The effect of exposure to cold on the pulse rate and respiration of man

Barcroft, Joseph; Verzár, Fritz

doi:10.1113/jphysiol.1931.sp002742

Cited by 20 publications

(9 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Zhhlava, Sobotka, Reinig & MysliveEek (1961) showed that the removal of the neopallium of the rat resulted in some disturbance to thermoregulation, but this was not of a gross nature. This essentially confirms and extends the observations of Bazett & Penfield (1922), Bazett et al (1933), Pinkston et al (1934), andRioch (1937) that removal of the forebrain in cats and dogs has little effect upon thermoregulation and those of Clark, Magoun & Ranson (19393) who found that damage to the thalamus causes no obvious disturbance to temperature regulation in the cat.…”

Section: Dependence Of Homoeothermy Upon the Integritysupporting

confidence: 89%

The Thermosensitivity of the Hypothalamus and Thermoregulation in Mammals

Bligh

1966

Biological Reviews

210

View full text Add to dashboard Cite

Section: Dependence Of Homoeothermy Upon the Integritysupporting

confidence: 89%

The Thermosensitivity of the Hypothalamus and Thermoregulation in Mammals

Bligh

1966

Biological Reviews

210

View full text Add to dashboard Cite

“…shivering) to regulate body temperatures, but does not prevent their activation. Given that skin wetness (Fukazawa & Havenith, ), which occurs subsequent to sweating (Hardy, ), and shivering (Barcroft & Verzar, ) are known to modulate thermal discomfort, it has been proposed that the activation of sweating and shivering in humans may be required inputs for thermal behaviour to be initiated (Schlader, ). On the contrary, our data indicate that sweat rate (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…At present, it remains unknown whether the activation of shivering or sweating is required for thermal behaviour to be initiated (Schlader, 2014). On the one hand, in hot and cold environments thermal discomfort can be brought about or exacerbated by skin wetness (Fukazawa & Havenith, 2009), which occurs subsequent to sweating (Hardy, 1970), and shivering (Barcroft & Verzar, 1931), respectively. This suggests that there might be a causal role for sweating or shivering in the initiation of thermal behaviour in humans (Schlader, 2014).…”

Section: Introductionmentioning

confidence: 99%

Activation of autonomic thermoeffectors preceding the decision to behaviourally thermoregulate in resting humans

Schlader

Coleman

Sackett

et al. 2016

Experimental Physiology

View full text Add to dashboard Cite

New Findings r What is the central question of this study?Do increases in metabolic heat production and sweat rate precede the initiation of thermoregulatory behaviour in resting humans exposed to cool and warm environments? r What is the main finding and its importance?Thermoregulatory behaviour at rest in cool and warm environments is preceded by changes in vasomotor tone in glabrous and non-glabrous skin, but not by acute increases in metabolic heat production or sweat rate. These findings suggest that sweating and shivering are not obligatory for thermal behaviour to be initiated in humans.We tested the hypothesis that acute increases in metabolic heat production and sweating precede the initiation of thermoregulatory behaviour in resting humans exposed to cool and warm environments. Twelve healthy young subjects passively moved between 17 and 40°C rooms when they felt 'too cool' (C→W) or 'too warm' (W→C). Skin and internal (intestinal) temperatures, metabolic heat production, local sweat rate (forearm and chest) and cutaneous vascular conductance (CVC; forearm and fingertip) were measured continually. Compared with pretest baseline (31.8 ± 0.3°C), skin temperature was higher at C→W (32.0 ± 0.7°C; P = 0.01) and W→C (34.5 ± 0.5°C; P < 0.01). Internal temperature did not differ (P = 0.12) between baseline (37.2 ± 0.3°C), C→W (37.2 ± 0.3°C) and W→C (37.0 ± 0.3°C). Metabolic heat production was not different from baseline (40 ± 9 W m −2 ) at C→W (39 ± 7 W m −2 ; P = 0.50). Forearm (0.06 ± 0.01 mg cm −2 min −1 ) and chest (0.04 ± 0.02 mg cm −2 min −1 ) sweat rate at W→C did not differ from baseline (forearm, 0.05 ± 0.02 mg cm −2 min −1 and chest, 0.04 ± 0.02 mg cm −2 min −1 ; P ࣙ 0.23). Forearm CVC was not different from baseline (0.30 ± 0.21 perfusion units (PU) mmHg −1 ) at C→W (0.24 ± 0.11 PU mmHg −1 ; P = 0.17), but was higher at W→C (0.65 ± 0.33 PU mmHg −1 ; P < 0.01). Fingertip CVC was different from baseline (2.6 ± 2.0 PU mmHg −1 ) at C→W (0.70 ± 0.42 PU mmHg −1 ; P < 0.01) and W→C (4.49 ± 1.66 PU mmHg −1 ; P < 0.01). Thermoregulatory behaviour at rest in cool and warm environments is preceded by changes in vasomotor tone in glabrous and non-glabrous skin, but not by acute increases in metabolic heat production or sweat rate.

