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PubMed1998

Metabolic and endocrine responses to cold air in women differing in aerobic capacity.

PURPOSE: The purpose of this study was to measure resting metabolic rate, plasma norepinephrine, and plasma immunoreactive beta endorphin during exposures to cold air during two consecutive 5-d periods, separated by 2 weekend days, in two groups of women differing in aerobic fitness. METHODS: Plasma norepinephrine (NE), plasma immunoreactive beta-endorphin (IBE), and resting metabolic response (RMR) were measured during repeated exposures to 3.5 degrees C air in two groups of women differing in aerobic fitness. Ten women, separated into highly fit (HFW) and less fit (LFW) groups, sat in 22 degrees C air for 45 min followed by 45 min in 3.5 degrees C air each day during two consecutive 5-d periods separated by two weekend days. RESULTS: Norepinephrine was not different between groups during warm air exposure; however, following 45 min of cold air, NE was two times higher in HFW compared with that in LFW (P < 0.001). Plasma IBE was elevated (P < 0.02) in HFW compared with that in LFW but was not affected by exposure to cold on any test day. Warm RMR was not different between groups and remained unchanged during the study period. Cold RMR was significantly higher in LFW compared with that in HFW (P < 0.01). Resting metabolic rate peaked at 30% of VO2peak in LFW by the 5th minute of cold exposure on day 1 before declining to 21% and remaining steady. In contrast, RMR in HFW peaked at about 13% and then fell to 9.4% before slowly increasing to 14% by the end of 45 min. On other test days HFW RMR increased to 14% of VO2peak and rose slowly through 45 min of cold exposure while LFW RMR peaked at 24% of VO2peak before declining to 20% and remaining steady. CONCLUSIONS: Our findings suggest that, in women, aerobic fitness alters the endocrine and metabolic responses to acute cold air exposure. The norepinephrine response is exaggerated in highly fit women exposed to cold but not the metabolic response. Immunoreactive beta endorphin was not affected by exposure to cold but was elevated in highly fit women. We further conclude that the temperature threshold for acclimation to cold air by women may be higher than the air temperature used in this study.

Acclimatization↗
PubMed2006

Visual evoked potentials of the blue-sensitive pathway under cold provocation in normals and glaucomas.

BACKGROUND: Vascular dysregulation in open-angle glaucomas can be identified by measuring the blood circulation during exposure to cold water. Aim of this study was to find out whether the same cold stimulus would lead to functional changes in the visual evoked potentials (VEP) of the short-sensitive pathway in normals and glaucoma patients. PATIENTS AND METHODS: Blue-on-yellow pattern-visual evoked potentials were studied in 22 healthy control persons and 47 patients with primary open-angle glaucoma (25 high-pressure glaucomas, 22 normal pressure glaucomas with clinical signs of vasospastic hyperreactivity). A blue stripe pattern, presented in onset-offset mode on a yellow adaptation light served as the stimulus. Cold provocation was initiated by dipping one hand of the patient into cold water of 3 degrees C to 5 degrees C. The onset amplitudes and peak times were measured without cold exposition as well as two and four minutes after the cold exposition began. RESULTS: In the group of vasospastic glaucoma patients a significant reduction of visual evoked potential-amplitudes was observed during cold provocation (amplitude before ice exposition: 4.17 microV, amplitude following two minutes of ice exposition: 3.52 microV; paired test: P < 0.01). Other subject groups showed no significant amplitude reductions after cold provocation. Peak times of both open-angle glaucoma groups (132.3 +/- 18.7 milliseconds in high pressure, 132.7 +/- 14.5 milliseconds in normal pressure) were significantly increased in comparison to normals (117.4 +/- 8.0 milliseconds). However, no significant influence of the cold provocation on peak times could be found in all groups. CONCLUSION: Peak times of the blue-on-yellow visual evoked potentials are significantly prolonged in patients with primary open-angle glaucomas. Cold provocation causes a significant amplitude reduction of the blue-on-yellow visual evoked potential in the present normal-pressure glaucoma patients and reflects vascular dysregulation in patients with vasospastic hyperreactivity.

Blood Pressure↗
PubMed2005

Chronic intermittent cold stress sensitises the hypothalamic-pituitary-adrenal response to a novel acute stress by enhancing noradrenergic influence in the rat paraventricular nucleus.

