Some characteristics of core temperature signals in the conscious goat

1984 ◽  
Vol 247 (3) ◽  
pp. R456-R464 ◽  
Author(s):  
C. Jessen ◽  
G. Feistkorn
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Temperature Difference ◽  
Heat Production ◽  
Heat Exchangers ◽  
Response Curve ◽  
Temperature Response ◽  
Warm Receptors ◽  
Core Sensors Of Temperature ◽  
Head Temperature

In three conscious goats, head and trunk temperatures were altered independently of each other by means of extracorporeal carotid heat exchangers and intravascular heat exchangers in the trunk veins. In 35 experiments heat production and heat loss were measured while head temperature was varied between 35.4 and 42.2 degrees C and trunk temperature between 34.5 and 42.4 degrees C. The largest temperature difference between head and trunk amounted to 6.6 degrees C. Head and trunk generated approximately equal fractions of the total core temperature input to the controller. The distribution of combinations of head and trunk temperatures resulting in constant levels of heat production and heat loss was consistent with the hypothesis that the total core temperature input to the controller equaled the sum of two identical inputs, both rising exponentially with temperature. The hypothesis implies that the input generated by core sensors of temperature in head and trunk is a continuum and conforms with the temperature-response curve of warm receptors.

Interaction of central and peripheral factors in physiological temperature regulation

1961 ◽  
Vol 200 (3) ◽  
pp. 572-580 ◽  
Author(s):  
M. M. Fusco ◽  
J. D. Hardy ◽  
H. T. Hammel
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Heat Production ◽  
Temperature Regulation ◽  
Physiological Temperature ◽  
Warm Environment ◽  
Quantitative Estimates ◽  
Cool Environment ◽  
Localized Heating ◽  
Environmental Temperatures

To evaluate the relative importance of central and peripheral factors in physiological temperature regulation, calorimetric measurements of thermal and metabolic responses in the unanesthetized dog to localized heating of the supraoptic and preoptic regions were made at various environmental temperatures. At all temperatures, heating the hypothalamus caused an imbalance in the over-all heat exchange, and lowered core temperature by 0.8°–1.0°C. In a neutral environment, this was effected by a 30–40% depression of the resting rate of heat production. In a cool environment, heating inhibited shivering so that heat production, relative to heat loss, was low. In a warm environment, vigorous panting and vasodilatation were elicited, thereby increasing heat loss. On cessation of heating, shivering occurred in response to the lowered core temperature, but differed in intensity depending upon the peripheral thermal drive. Reapplication of heating suppressed shivering in all cases. From these data some quantitative estimates were made of the sensitivity of the hypothalamic thermoregulatory ‘centers’, and of the interaction and relative contributions of central and peripheral control.

No dynamic effector responses to fast changes of core temperature at constant skin temperature

1987 ◽  
Vol 65 (6) ◽  
pp. 1339-1346 ◽  
Author(s):  
Ulrike Roos ◽  
Claus Jessen
Keyword(s):  
Skin Temperature ◽  
Heat Loss ◽  
Core Temperature ◽  
Heat Production ◽  
Control Level ◽  
Time Derivative ◽  
Rate Of Change ◽  
Dynamic Responses ◽  
Evaporative Heat Loss ◽  
Blood Temperature

Experiments in conscious goats were done to see whether heat production and respiratory evaporative heat loss show dynamic responses to changing core temperature at constant skin temperature. Core temperature was altered by external heat exchangers acting on blood temperature, while skin temperature was maintained constant by immersing the animals up to the neck in a rapidly circulating water bath. Core temperature was altered at various rates up to 0.9 °C/min. Step deviations of core temperature from control values were always followed by a positive time derivative of effector response, but never by a negative time derivative during sustained displacement of core temperature. Ramp experiments showed that the slopes at which heat production or heat loss rose with core temperature deviating from its control level grew smaller at higher rates of change of core temperature. It is concluded that neither heat production nor respiratory evaporative heat loss respond to the rate of change of core temperature. At constant skin temperature, thermoregulatory effector responses appear to be proportional to the degree to which core temperature deviates from its set level.

scholarly journals Blunted sweating does not alter the rise in core temperature in people with multiple sclerosis exercising in the heat

2020 ◽  
Author(s):  
Georgia K Chaseling ◽  
Davide Filingeri ◽  
Dustin R. Allen ◽  
Michael Barnett ◽  
Steve Vucic ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Heat Loss ◽  
Core Temperature ◽  
Heat Production ◽  
Sweat Rate ◽  
Onset Time ◽  
Local Sweat Rate ◽  
Temperature Heat ◽  
C 30 ◽  
Exercise Induced

