Effect of Hypoxia Upon Temperature Regulation of Mice, Dogs, and Man

Kottke, Frederic J.; Phalen, J. S.; Taylor, C. B.; Visscher, Maurice B.; Evans, Gerald

doi:10.1152/ajplegacy.1948.153.1.10

Cited by 50 publications

(34 citation statements)

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“…However, after the core temperature stabilized fo llo wing the posture change the introduction of hypoxia had no further effect. Prev ious studies that proposed acute hypoxia to decrease core temperature also found a 0.4 ℃ decrease, although, the methods used in these studies did not control for posture [1,2,5]. Subjects in these studies transitioned fro m standing to lying when exposed to hypoxia.…”

Section: Posture Not Acute Hypoxia Decreases Core Temperaturementioning

confidence: 94%

“…Previous studies have reported that core temperature in humans decreases with acute exposure to hypoxia [1,2]. It was hypothesized that this occurs due to both a decrease in metabolic rate and an increase in skin b lood flo w [2].…”

Section: Introductionmentioning

confidence: 99%

“…The methods in previous studies that reported acute hypoxia to decrease core temperature did not control for postural changes. For example, one study found that when oxygen content was progressively lowered, body temperature also decreased; however, during this time, subjects went from a standing position to a lying position [1]. Thus, further study on the effect of acute hypoxia on core temperature wh ile controlling for posture is warranted.…”

Section: Introductionmentioning

confidence: 99%

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When Posture is Controlled, Acute Hypoxia does not Decrease Core Temperature

Dalton¹,

Brautigam²,

Buono³

2012

ALS

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It has been reported that acute hypoxia causes a reduction in core temperature in humans. It was hypothesized that this occurs due to both a decrease in metabolic rate and an increase in skin b lood flo w. Ho wever, other studies have found that core temperature decreases with changes in posture. The methods in prev ious studies finding hypo xia to decrease core temperature did not control for postural changes. Thus, further examination is warranted to examine the effect of hypo xia on core temperature while controlling for posture change. Ten healthy adults, between the ages of 18 and 45 were recruited to participate. Subjects completed one trial consisting of breathing normo xic air (20.9%) for a 2 hour period and hypoxic air for a 1 hour period, while systematically changing posture. During this time core temperature and skin blood flow were recorded every 5 minutes. The results showed that mean core body temperature significantly (p < 0.05) decreased by 0.4℃ when the subjects transitioned from a standing to lying position. Ho wever, acute hypoxia, which reduced the mean o xygen saturation to 85%, d id not significantly affect core temperature. Such results suggest that when posture is controlled, acute hypoxia does not significantly decrease core body temperature. Thus, the results of previous studies that have reported decreases in core temperature with acute hypoxia, but failed to control for posture, need to be questioned.

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Section: Posture Not Acute Hypoxia Decreases Core Temperaturementioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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When Posture is Controlled, Acute Hypoxia does not Decrease Core Temperature

Dalton¹,

Brautigam²,

Buono³

2012

ALS

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“…A method to induce anapyrexia in small animals is by subjecting the animals to hypoxia, which triggers regulated hypothermia and corollary hypometabolism in some species as a countermeasure against the hypoxic, and thus potentially lethal, conditions [14][15][16][17]. One of the putative regulatory mechanisms is centered on carotid body sensing [18,19].…”

Section: Introductionmentioning

confidence: 99%

“…When hypoxia is sensed, anapyrexia is induced through the inhibition of thermogenic effectors and activation of cooling effectors [1,16,[22][23][24], which are under control of the POAH [7,8,11,25]. This protective mechanism (Figure 1) is believed to be rooted in evolution, and there is evidence that such a mechanism is preserved in man, at least to an extent [14,26]. However, hypoxia is generally not employed in the clinical setting as a patient's already compromised state may be exacerbated at low oxygen tensions.…”

Section: Introductionmentioning

confidence: 99%

Survey and critical appraisal of pharmacological agents with potential thermo-modulatory properties in the context of artificially induced hypometabolism

Dirkes

Gulik

Heger

2015

JCTRes

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A reduction in body temperature can be achieved by a downward adjustment of the termoneutral zone, a process also described as anapyrexia. Pharmacological induction of anapyrexia could enable numerous applications in medicine. However, little is known about the potential of pharmacological agents to induce anapyrexic signaling. Therefore, a review of literature was performed and over a thousand pharmacologically active compounds were analyzed for their ability to induce anapyrexia in animals. Based on this analysis, eight agents (helium, dimethyl sulfoxide, reserpine, (oxo)tremorine, pentobarbital, (chlor) promazine, insulin, and acetaminophen) were identified as potential anapyrexia-inducing compounds and discussed in detail. The translational pitfalls were also addressed for each candidate compound. Of the agents that were discussed, reserpine, (oxo)tremorine, and (chlor) promazine may possess true anapyrexic properties based on their ability to either affect the thermoneutral zone or its effectors and facilitate hypothermic signaling. However, these properties are currently not unequivocal and warrant further examination in the context of artificially-induced hypometabolism. Keywords:thermoneutral zone hypothermia induction pharmacological agents animals body temperature

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Integrated Physiological Mechanisms of Exercise Performance, Adaptation, and Maladaptation to Heat Stress

Sawka

Leon

Montain

et al. 2011

Comprehensive Physiology

395

444

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This article emphasizes significant recent advances regarding heat stress and its impact on exercise performance, adaptations, fluid electrolyte imbalances, and pathophysiology. During exercise-heat stress, the physiological burden of supporting high skin blood flow and high sweating rates can impose considerable cardiovascular strain and initiate a cascade of pathophysiological events leading to heat stroke. We examine the association between heat stress, particularly high skin temperature, on diminishing cardiovascular/aerobic reserves as well as increasing relative intensity and perceptual cues that degrade aerobic exercise performance. We discuss novel systemic (heat acclimation) and cellular (acquired thermal tolerance) adaptations that improve performance in hot and temperate environments and protect organs from heat stroke as well as other dissimilar stresses. We delineate how heat stroke evolves from gut underperfusion/ischemia causing endotoxin release or the release of mitochondrial DNA fragments in response to cell necrosis, to mediate a systemic inflammatory syndrome inducing coagulopathies, immune dysfunction, cytokine modulation, and multiorgan damage and failure. We discuss how an inflammatory response that induces simultaneous fever and/or prior exposure to a pathogen (e.g., viral infection) that deactivates molecular protective mechanisms interacts synergistically with the hyperthermia of exercise to perhaps explain heat stroke cases reported in low-risk populations performing routine activities. Importantly, we question the "traditional" notion that high core temperature is the critical mediator of exercise performance degradation and heat stroke. Published 2011. This article is a U.S. Government work and is in the public domain in the USA.

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Effect of Hypoxia Upon Temperature Regulation of Mice, Dogs, and Man

Cited by 50 publications

References 0 publications

When Posture is Controlled, Acute Hypoxia does not Decrease Core Temperature

When Posture is Controlled, Acute Hypoxia does not Decrease Core Temperature

Survey and critical appraisal of pharmacological agents with potential thermo-modulatory properties in the context of artificially induced hypometabolism

Integrated Physiological Mechanisms of Exercise Performance, Adaptation, and Maladaptation to Heat Stress

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