Chronic intermittent cold stress sensitises activation of the hypothalamic-pituitary-adrenal (HPA) axis by novel acute stress. We have shown that enhanced noradrenergic function in limbic forebrain contributes to HPA sensitisation. In the present study, we investigated whether chronic intermittent cold also induced changes in noradrenergic function in the paraventricular nucleus (PVN), the primary mediator of the HPA stress response. Rats were exposed to chronic intermittent cold (7 days, 6 h per day, 4 degrees C). On the day after final cold exposure, there were no differences in baseline plasma ACTH, but the peak ACTH response to 30 min of acute immobilisation stress was greater in cold-stressed rats compared to controls. Bilateral microinjection of the alpha(1)-adrenergic receptor antagonist benoxathian into the PVN reduced acute stress-induced adrenocorticotrophic hormone (ACTH) levels by approximately 25% in controls. Furthermore, in cold-stressed rats, all of the sensitisation of the ACTH response was blocked by benoxathian, to a level comparable to benoxathian-treated controls. In a second study using microdialysis to measure norepinephrine release in the PVN, there were no differences in either baseline or acute stress-induced increases in norepinephrine release in the PVN of cold-stressed rats compared to controls. Thus, in a third study, we tested potential alterations in postsynaptic alpha(1)-receptor sensitivity after chronic cold stress. Dose-dependent activation of ACTH secretion by microinjection of the alpha(1)-adrenergic receptor agonist, phenylephrine, into the PVN was significantly enhanced in cold-stressed rats compared to controls. Thus, the sensitised HPA response to acute stress after chronic intermittent cold exposure is at least partly attributable to an enhanced response to alpha1-adrenergic receptor activation in the PVN. Chronic stress-induced plasticity in the acute stress response may be important for stress adaptation, but may also contribute to pathophysiological conditions associated with stress. Thus, understanding the neural mechanisms underlying such adaptations may help us understand the aetiology of such disorders, and contribute to the future development of more effective treatment or prevention strategies.

Adrenergic alpha-Agonists↗
PubMed2005

Occurrence of cold activation of transfusion plasma during storage at +4 degrees C.

BACKGROUND AND OBJECTIVES: The storage of transfusion plasma at +4 degrees C sometimes leads to the activation of several proteolytic systems. In this study the frequency of cold activation was investigated, as well as whether cold activation of plasma is an individually recurrent property of the donor. MATERIALS AND METHODS: Plasma units prepared from whole blood obtained from 100 male donors were stored at +2 degrees to +5 degrees C, in bags for 28 days and in cryotubes for up to 42 days. Samples from plasma units, collected by apheresis from 100 male donors, were stored in cryotubes for up to 42 days. Cold activation was measured weekly as kallikrein-like activity of plasma. Samples from repeat apheresis plasma units from 32 donors were measured 12-20 months later. The effects of storage on the contact, coagulation and fibrinolytic systems were determined. RESULTS: The cumulative frequency of cold-activated plasma units stored in bags was 5% on day 7 and 18% on day 28. After 42 days in cryotubes, 49% of the plasma units were cold activated. Large intraindividual differences in the onset-day of cold activation were observed in plasma samples of some donors. During cold activation, an increase in kallikrein-like activity was accompanied by a decrease in C1 esterase inhibitor activity and an increase in the concentrations of activated factor VII and fibrinopeptide A. The functional plasminogen level was unchanged, while a minor decrease in plasmin inhibitor activity was combined with a corresponding increase in the concentration of plasmin-plasmin inhibitor complex. CONCLUSIONS: The cumulative frequency of cold-activated plasma units increased in a time-dependent manner during storage at +2 degrees to +5 degrees C for 42 days. The intraindividual onset-day of cold activation varied widely between plasma samples of some donors. Cold activation was associated with a high degree of activation of the contact and coagulation systems. The fibrinolytic system was scarcely affected.

Blood Coagulation Factors↗
PubMed1990

Effects of cold exposure on rat adrenal tyrosine hydroxylase: an analysis of RNA, protein, enzyme activity, and cofactor levels.

Long-term cold exposure (5-7 days) is known to induce concomitant increases in the levels of adrenomedullary tyrosine hydroxylase (TH) RNA, protein, and enzyme activity. In this report, we compare the time courses of these changes and investigate the effects of cold exposure on the levels of biopterin, the cofactor required for tyrosine hydroxylation. After only 1 h of cold exposure, TH mRNA abundance increased 71% compared with nonstressed controls. Increases in total cellular TH RNA levels were maximal (threefold over control values) within 3-6 h of cold exposure and remained elevated throughout the duration of the experiment (72 h). TH protein levels increased rapidly after 24 h of cold exposure and reached a maximal value threefold above that of controls at 48-72 h. Despite the relatively rapid and large elevations in TH RNA and protein content, only modest increases in TH activity were detected during the initial 48 h of cold exposure. Adrenomedullary biopterin increased rapidly after the onset of cold exposure, rising to a level approximately twofold that of the nonstressed controls at 24 h, and remained at this level throughout the duration of the stress period. Taken together, the results of this time course study indicate that cold-induced alterations in adrenal TH activity are mediated by multiple cellular control mechanisms, which may include pre- and posttranslational regulation. Our findings also suggest that cold stress-induced increases in the levels of the TH cofactor may represent another key event in the sympathoadrenal system's response to cold stress.

