Hypoglycaemia, Hypothermia and Shivering in Man

1981 ◽  
Vol 61 (4) ◽  
pp. 463-469 ◽  
Author(s):  
E. A. M. Gale ◽  
T. Bennett ◽  
J. Hilary Green ◽  
I. A. MacDonald

1. The present experiments were designed to elucidate the reasons for the fall in central body temperature during hypoglycaemia. 2. The first experiment was carried out at a room temperature of 25 °C on 11 male subjects. Hypoglycaemia was induced by infusion of insulin. Heat production (calculated from respiratory gas exchange) rose from a baseline of 5.10 ± 0.13 kJ/min (mean ± sem) to a peak of 6.25 ± 0.21 kJ/min (P < 0.001), but core temperature fell concurrently by 0.51 ± 0.08°C and skin temperature fell by 1.1 ± 0.2°C. The net heat loss was due to peripheral vasodilatation and sweating. 3. To determine the effect of insulin-induced hypoglycaemia on thermoregulation in a cool environment, the experiment was repeated at a room temperature of 18–19°C on five of the subjects who had air blown over them until shivering was sustained. During this time heat production rose to 10.13 ± 1.67 kJ/min, but core temperature remained constant. Shivering stopped as plasma glucose fell below 2.5 mmol/l during insulin infusion and the subjects said they no longer felt cold. 4. During hypoglycaemia in the cold peripheral vasodilatation and sweating occurred, skin temperature fell by up to 0.8°C and core temperature fell below 35°C, so subjects had to be rewarmed. 5. Recovery of plasma glucose after hypoglycaemia in the cold was impaired at low body temperatures, but shivering was restored within seconds when glucose was given intravenously.

1982 ◽  
Vol 63 (3) ◽  
pp. 301-310 ◽  
Author(s):  
I. A. Macdonald ◽  
T. Bennett ◽  
E. A. M. Gale ◽  
J. Hilary Green ◽  
S. Walford

1. The effects of metoprolol and propranolol on heat production and body temperature have been studied in six male subjects during insulin-induced hypoglycaemia in a thermoneutral environment. Hypoglycaemia was induced by insulin infusion on three occasions in each subject, accompanied by the infusion of sodium chloride solution (154 mmol/l) (control), metoprolol (β1-selective antagonist) or propranolol (non-selective antagonist). 2. During the period of hypoglycaemia in the control experiments mean heat production (calculated from respiratory gas exchange) increased by 1·07 ± sem 0·13 kJ/min and remained elevated for 30−40 min. This heat production response was reduced by metoprolol and abolished by propranolol. During the recovery period, heat production was significantly reduced in the presence of propranolol. 3. Skin and core temperatures fell during the period of hypoglycaemia in all three experiments. The fall in skin temperature was significantly greater in the presence of propranolol (−2·51 ± 0·47°C). The reductions in core temperature recorded during the three experiments were similar (control −0·73 ± 0·17, metoprolol −0·99 ± 0·21, propranolol −0·88 ± 0·22°C), but core temperature was still falling at the end of the propranolol experiment. 4. The cardiovascular responses to hypoglycaemia were similar in the control and metoprolol experiments but were substantially modified by propranolol. During the period of hypoglycaemia in the control experiments, plasma adrenaline levels rose to 7·78 ± 1·79 nmol/l; significantly higher levels were measured in the metoprolol (10·11 ± 1·64) and propranolol (22·76 ± 7·02) experiments. The very high adrenaline levels may have been responsible for the modified cardiovascular responses to hypoglycaemia observed in the propranolol experiment.


1961 ◽  
Vol 200 (3) ◽  
pp. 572-580 ◽  
Author(s):  
M. M. Fusco ◽  
J. D. Hardy ◽  
H. T. Hammel

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.


1987 ◽  
Vol 65 (6) ◽  
pp. 1339-1346 ◽  
Author(s):  
Ulrike Roos ◽  
Claus Jessen

Experiments in conscious goats were done to see whether heat production and respiratory evaporative heat loss show dynamic responses to changing core temperature at constant skin temperature. Core temperature was altered by external heat exchangers acting on blood temperature, while skin temperature was maintained constant by immersing the animals up to the neck in a rapidly circulating water bath. Core temperature was altered at various rates up to 0.9 °C/min. Step deviations of core temperature from control values were always followed by a positive time derivative of effector response, but never by a negative time derivative during sustained displacement of core temperature. Ramp experiments showed that the slopes at which heat production or heat loss rose with core temperature deviating from its control level grew smaller at higher rates of change of core temperature. It is concluded that neither heat production nor respiratory evaporative heat loss respond to the rate of change of core temperature. At constant skin temperature, thermoregulatory effector responses appear to be proportional to the degree to which core temperature deviates from its set level.