show abstract

“…Changes of Heart Rate in the Still Stirred Unclothed Immersions.-A rise of heart rate in warm, or a fall in cool, surroundings has often been observed [Barcroft and Verzar, 1931;Swift, 1932;Barcroft and Marshall, 1923-24;Bazett, Scott, Maxfield and Blithe, 1937;Cooper and Kerslake, 1955]; the last authors considered that the rapid increase in heart rate after exposure of men to radiant heat indicated that the change was a direct reflex response from the skin and not a result of vasodilatation, but the continuing rise in rate during the present 37 80 C. immersions makes it likely that vasodilatation and perhaps an increase in the temperature of the heart played a part in this case. The men's immediate fall in heart rate in water at 250 C. must have been brought about either by a direct reflex from the skin or indirectly by vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

The Respiratory and Cardiovascular Response to Immersion in Cold and Warm Water

Keatinge

Evans

1961

Exp Physiol

View full text Add to dashboard Cite

During their first few minutes of immersion in stirred water at 5 and 150 C. the pulmonary ventilation of twelve unclothed men was high, and their end-tidal PCO2 fell. The pCO2 then returned to or a little above its original level but did not greatly exceed it even in working experiments lasting 20 min. in water at 50 C. or 40 min. in water at 150 C. Although work reduced or reversed the initial fall in pCO2, these results therefore do not bear out predictions that the pCO2 would rise to dangerous levels during hard work in cold water, at least in immersions of moderate duration.In water at 37.80 C. the men's heart rates rose steadily, in water at 250 C. they fell and remained low, and in water at 5 and 150 C. they rose and then fell. Repeated immersion at 150 C. reduced or abolished the early respiratory and heart rate responses to immersion and the metabolic response, but did not significantly increase the falls in rectal temperature. Clothing also reduced the reflex responses to immersion. A number of ventricular extrasystoles were observed during the first 2 min. of immersion in water at 150 C., and it is suggested that ventricular fibrillation due to increased venous and arterial pressures, adrenaline, and hyperventilation, may be responsible for some cases of sudden death in cold water. THIS paper describes observations on the end-tidal pCO2, pulmonary ventilation, heart rate, and electrocardiographs of twelve men during immersion in water at temperatures between 5 and 37.80 C. Cotes [1954 and 1955] has reported that the pulmonary ventilation of a man could be predicted from his alveolar pCO2 and deep body temperature, and anticipated that CO2 would accumulate in the body to reach dangerous concentrations during hard work in cold water.Sudden death in cold water without drowning is generally [Simpson, 1958] attributed to vagal arrest of the heart following inhalation of cold water into the naso-pharynx and glottis. However, it has seemed possible that ventricular fibrillation might be responsible for some of these cases; an increase in venous pressure may follow sudden exposure to cold [Bondurant, Hickam and Isley, 1957; Keatinge and McCance, 1957] and a rise in filling pressure may precipitate ventricular fibrillation in isolated hearts [Keatinge, 1959], while adrenaline is known sometimes to cause ventricular fibrillation after chloroform [Levy, 1914] and to facilitate it without chloroform in isolated hearts [Goodford, 1958].The effect of adaptation by repeated immersion in cold water has also been assessed, since the heart rate and blood pressure responses to the immersion of a hand in ice water [Glaser and Whittow, 1957] are reduced by repetition. The design of the experiments and the subjects have been described in the preceding paper.*

show abstract

The effect of exposure to cold on the pulse rate and respiration of man

Cited by 20 publications

References 2 publications

The Thermosensitivity of the Hypothalamus and Thermoregulation in Mammals

The Thermosensitivity of the Hypothalamus and Thermoregulation in Mammals

Activation of autonomic thermoeffectors preceding the decision to behaviourally thermoregulate in resting humans

The Respiratory and Cardiovascular Response to Immersion in Cold and Warm Water

Contact Info

Product

Resources

About