Purpose: To determine whether thermoregulatory capacity is altered by MS during exercise in the heat. Methods: Sixteen MS (EDSS: 2.9±0.9; 47±8 y; 77.6±14.0 kg) and 14 healthy (CON) control participants (43±11 y; 78.6±17.0 kg) cycled at a heat production of 4 W.kg-1 for 60 minutes at 30˚C, 30%RH (WARM). A subset of 8 MS (EDSS: 2.6±0.5; 44±8 y; 82.3±18.2 kg) and 8 CON (44±12 y; 81.2±21.1 kg) also exercised at 35°C, 30%RH (HOT). Rectal (Tre), mean skin (Tsk) temperature, and local sweat rate on the upper-back (LSRback) and forearm (LSRarm), were measured. Results: All CON, yet only 9 of 16, and 7 of 8 MS participants completed 60 min of exercise in WARM and HOT trials, respectively. All MS participants unable to complete exercise stopped with ∆Tre between 0.2-0.5˚C. The time to reach a ∆Tre of 0.2˚C was similar (MS:28±15 min, CON: 32±18 min; P=0.51). For MS participants completing 60-min of exercise in WARM, ∆Tre (P=0.13), ∆Tsk (P=0.45), LSRback (P=0.69) and LSRarm (P=0.54) were similar to CON, but ΔTb (MS:0.16±0.13˚C, CON:0.07±0.06˚C; P=0.02) and onset time (MS:16±10 min, CON:8±5 min; P=0.02) for sweating were greater. Similarly, in HOT, ∆Tre (P=0.52), ∆Tsk (P=0.06), LSRback (P=0.59) and LSRarm (P=0.08) were similar, but ΔTb (MS: 0.19±0.16˚C, CON: 0.06±0.04˚C; P=0.04) and onset time (MS:13±7 min, CON:6±3 min; P=0.02) for sweating were greater with MS. Conclusion: Even at 35˚C, a delayed sweating onset didn't alter heat loss to sufficiently affect exercise-induced rises in core temperature. Heat intolerance with MS does not seem attributable to thermoregulatory impairments.

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.

Heat Balance and Distribution during the Core-Temperature Plateau in Anesthetized Humans

1995 ◽  
Vol 83 (3) ◽  
pp. 491-499. ◽  
Author(s):  
Andrea Kurz ◽  
Daniel I. Sessler ◽  
Richard Christensen ◽  
Martha Dechert
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Heat Production ◽  
Heat Balance ◽  
Thermal Flux ◽  
The Body ◽  
Metabolic Heat Production ◽  
The Core ◽  
Metabolic Heat ◽  
Temperature Plateau

Background Once triggered, intraoperative thermoregulatory vasoconstriction is remarkably effective in preventing further hypothermia. Protection results from both vasoconstriction-induced decrease in cutaneous heat loss and altered distribution of body heat. However, the independent contributions of each mechanism have not been quantified. Accordingly, we evaluated overall heat balance and distribution of heat within the body during the core-temperature plateau. Methods Nine minimally clothed male volunteers were anesthetized with propofol and isoflurane and maintained in an approximately 22 degrees C environment. They were monitored for approximately 2 h before vasoconstriction and for 3 h subsequently. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular temperatures, ten skin temperatures, and "deep" foot temperature. Heat constrained by vasoconstriction to the trunk and head was calculated by subtracting the expected change in that region (overall heat balance multiplied by the fractional weight of the trunk and head) from the actual change (change in distal esophageal temperature multiplied by the specific heat of human tissue and the weight of the trunk and head); the result represents the amount by which core heat exceeded that which would be expected based on overall heat balance, assuming that the change was evenly distributed throughout the body. Results Vasoconstriction and passive tissue cooling decreased heat loss but not to the level of heat production. Consequently, heat loss exceeded metabolic heat production throughout the study. Core temperature decreased approximately 1.3 C during the 2-h prevasoconstriction period; however, core temperature remained virtually constant during the subsequent 3 h. In the 3 h after vasoconstriction, arm and leg heat content decreased 57 +/- 9 kcal, and vasoconstriction constrained 22 +/- 8 kcal to the trunk and head. Conclusions These results confirm the efficacy of thermo-regulatory vasoconstriction in preventing additional core hypothermia. Decreased cutaneous heat loss and constraint of metabolic heat to the core thermal compartment contributed to the plateau.