1960 ◽  
Vol 198 (3) ◽  
pp. 471-475 ◽  
Author(s):  
T. R. A. Davis ◽  
D. R. Johnston ◽  
F. C. Bell ◽  
B. J. Cremer

When cold acclimating rats are treated with diathermy, curare and a combination of both, two main fractions of the increase in cold-induced oxygen consumption can be delineated. First, a fraction which diathermy replaces by virtue of the fact that it, in the intensities used, can raise core temperature without altering the temperature of the skin; therefore this fraction appears to be dependent upon changes in central temperature and is found to persist throughout the period of acclimation investigated. Second, a fraction of cold-induced oxygen consumption which is not replaced by diathermy and which is presumed to be dependent upon changes in skin temperature. By the administration of curare, this second fraction can be separated into two further fractions acting reciprocally depending upon the duration of cold exposure. In the early stages of acclimation, the curare-suppressed fraction of oxygen consumption appears to be entirely due to shivering. As shivering disappears with acclimation, it is replaced by a peripherally regulated nonshivering heat source which eventually takes over all the duties of heat production previously performed by shivering.


2001 ◽  
Author(s):  
K. B. Emerton ◽  
W. H. Cooke ◽  
D. A. Nelson

Abstract Some symptoms of Multiple Sclerosis (MS) are mitigated by lowering the patient’s core temperature. Personal cooling garments, similar to those developed for cooling crewmembers in military aircraft, have been developed and marketed for the treatment of MS symptoms. This study investigated the effectiveness of a water-cooled vest in reducing the skin surface and core (rectal) temperatures in healthy male subjects. Results show no effect on core temperature, and modest increases in skin temperature over a 30-min session. It is not known whether similar results would obtain with healthy female subjects, or with MS subjects of either gender.


1980 ◽  
Vol 239 (3) ◽  
pp. R265-R269 ◽  
Author(s):  
T. Shiraishi ◽  
M. Mager

From our previous studies with 2-deoxy-D-glucose (2-DG) an inhibitor of glucose utilization, we postulated that the resultant intracellular glucopenia affects central neuronal pathways involved in the control of peripheral heat production. In this investigation, we have delineated these thermoregulatory sites by stereotaxically injecting microquantities of 2-DG into the hypothalamus of the rat and monitoring core temperature (Tre). After stabilization of Tre at a room temperature of 23 +/- 1 degree C, 20 microgram of 2-DG in 2 microliter was injected into 350- to 400-g rats. Significant decreases in Tre were noted after injections into the anterior hypothalamic, ventromedial, and dorsomedial nuclei as well as the lateral and posterior hypothalamic areas. Mean nadir Tre decreased 1.5 degrees C 1 h after, was significantly depressed 3.5 h after, and returned to basal values 4 h after administration of 2-DG into the ventral premammillary nucleus (PMV). Dose-dependent response was observed for injections into the PMV only. Of a total of 21 sites studied in the anterior and posterior hypothalamus, the PMV, an area of unknown physiological function, was the most sensitive to glucose deprivation.


2014 ◽  
Vol 54 (10) ◽  
pp. 1877 ◽  
Author(s):  
K. DiGiacomo ◽  
L. C. Marett ◽  
W. J. Wales ◽  
B. J. Hayes ◽  
F. R. Dunshea ◽  
...  

It is suggested that one-third of the inter-animal differences in efficiency is explained by differences in digestion, heat production, body composition and activity; while the remaining variation is the result of energy expenditure due to biological processes such as ion pumps and mitochondrial function. Inefficient animals may be wasting energy on inefficient processes resulting in increased heat production that may be reflected by differences in skin and core temperature. While the association between heat production and residual feed intake (RFI) has been touched on, it is yet to be fully elucidated. It is hypothesised that more efficient animals will expend less energy as heat, which will be reflected by differences in core and skin temperature measures. Fifty-four primiparous, Holstein-Friesian cows previously assessed for RFI (26 inefficient/high RFI, 28 efficient/low RFI) were selected and drafted into outdoor holding yards for measurements on two occasions (once during lactation and once during the non-lactating ‘dry’ period). Measures of body temperature were obtained using an infrared (IR) camera to obtain skin (surface) temperatures at multiple locations [muzzle, eye, jaw, ear, leg (front and back), rump, shoulder, teat, udder, side and tail] and rectal temperatures were measured using a digital thermometer. Respiration rates (RR) were obtained by counting the number of flank movements in 1 min. A subset of 16 cows (8 efficient and 8 inefficient) were utilised for further IR imagery in an undercover environment (to eliminate the influences of external environments). Skin temperature measurement obtained using an IR camera during the outdoor period demonstrated that inefficient cows had higher (0.65°C) teat temperatures (P = 0.05). Rectal temperature and RR were not influenced by efficiency group. When IR images were obtained undercover inefficient cows tended to have higher shoulder (0.85°C) and neck (0.98°C) temperatures than efficient cows (P < 0.087); while udder temperature was significantly greater (1.61°C) for inefficient than efficient cows (P = 0.018). These data indicate that some of the differences in efficiency may be attributed to differences in thermoregulation, as reflected by differences in skin (but not core) temperature and that IR imagery is a suitable method for determining these differences in a non-invasive manner. Further research is required to further establish these relationships, and the measurement of skin temperatures should be undertaken indoors to eliminate external environmental influences.


