Influence of carotid denervation on the body-core temperature and metabolic responses to changes in ambient temperature during normoxemia and acute hypoxemia in guinea pigs during postnatal maturation

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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Thermal regulatory dysfunction of growth hormone in classical heat stroke?

Acta Endocrinologica ◽

10.1530/eje.0.1340727 ◽

1996 ◽

Vol 134 (6) ◽

pp. 727-730

Author(s):

Abdulaziz Alzeer ◽

Abdullah Al Arifi ◽

Mohsen El-Hazmi ◽

Arjumand S Warsy ◽

Eric S Nylen

Keyword(s):

Growth Hormone ◽

Core Temperature ◽

Heat Stroke ◽

The Body ◽

Body Core Temperature ◽

Treatment Unit ◽

Gh Secretion ◽

Body Core ◽

Time Of Admission ◽

Regulatory Dysfunction

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

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Keeping a Cool Head

Physiology ◽

10.1152/physiologyonline.1986.1.2.41 ◽

1986 ◽

Vol 1 (2) ◽

pp. 41-44 ◽

Cited By ~ 3

Author(s):

M Cabanac

Keyword(s):

Heat Stress ◽

Core Temperature ◽

Heat Exchangers ◽

The Body ◽

Body Core Temperature ◽

Mammalian Brain ◽

Poor Tolerance ◽

Selective Cooling ◽

Body Core ◽

The Brain

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.

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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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An intra ruminal heat exchanger for use in large concious animals

Rangifer ◽

10.7557/2.5.1.536 ◽

1985 ◽

Vol 5 (1) ◽

pp. 10 ◽

Cited By ~ 1

Author(s):

James B. Mercer ◽

Helge K. Johnsen ◽

Svein D. Mathiesen ◽

Arnoldus Schytte Blix

Keyword(s):

Heat Exchanger ◽

Core Temperature ◽

Heat Production ◽

The Body ◽

Body Core Temperature ◽

Ruminant Species ◽

Large Ruminant ◽

Body Core ◽

Total Body

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.En intra-rumenal varmeveksler til bruk i større, uanesteserte dyr.Abstract in Norwegian / Sammendrag: Vi har i denne undersøkelsen beskrevet en metode for hvordan kroppstemperatur hos uanesteserte reinsdyr kan endres uavhengig av omgivelsestemperatur og om dyret løper eller ikke. Metoden innebærer bruk av en enkel varmeveksler som plasseres i dyrets vom gjennom en permanent vom-fistel. Varmeveksleren består av en 7 m lang kveil av fleksibel plastslange (ytre diameter 10.0 mm, indre diameter 8.0 mm). Ved å perfundere slangen med vann av en bestemt temperatur er det mulig å fjerne eller tilføre kroppen en varmemengde som tilsvarer flere ganger dyrets varmeproduksjon. Vi mener at denne metoden kan tilpasses alle store drøvtyggere.Potsiin asetettavan låmpotilan muuttajan kåytto suurilla nukkumattomilla elåimillå.Abstract in Finnish / Yhteenveto: Tutkimuksessa olemme kuvanneet menetelman, jolla voidaan muuttaa nukuttamattoman poron ruumiinlåmpotilaa riippumatta ulkolampotilasta tai siita juokseeko elåin vai ei. Menetelmassa kåytaan yksinkertaista låmpotilan muuttajaa, joka asetetaan elaimeen pysyyan potsifistulan kautta. Låmpotilan muuttaja kasittåa 7 m pitkan muoviletkurullan (letkun halkaisija 10.6 mm, reian halkaisija" 8.0 mmJTTayttåmålla letku tietyn lampoisellå vedella on mahdollista joko laskea tai nostaa ruumiin lampomååråa niin, etta se vastaa moninkertaisesti elaimen omaa låmmontuottoa. Oletamme, etta menetelmåa voidaan kayttaå kaikille suurille mårehtijoille.

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Pregnancy alters body-core temperature response to a simulated open field in rats

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.5.1406 ◽

1997 ◽

Vol 82 (5) ◽

pp. 1406-1410 ◽

Cited By ~ 12

Author(s):

James E. Fewell ◽

Patricia A. Tang

Keyword(s):

Open Field ◽

Core Temperature ◽

Temperature Response ◽

The Body ◽

Body Core Temperature ◽

Sprague Dawley ◽

Induced Hyperthermia ◽

Sprague Dawley Rats ◽

Functional Consequences ◽

Body Core

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.

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