Human heat balance during postexercise recovery: separating metabolic and nonthermal effects

2008 ◽  
Vol 294 (5) ◽  
pp. R1586-R1592 ◽  
Author(s):  
Ollie Jay ◽  
Daniel Gagnon ◽  
Michel B. DuCharme ◽  
Paul Webb ◽  
Francis D. Reardon ◽  
...  
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Heat Production ◽  
Heat Balance ◽  
Heat Content ◽  
Total Heat ◽  
Whole Body ◽  
Active Recovery ◽  
Total Heat Loss ◽  
Body Heat

Previous studies report greater postexercise heat loss responses during active recovery relative to inactive recovery despite similar core temperatures between conditions. Differences have been ascribed to nonthermal factors influencing heat loss response control since elevations in metabolism during active recovery are assumed to be insufficient to change core temperature and modify heat loss responses. However, from a heat balance perspective, different rates of total heat loss with corresponding rates of metabolism are possible at any core temperature. Seven male volunteers cycled at 75% of V̇o2peak in the Snellen whole body air calorimeter regulated at 25.0°C, 30% relative humidity (RH), for 15 min followed by 30 min of active (AR) or inactive (IR) recovery. Relative to IR, a greater rate of metabolic heat production (Ṁ − Ẇ) during AR was paralleled by a greater rate of total heat loss (ḢL) and a greater local sweat rate, despite similar esophageal temperatures between conditions. At end-recovery, rate of body heat storage, that is, [(Ṁ − Ẇ) − ḢL] approached zero similarly in both conditions, with Ṁ − Ẇ and ḢL elevated during AR by 91 ± 26 W and 93 ± 25 W, respectively. Despite a higher Ṁ − Ẇ during AR, change in body heat content from calorimetry was similar between conditions due to a slower relative decrease in ḢL during AR, suggesting an influence of nonthermal factors. In conclusion, different levels of heat loss are possible at similar core temperatures during recovery modes of different metabolic rates. Evidence for nonthermal influences upon heat loss responses must therefore be sought after accounting for differences in heat production.

Assessment of heat production, heat loss, and core temperature during nitrous oxide exposure: a new paradigm for studying drug effects and opponent responses

2005 ◽  
Vol 288 (3) ◽  
pp. R692-R701 ◽  
Author(s):  
Karl J. Kaiyala ◽  
Douglas S. Ramsay
Keyword(s):  
Nitrous Oxide ◽  
Heat Loss ◽  
Core Temperature ◽  
Heat Production ◽  
Drug Effects ◽  
Acute Tolerance ◽  
New Paradigm ◽  
Tolerance Development ◽  
Drug Induced ◽  
Opponent Processes

Studies using core temperature (Tc) have contributed greatly to theoretical explanations of drug tolerance and its relationship to key features of addiction, including dependence, withdrawal, and relapse. Many theoretical accounts of tolerance propose that a given drug-induced psychobiological disturbance elicits opponent responses that contribute to tolerance development. This proposal and its theoretical extensions (e.g., conditioning as a mechanism of chronic tolerance) have been inferred from dependent variables, such as Tc, which represent the summation of multiple underlying determinants. Direct measurements of determinants could increase the understanding of opponent processes in tolerance, dependence, and withdrawal. The proximal determinants of Tc are metabolic heat production (HP) and heat loss (HL). We developed a novel system for simultaneously quantifying HP (indirect calorimetry), HL (direct gradient layer calorimetry), and Tc (telemetry) during steady-state administrations of nitrous oxide (N2O), an inhalant with abuse potential that has been previously used to study acute and chronic tolerance development to its hypothermia-inducing property. Rats were administered 60% N2O ( n = 18) or placebo gas ( n = 16) for 5 h after a 2-h placebo baseline exposure. On average, N2O rapidly but transiently lowered HP and increased HL, each by ∼16% ( P < 0.001). On average, rats reestablished and maintained thermal equilibrium (HP = HL) at a hypothermic Tc (−1.6°C). However, some rats entered positive heat balance (HP > HL) after becoming hypothermic such that acute tolerance developed, i.e., Tc rose despite continued drug administration. This work is the first to directly quantify the thermal determinants of Tc during administration of a drug of abuse and establishes a new paradigm for studying opponent processes involved in acute and chronic hypothermic tolerance development.

Temperature Response of the Rat to Action and Interaction of Chlorpromazine, Reserpine and Serotonin

1958 ◽  
Vol 195 (3) ◽  
pp. 755-758 ◽  
Author(s):  
Roger A. Hoffman
Keyword(s):  
Oxygen Consumption ◽  
Heat Loss ◽  
Heat Production ◽  
Temperature Response ◽  
Prior Treatment ◽  
Antagonistic Interaction

Reserpine was found to cause a prolonged increase in oxygen consumption while chlorpromazine and serotonin produced a comparable decline. Consequently, reserpine and chlorpromazine exhibited antagonistic interaction on the temperature response. Serotonin had little effect in modifying the temperature response to chlorpromazine, while prior treatment with serotonin appeared to delay the temperature decline seen with reserpine alone. Since the temperature declined following reserpine, in spite of an increased oxygen consumption, there was indicated both an increased heat production and a greatly increased heat loss. The data suggest that reserpine and chlorpromazine act by different mechanisms. Likewise, it is suggested that while reserpine and serotonin may act at similar sites, it is also apparent that different effector sites are differentially affected as well, at least insofar as thermoregulation is concerned.

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