Temperature regulation by hypothalamic proportional control with an adjustable set point

1963 ◽  
Vol 18 (6) ◽  
pp. 1146-1154 ◽  
Author(s):  
H. T. Hammel ◽  
D. C. Jackson ◽  
J. A. J. Stolwijk ◽  
J. D. Hardy ◽  
S. B. Stromme
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Temperature Regulation ◽  
Thermal Response ◽  
Hypothalamic Temperature ◽  
Set Point ◽  
Cold Environments ◽  
Hot Environment ◽  
Skin Temperatures

The role of the hypothalamic and skin temperatures in controlling the thermal response of a resting animal was studied by measurements of 1) hypothalamic, rectal, ear skin, and trunk skin temperatures on the resting dog and rhesus monkey in hot, neutral, and cold environments; and 2) the thermal and metabolic responses of a dog in neutral and cold environments during and immediately after holding the hypothalamus at approximately 39.0 C by means of six thermodes surrounding the hypothalamus and perfused with water. The results indicate that 1) a resting animal shivers in a cold environment with the same or higher hypothalamic temperature as the same animal in a neutral environment; 2) a resting animal pants in a hot environment with the same or lower hypothalamic temperature as the same animal in a neutral environment; 3) the hypothalamus is nonetheless strongly responsive to an increase or decrease of 1 C; 4) the rate of heat loss increases at the onset of sleep while the hypothalamic temperature is falling; 5) the hypothalamic temperature is 1–2 C lower during sleep even though thermoregulatory responses are the same as when awake; 6) the rate of heat loss decreases upon awakening while the hypothalamic temperature is rising. The discussion of these results includes a suggestion that the set point for temperature regulation is 1) decreased by a rising or elevated skin and extrahypothalamic core temperature, 2) increased by a falling or lowered skin and extrahypothalamic core temperature, 3) decreased upon entering and during sleep and is increased upon awakening. hypothalamic temperature; temperature set point; hypothalamic stimulation; dog temperature regulation; monkey temperature regulation Submitted on October 15, 1962

The Mechanisms and Energetics of Honeybee Swarm Temperature Regulation

1981 ◽  
Vol 91 (1) ◽  
pp. 25-55
Author(s):  
BERND HEINRICH
Keyword(s):  
Metabolic Rate ◽  
Heat Loss ◽  
Temperature Regulation ◽  
Resting Metabolic Rate ◽  
Primary Role ◽  
Set Point ◽  
Ambient Temperatures ◽  
Thermal Environments ◽  
Lower Temperature

1. Free (active) honeybee swarms regulated their core temperature (Tc) generally within 1 °C of 35 °C. They maintained the same temperature around freshly built honeycomb, and in the brood nest of the hive, from ambient temperatures of between at least 1 and 25 °C. Captive (inactive) swarms in the laboratory often allowed Tc to decline below 35 °C. 2. The temperature of the swarm mantle (Tm) varied with the general activity of the swarm as well as with ambient temperature (TA), but in captive swarms (and sometimes at night in free swarms), Tm was generally held above 17 °C, even at TA < 5 °C. 3. Within the swarm, temperatures varied between 36 °C, an upper temperature set-point, and 17 °C, a lower temperature set-point. 4. Before swarm take-off, all temperature gradients in the swarm were abolished and Tm equalled Tc. 5. The regulated Tc and Tm were unrelated to size and passive cooling rates in swarms ranging from 1000 to 30000 bees. 6. The weight-specific metabolic rate of swarms was correlated with TA and Tc, but relatively little affected by swarm size. 7. Bees on the mantle experiencing low temperatures pushed inward, thus contracting the mantle, diminishing the mantle porosity, and filling interior passageways. As a result, their own rate of heat loss, as well as that from the swarm core, decreased. 8. In large tightly clumped swarms, even at TA < 5 °C, the resting metabolic rate of the bees in the swarm core was more than sufficient to maintain Tc at 35 °C or above. The active thermoregulatory metabolism was due to the bees on the swarm mantle. 9. There was little physical exchange of bees between core and mantle at low (< 5 °C) TA. In addition, there was no apparent chemical or acoustic communication between the bees in the swarm mantle that are subjected to the changes of the thermal environments and the bees in the swarm interior that constantly experience 35 °C regardless of TA. 10. The data are summarized in a model of Tc control indicating a primary role of the mantle bees in controlling heat production and heat loss. 11. The possible ecological significance of swarm temperature regulation is discussed.

