamic control of body temperature: insights from the past

2004 ◽  
Vol 97 (5) ◽  
pp. 1593-1594 ◽  
Author(s):  
Gary W. Mack
Keyword(s):  
Body Temperature ◽  
Temperature Regulation ◽  
Proportional Control ◽  
Set Point ◽  
Historical Significance ◽  
The Past ◽  
Thermoregulatory Responses ◽  
Hypothalamic Control ◽  
Classic Papers

This essay looks at the historical significance of three APS classic papers that are freely available online: Hammel HT, Hardy JD, and Fusco MM. Thermoregulatory responses to hypothalamic cooling in unanesthetized dogs. Am J Physiol 198: 481—486, 1960 ( http://ajplegacy.physiology.org/cgi/reprint/198/3/481 ). Hammel HT, Jackson DC, Stolwijk JAJ, Hardy JD, and Strømme SB. Temperature regulation by hypothalamic proportional control with an adjustable set point. J Appl Physiol 18: 1146—1154, 1963 ( http://jap.physiology.org/cgi/reprint/18/6/1146 ). Hellstrøm B and Hammel HT. Some characteristics of temperature regulation in the unanesthetized dog. Am J Physiol 213: 547—556, 1967 ( http://ajplegacy.physiology.org/cgi/reprint/213/2/547 ).

scholarly journals Altered Febrile Responses in Older Adults: A Systematic Review

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 224-224
Author(s):  
Barbara Holtzclaw
Keyword(s):  
Systematic Review ◽  
Older Adults ◽  
Body Temperature ◽  
Animal Studies ◽  
Clinical Medicine ◽  
Signs And Symptoms ◽  
Set Point ◽  
Age Related ◽  
Research Findings ◽  
Fever Response

Abstract Human and animal studies support generalizations that older adults are less able than younger adults to mount an effective febrile response. Beyond difficulties this presents for assessing signs and symptoms of infection, concern exists that older adults may lack fever’s protective immuno-stimulant benefits. Fever is a systemic physiological host response to a pyrogen resulting in release of proinflammatory cytokines that produce a regulated elevation of thermoregulatory set-point. Heat is generated, by shivering and molecular activity, and conserved, by vasomotor activity, elevating and maintaining body temperature at the higher set-point level. Because immunological, vasomotor, and kinetic activities raise body temperature, age-associated alterations have been hypothesized to explain blunted febrile responses in older adults. Purpose: A systematic review was done to 1) determine factors underlying presumed origins and alterations in older adults’ febrile responses. 2) assess for gaps and controversies in emerging research that could inform care decisions. Comparisons of disciplinary assumptions, perspectives, and cross-disciplinary interpretations sought relevance to interdisciplinary care. Methods: Search of literature databases: Medline (OVID), and CINAHL (EBSCO). PubMed, and included relevant animal and human research findings since 2000 from physiology, gerontology, immunology, infectious disease, clinical medicine, and nursing. Findings: Altered innate immunity in sepsis shows early hyper-reactive response, prolonged inflammatory activity, and fever response contributing to cardiovascular and neurological morbidity, not temperature elevation. Morbidly was attributed to disease not age. Conclusions: Hazards of blunted febrile temperatures include undetected infections and possible loss of immune benefits. Significant evidence of age-related diminished febrile temperature’s immune consequences shown with animal models.

Effect of antipyretic drugs on circadian rhythm in body temperature of rats

1987 ◽  
Vol 253 (2) ◽  
pp. R306-R313 ◽  
Author(s):  
W. E. Scales ◽  
M. J. Kluger
Keyword(s):  
Circadian Rhythm ◽  
Body Temperature ◽  
Acetylsalicylic Acid ◽  
Sodium Salicylate ◽  
Prostaglandin Synthesis ◽  
Plateau Phase ◽  
Considerable Evidence ◽  
Set Point ◽  
Significant Fall ◽  
Prostaglandin Synthesis Inhibitors

In many species, including the laboratory rat, body temperature varies on a circadian (24 h) basis. There is considerable evidence that the circadian rise in body temperature is attributable to an elevation in thermoregulatory set point. We hypothesized that this rise in set point may be mediated by prostaglandins. If this hypothesis is correct, then it should be possible to block or reduce the nighttime rise in body temperature by the administration of prostaglandin synthesis inhibitors. Rats were injected with the prostaglandin synthesis inhibitors sodium salicylate, acetylsalicylic acid, and indomethacin at 5:00 P.M. and at 9:00 A.M. Administration of these drugs had little effect on body temperature during the day but caused a significant fall in body temperature at night when temperature is normally in the rising or plateau phase of the cycle. We conclude that prostaglandin synthesis is an important component of the circadian rise in body temperature in the rat. In addition, evidence is presented that there exists a cryogenic factor that opposes the nighttime prostaglandin-mediated rise in body temperature.

Fever Revisited

PEDIATRICS ◽  
1992 ◽  
Vol 90 (6) ◽  
pp. 846-850
Author(s):  
Matthew J. Kluger
Keyword(s):  
Body Temperature ◽  
Heat Loss ◽  
Core Body Temperature ◽  
Interleukin 1 ◽  
Defense Responses ◽  
Tropical Fish ◽  
Small Molecular Weight ◽  
Set Point ◽  
Warm Environment ◽  
The Individual

It has been 12 years since I last wrote a Commentary on fever for Pediatrics.29 As I pointed out in that review, fever, which occurs in response to infection or trauma, should be differentiated from "hyperthermia." During fever, the host behaves as if the temperature around which it is regulating (its thermoregulatory "set-point") were elevated. As such, during the rising phase of fever, the infected person will often shiver (increases heat production), will be peripherally vasoconstricted (a response that reduces heat loss), and will crawl under the covers or wear heavier clothing (behavioral responses that decrease heat loss). During hyperthermia, the core body temperature is above the thermoregulatory set-point, and the individual uses both physiological and behavioral means to lower body temperature. This is what happens as a result of exercising, particularly in a warm environment, or as a result of sitting in a sauna. When a fever "breaks" it is thought that the thermoregulatory set-point has returned toward normal, and it is at this time that the individual is hyperthermic. This is why the person will feel warm and will sweat during defervescence. Since 1974 it has been known that fever has had a long phylogenetic history.63 Fevers occur not only in infected birds and mammals, but also in infected reptiles, amphibians, fishes, and even insects (Table 1). The thermoregulatory set-point has risen in the infected "cold-blooded" organisms; and as a result, they behaviorally seek a warmer microclimate. Individuals who have tropical fish may have noticed that when their fish are sick, they tend to congregate near the light (or heat source). I suspect this is an attempt to get their body temperatures up to their raised thermoregulatory set-point. WHAT CAUSES THE RISE IN THERMOREGULATORY SET-POINT? Most evidence indicates that some stimulus (eg, bacterial endotoxin or viruses) causes the release of an endogenous pyrogen (EP), a small molecular weight protein, from macrophages. EP travels through the circulation to the brain, where in the anterior hypothalamus it causes a rise in set-point, presumably by causing an increase in prostaglandin E2. Shortly after the first cytokines were identified, most investigators working in the area of temperature regulation and fever concluded that the cytokine, interleukin-1 (IL-1), was the circulating EP. IL-1, of which there are two forms: α and β, are thought to be responsible for numerous immune and nonimmune host-defense responses.

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