Control of respiratory evaporative heat loss in exercising goats

1979 ◽  
Vol 46 (5) ◽  
pp. 978-983 ◽  
Author(s):  
J. B. Mercer ◽  
C. Jessen

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.

1980 ◽  
Vol 49 (6) ◽  
pp. 979-984 ◽  
Author(s):  
J. B. Mercer ◽  
C. Jessen

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.


2017 ◽  
Vol 122 (4) ◽  
pp. 933-944 ◽  
Author(s):  
Glen P. Kenny ◽  
Ryan McGinn

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.


1990 ◽  
Vol 68 (1) ◽  
pp. 66-70 ◽  
Author(s):  
O. Shido ◽  
T. Nagasaka

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)


Physiology ◽  
1986 ◽  
Vol 1 (2) ◽  
pp. 41-44 ◽  
Author(s):  
M Cabanac

The mammalian brain has poor tolerance to increased temperature. However, when body core temperature rises during exercise or heat stress, the temperature of the brain can remain at a lower level, somewhat independent of the rest of the body. In several mammals the cooling of the brain is related to anatomically well-defined countercurrent heat exchangers. Humans lack these distinct anatomic structures, but significant cooling of the brain can nevertheless occur. Such selective cooling of the brain may have important medical implicantions.


Rangifer ◽  
1985 ◽  
Vol 5 (1) ◽  
pp. 10 ◽  
Author(s):  
James B. Mercer ◽  
Helge K. Johnsen ◽  
Svein D. Mathiesen ◽  
Arnoldus Schytte Blix

<p>A method is described whereby it is possible to alter total body core temperature independently of environmetal temperature and/or exercise in conscious reindeer. The method employs the use of a simple heat exchanger introduced through a permanent rumen fistula. The heat exchanger consists of a 7 m long coil of flexible plastic tubing (OD, 10.0 mm, ID, 8.0 mm). By perfusing the tubing with thermostatically controlled water, heat can be added to or subtracted from the body core at rates equalling several times resting heat production. It is suggested that the method could be used in any large ruminant species.</p><p>En intra-rumenal varmeveksler til bruk i st&oslash;rre, uanesteserte dyr.</p><p>Abstract in Norwegian / Sammendrag: Vi har i denne unders&oslash;kelsen beskrevet en metode for hvordan kroppstemperatur hos uanesteserte reinsdyr kan endres uavhengig av omgivelsestemperatur og om dyret l&oslash;per eller ikke. Metoden inneb&aelig;rer bruk av en enkel varmeveksler som plasseres i dyrets vom gjennom en permanent vom-fistel. Varmeveksleren best&aring;r av en 7 m lang kveil av fleksibel plastslange (ytre diameter 10.0 mm, indre diameter 8.0 mm). Ved &aring; perfundere slangen med vann av en bestemt temperatur er det mulig &aring; fjerne eller tilf&oslash;re kroppen en varmemengde som tilsvarer flere ganger dyrets varmeproduksjon. Vi mener at denne metoden kan tilpasses alle store dr&oslash;vtyggere.</p><p>Potsiin asetettavan l&aring;mpotilan muuttajan k&aring;ytto suurilla nukkumattomilla el&aring;imill&aring;.</p><p>Abstract in Finnish / Yhteenveto: Tutkimuksessa olemme kuvanneet menetelman, jolla voidaan muuttaa nukuttamattoman poron ruumiinl&aring;mpotilaa riippumatta ulkolampotilasta tai siita juokseeko el&aring;in vai ei. Menetelmassa k&aring;ytaan yksinkertaista l&aring;mpotilan muuttajaa, joka asetetaan elaimeen pysyyan potsifistulan kautta. L&aring;mpotilan muuttaja kasitt&aring;a 7 m pitkan muoviletkurullan (letkun halkaisija 10.6 mm, reian halkaisija" 8.0 mmJTTaytt&aring;m&aring;lla letku tietyn lampoisell&aring; vedella on mahdollista joko laskea tai nostaa ruumiin lampom&aring;&aring;r&aring;a niin, etta se vastaa moninkertaisesti elaimen omaa l&aring;mmontuottoa. Oletamme, etta menetelm&aring;a voidaan kaytta&aring; kaikille suurille m&aring;rehtijoille.</p>


2013 ◽  
Vol 84 (11) ◽  
pp. 1153-1158 ◽  
Author(s):  
Jayme D. Limbaugh ◽  
Gregory S. Wimer ◽  
Lynn H. Long ◽  
William H. Baird

1996 ◽  
Vol 134 (6) ◽  
pp. 727-730
Author(s):  
Abdulaziz Alzeer ◽  
Abdullah Al Arifi ◽  
Mohsen El-Hazmi ◽  
Arjumand S Warsy ◽  
Eric S Nylen

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


1997 ◽  
Vol 82 (5) ◽  
pp. 1406-1410 ◽  
Author(s):  
James E. Fewell ◽  
Patricia A. Tang

Fewell, James E., and Patricia A. Tang. Pregnancy alters body-core temperature response to a simulated open field in rats. J. Appl. Physiol. 82(4): 1406–1410, 1997.—Exposure of a rat to a novel environment (e.g., a simulated open field) induces a transient increase in body-core temperature, which is often called stress-induced hyperthermia. Although pregnancy is known to influence thermoregulatory control, its effect on stress-induced hyperthermia is unknown. Therefore, 24 Sprague-Dawley rats (8 nonpregnant and 16 pregnant) were studied to test the hypothesis that pregnancy would alter the development of stress-induced hyperthermia after exposure to a simulated open field. Body-core temperature index increased significantly after exposure to a simulated open field in nonpregnant and gestation day-10 rats but not in gestation day-15 and day-20 rats. Thus our data provide evidence that pregnancy influences the body-core temperature response of rats exposed to a simulated open field in a gestation-dependent fashion. The functional consequences as well as the mechanisms involved remain to be determined.


1984 ◽  
Vol 57 (6) ◽  
pp. 1655-1661 ◽  
Author(s):  
G. Feistkorn ◽  
A. Nagel ◽  
C. Jessen

Thirty experiments were performed in two goats at an air temperature of +35 degrees C and a relative humidity of 33%. By means of heat exchangers, body core temperature (Tpaor) was adjusted to 39, 40.5, or 42 degrees C and maintained at these levels for 120 min. During the last 60 min the animals worked at a rate of 1.2 W/kg (treadmill, 3 km/h, 15%). Blood gases (arteriovenous O2 difference, Po2, Pco2), hemoglobin (Hb), blood lactate (LA), cardiac output (CO), blood pressure (MAP), heart rate (HR), metabolic rate (M), and respiratory evaporative heat loss (REHL) were determined. M, CO, HR, and Hb increased with exercise and were independent of Tpaor. At rest and exercise, REHL increased and Pco2 decreased at higher levels of Tpaor resulting in a respiratory alkalosis. During exercise this was accompanied by an increase in LA. At all instants, the concentrations of LA were higher at higher Tpaor. It is concluded that in a virtually nonsweating species like the goat the overall stress on the circulatory system caused by hyperthermia during exercise is relatively small while the behavior of blood LA is indicative of a temperature-dependent accumulation of LA also in the exercising muscle.


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