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.

Role of the adrenal gland in the thermal response to morphine withdrawal in rats

1992 ◽  
Vol 70 (8) ◽  
pp. 1090-1095 ◽  
Author(s):  
Michael J. Katovich ◽  
David Pitman ◽  
Orit Schechtman
Keyword(s):  
Adrenal Gland ◽  
Skin Temperature ◽  
Core Temperature ◽  
Temperature Response ◽  
Thermal Response ◽  
Morphine Withdrawal ◽  
Ovariectomized Rats ◽  
Moderate Increase ◽  
Adrenalectomized Rats

Administration of naloxone to morphine-dependent rats results in an elevation of tail skin temperature and a fall in core temperature. Previous studies have demonstrated a role of the adrenal gland in the thermal responses that accompany morphine withdrawal in the rat. In the present study, experiments were designed to determine if the duration of adrenalectomy significantly influenced the thermal response observed in morphine withdrawal. In addition we evaluated the influence of the adrenal medulla and glucocorticoid replacement in adrenalectomized rats in mediating the thermal responses of the morphine-dependent rat. Ovariectomized rats were addicted to morphine and subsequently withdrawn by administration of naloxone. This treatment results in a significant rise in tail skin temperature and subsequent fall in colonic temperature. These thermal responses were not observed in morphine-naive rats. Adrenalectomy resulted in a significant attenuation of the rise in tail skin temperature associated with withdrawal. This reduced tail skin temperature response was not different among animals adrenalectomized for 1, 7, 14, 21, or 28 days. Likewise, the moderate increase in core temperature associated with morphine treatment was not observed in the adrenalectomized rats. Serum corticosteroid determinations confirmed the loss of the adrenal steroids in the adrenalectomized rats. In a subsequent experiment it was determined that adrenal demedullation did not reduce the tail skin temperature response during morphine withdrawal, and corticosteroids restored the naloxone-induced surge in tail skin temperature in morphine-dependent, adrenalectomized rats. Collectively, these data suggest a role for the adrenal gland, especially the cortical region, in allowing for full expression of the skin temperature changes associated with withdrawal in morphine-dependent animals.Key words: corticosterone, tail skin temperature, morphine withdrawal, adrenal gland, thermal response, naloxone.

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)

Neuronal basis of Hammel's model for set-point thermoregulation

2006 ◽  
Vol 100 (4) ◽  
pp. 1347-1354 ◽  
Author(s):  
Jack A. Boulant
Keyword(s):  
Heat Loss ◽  
Heat Production ◽  
Temperature Sensitive ◽  
Excitatory Postsynaptic Potential ◽  
Hypothalamic Temperature ◽  
Set Point ◽  
Synaptic Excitation ◽  
Morphological Studies ◽  
Postsynaptic Potential ◽  
To Receive

In 1965, H. T. Hammel proposed a neuronal model to explain set-point thermoregulation. His model was based on a synaptic network encompassing four different types of hypothalamic neurons: i.e., warm-sensitive and temperature-insensitive neurons and heat loss and heat production effector neurons. Although some modifications to this model are suggested, recent electrophysiological and morphological studies support many of the model's major tenets. Hypothalamic warm-sensitive neurons integrate core and peripheral thermal information. These neurons sense changes in hypothalamic temperature, and they orient their dendrites medially and laterally to receive ascending afferent input from cutaneous thermoreceptors. Temperature-insensitive neurons have a different dendritic orientation and may provide constant reference signals, which are important in determining thermoregulatory set points. In Hammel's model, temperature-sensitive and -insensitive neurons send mutually antagonistic synaptic inputs to effector neurons controlling various thermoregulatory responses. The model predicts that warm-sensitive neurons synaptically excite heat loss effector neurons and inhibit heat production effector neurons. In recent studies, one counterpart of these effector neurons may be “excitatory postsynaptic potential-driven neurons,” the activity of which is dependent on synaptic excitation from nearby cells. Excitatory postsynaptic potential-driven neurons have sparse dendrites that appear to be specifically oriented, either medially or laterally, presumably to receive selective synaptic input from a discrete source. Another counterpart of effector neurons may be “silent neurons,” which have extensive dendritic branches that may receive synaptic excitation from remote sources. Because some silent neurons receive synaptic inhibition from nearby warm-sensitive neurons, Hammel's model would predict that they have a role in heat production or heat retention responses.