1978 ◽  
Vol 56 (6) ◽  
pp. 993-998 ◽  
Author(s):  
Stefan A. Carter

To test whether man can increase voluntarily skin temperature in a cool environment, 14 subjects (age 15–51) were studied. They came once or twice a week for five to eight sessions of 1 h. The room temperature of various sessions varied from 21.2 to 15.6 °C. Temperatures of six fingers were recorded using thermocouples. During trials to increase temperature, subjects were shown a dial indicating temperature of an index linger and were instructed to try to warm their hands. The trials were begun when skin temperatures were stable or were falling, indicating that vasoconstriction was occurring. They were preceded and followed by a rest period. The differences between changes in temperature during the trials and the rest periods were significant for the group of 14 subjects (p < 0.01). In 10 subjects with individually significant results, differences between the trial and rest periods averaged 5.0 °C for 'the best' and 3.9 °C for 'the worst' finger. The maximum temperatures during the trials averaged 30.9 ± 1.0 °C(mean ± SE) in 'the best' finger. During later sessions, subjects were able to increase temperatures without seeing the dial. The results indicate that humans are able to increase voluntarily cutaneous finger blood How in a cool environment.


1966 ◽  
Vol 44 (1) ◽  
pp. 139-146 ◽  
Author(s):  
G. E. Thompson ◽  
J. A. F. Stevenson

Colonic and tail-skin temperatures of cold-acclimatized (4 °C for 4 weeks) and unacclimatized (4 °C for 1 day) rats were measured while they were being exercised on a treadmill (4.6 m/minute) in the cold (4 °C). In unacclimatized animals the colonic temperature increased to the same level as when they were previously exercised at 24 °C, but the changes in tail-skin temperature indicated only a small vasodilatation. In cold-acclimatized animals the colonic temperature increased to a significantly higher level than in unacclimatized animals before peripheral vasodilatation appeared, and this higher colonic temperature was maintained as exercise continued. In addition, the cold-acclimatized animals showed a higher tail-skin temperature during rest and a greater vasodilatation during exercise than the unacclimatized controls. Rats treated for 6 days at room temperature (24 °C) with a mixture of thyroxine (25 μg/100 g body weight per day) and cortisone (1 mg per rat per day) were exercised at 4 °C after being exposed to this temperature for only 1 day. The colonic temperature was controlled at a higher level in these animals than in saline-injected controls but peripheral vasodilatation was not greater.


1996 ◽  
Vol 81 (3) ◽  
pp. 1128-1137 ◽  
Author(s):  
R. L. Thompson ◽  
J. S. Hayward

Simulated conditions of hiking in rain, wind, and cold, without protective rainwear, were used to investigate wet-cold hypothermia in 18 male subjects. Thermal, metabolic, and motor responses were monitored during an attempted 5-h walk (5.1 km/h) at 5 degrees C, with continuous exposure to rain (7.4 cm/h) and wind (8.0 km/h) over the final 4 h. The majority of subjects (11) could not complete the protocol because of intolerance of wet-cold conditions during the last 2 h. Therefore, data from 5 subjects who completed the protocol in rain and control conditions were used to describe the general pattern of response. During the 1st h of walking, core temperature rose 1 degree C to 38.1 degrees C. The subsequent 2 h of rain caused substantial cold stress, indicated by a 40% increase in heat production due to shivering and significant loss of strength and manual dexterity. However, core temperature only decreased to 37.1 degrees C, merely eliminating the initial exercise hyperthermia. Over the last 2 h of rain, core temperature remained relatively stable at 36.8 degrees C, decreasing slightly to 36.4 degrees C by 5 h. Two other subjects developed significant hypothermia (35 degrees C). One demonstrated fatigue of shivering after 2.5 h of rain, confirming the exhaustion hypothesis of wet-cold hypothermia. The older cooled rapidly when he failed to maintain the walking pace. We conclude that if a person can tolerate the intense discomfort of prolonged wet-cold exposure, he or she has the potential to resist significant core hypothermia for at least 4 h of walking under the conditions of this experiment. Exceptions to this generalization occur, making exposure of < 4 h a hypothermia risk for some individuals. Exposures > 4 h would involve increasing probability of rapid decline into hypothermia, associated with exhaustion of shivering and exercise heat production.


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