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.

Air velocity influences thermoregulation and endurance exercise capacity in the heat

2018 ◽  
Vol 43 (2) ◽  
pp. 131-138 ◽  
Author(s):  
Hidenori Otani ◽  
Mitsuharu Kaya ◽  
Akira Tamaki ◽  
Phillip Watson ◽  
Ronald J. Maughan
Keyword(s):  
Skin Temperature ◽  
Heat Loss ◽  
Exercise Capacity ◽  
Core Temperature ◽  
Endurance Exercise ◽  
Temperature Rise ◽  
Time To Exhaustion ◽  
Evaporative Heat Loss ◽  
Air Velocity ◽  
Hot Environment

This study examined the effects of variations in air velocity on time to exhaustion and thermoregulatory and perceptual responses to exercise in a hot environment. Eight male volunteers completed stationary cycle exercise trials at 70% peak oxygen uptake until exhaustion in an environmental chamber maintained at 30 °C and 50% relative humidity. Four air velocity conditions, 30, 20, 10, and 0 km/h, were tested, and the headwind was directed at the frontal aspect of the subject by 2 industrial fans, with blade diameters of 1 m and 0.5 m, set in series and positioned 3 m from the subject’s chest. Mean ± SD time to exhaustion was 90 ± 17, 73 ± 16, 58 ± 13, and 41 ± 10 min in 30-, 20-, 10-, and 0-km/h trials, respectively, and was different between all trials (P < 0.05). There were progressive elevations in the rate of core temperature rise, mean skin temperature, and perceived thermal sensation as airflow decreases (P < 0.05). Core temperature, heart rate, cutaneous vascular conductance, and perceived exertion were higher and evaporative heat loss was lower without airflow than at any given airflow (P < 0.05). Dry heat loss and plasma volume were similar between trials (P > 0.05). The present study demonstrated a progressive reduction in time to exhaustion as air velocity decreases. This response is associated with a faster rate of core temperature rise and a higher skin temperature and perceived thermal stress with decreasing airflow. Moreover, airflow greater than 10 km/h (2.8 m/s) might contribute to enhancing endurance exercise capacity and reducing thermoregulatory, cardiovascular, and perceptual strain during exercise in a hot environment.

THE TAIL OF THE RAT, IN TEMPERATURE REGULATION AND ACCLIMATIZATION

1965 ◽  
Vol 43 (2) ◽  
pp. 257-267 ◽  
Author(s):  
R. P. Rand ◽  
A. C. Burton ◽  
T. Ing
Keyword(s):  
Thermal Conductivity ◽  
Blood Flow ◽  
Critical Temperature ◽  
Heat Loss ◽  
Temperature Regulation ◽  
Venous Occlusion ◽  
Maximum Heat ◽  
Cold Acclimatization ◽  
Environmental Temperatures

The role of the tail of the Wistar white rat in its temperature regulation was studied, and a new index of acclimatization was found. Blood flow in the tail was measured by venous-occlusion plethysmography at environmental temperatures from 17 to 33 °C. There is an abrupt vasodilation between 27 and 30° with flow rising from less than 5 ml to about 40 ml/100 ml tissue per minute. Measurement of heat loss by a gradient calorimeter on the tail showed a similar reflex vasodilation at a critical vasodilation temperature (TCVD). After vasodilation the tail can lose up to 20% of the total heat production of the rat. The skin temperature of the tail was used as an index of vasodilation to determine whether the critical temperature shifted with acclimatization to 11 °C, 20 °C, and 30 °C. There is a decrease in TCVD of about 6° after acclimatization to cold (TCVD = 20 °C for 11 °C, 26 °C for 20 °C). After acclimatization to 30 °C, no vasodilation was found at temperatures up to 33 °C. The maximum heat loss of the tail is greatly increased after cold acclimatization. The mechanism of the shift is probably a change in sensitivity of thermal receptors on the tail, due to an increased vascularity (increased thermal conductivity) of the local tissues.

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