Adrenal Glands↗
PubMed1977

Effect of cold exposure on mammary circulation oxygen consumption and milk secretion in the goat.

1. Measurements of milk secretion, mammary oxygen consumption and blood flow, cardiac output and blood pressure have been made in lactating goats exposed to a thermoneutral environment and to two levels of cold stress which were sufficient to raise total body oxygen consumption by an average of 18 and 46% above that in a thermoneutral environment. 2. Mammary blood flow and oxygen consumption were not appreciably affected by the milder cold stress but fell to 63 and 70%, respectively, of their thermoneutral value in the moderately cold environment. Resistance to blood flow through the udder was increased by this level of cold stress and the gland took a smaller fraction of an increased cardiac output. 3. Both levels of cold exposure caused a reduction in milk secretion, to 80 and 40% of its thermoneutral value in the mild and moderate cold respectively. The amount of milk secreted per unit volume of blood flowing through the gland decreased as the severity of the cold stress increased. 4. Voluntary food intake was not affected by the change in environmental temperature but the intake of water was reduced to 55% of the thermoneutral value during mild cold exposure and to 40% of the thermoneutral value during the moderate cold stress. 5. It is concluded that a reduction in blood flow to the mammary gland could be one of several possible mechanisms underlying the depression of milk secretion during cold exposure.

Animals↗
PubMed1995

Hsc66, an Hsp70 homolog in Escherichia coli, is induced by cold shock but not by heat shock.

Hsc66 is the second identified Hsp70 protein in Escherichia coli. Mutations in hscA, the gene encoding Hsc66, compensate for some phenotypic effects of a mutation in hns, a gene encoding the cold-inducible, nucleoid-associated protein H-NS. Expression of hscA was not induced upon heat shock but was induced approximately 11-fold 3 h after a shift from 37 to 10 degrees C. Furthermore, hscA was induced upon chloramphenicol addition, which induces the synthesis of other cold-inducible genes. Mapping of the transcription initiation site showed that hscA was cotranscribed with an upstream dnaJ-like gene, hscB; thus, hscB was also cold inducible. The hscBA promoter did not contain a Y-box element found in some cold-inducible promoters. Using two-dimensional electrophoresis, we identified Hsc66 under static 37 degrees C growth conditions and showed that Hsc66 was induced, as well as hscA, 3 h after a cold shock. Growth of an hscA mutant following cold shock was monitored relative to that of an isogenic wild-type strain. While cold shock adaptation as a function of growth rate was not significantly impaired in an hscA mutant, the expression of at least five other proteins was altered in this mutant following cold shock. On the basis of the homology to Hsp70 proteins and the induction following cold shock, we speculate that Hsc66 functions as a cold shock molecular chaperone.

Bacterial Proteins↗
PubMed1998

Role of the cold-box region in the 5' untranslated region of the cspA mRNA in its transient expression at low temperature in Escherichia coli.

Upon temperature downshift, a group of proteins called cold shock proteins, such as CspA, CspB, and CsdA, are transiently induced in Escherichia coli. However, when the 5' untranslated region (5' UTR) of cspA mRNA is overproduced at low temperature, the expression of cold shock genes is prolonged or derepressed. It has been proposed that this effect is due to highly conserved 11-base sequences designated the "cold box" existing in the 5' UTRs of cspA, cspB, and csdA. Here, we demonstrate that the overproduction of the 5' UTR of not only cspA but also cspB and csdA mRNAs causes derepression of all three genes at the same time. Conversely, when the cold-box region was deleted from the cspA 5' UTR its derepression function was abolished. The amount of mRNA from the chromosomal cspA gene was much higher in cells overproducing the wild-type 5' UTR by means of a plasmid than it was in cells overproducing the cold-box-deleted 5' UTR. The stability of the chromosomal cspA mRNA in cells overproducing the wild-type 5' UTR was almost identical to that in cells overproducing the cold-box-deleted 5' UTR. Therefore, the derepression of cspA caused by overproduction of 5' UTR at the end of the acclimation phase occurs at the level of transcription but not by mRNA stabilization, indicating that the cold-box region plays a negative role in cspA transcription in cold shock-adapted cells. The role of the cold-box region was further confirmed with a cspA mutant strain containing a cold-box-deleted cspA gene integrated into the chromosome, which showed a high level of constitutive production of CspA but not CspB during exponential growth at low temperature.

Bacterial Proteins↗
PubMed2002

Genomewide transcriptional analysis of the cold shock response in Bacillus subtilis.

Previous studies with two-dimensional gel electrophoresis techniques revealed that the cold shock response in Bacillus subtilis is characterized by rapid induction and accumulation of two classes of specific proteins, which have been termed cold-induced proteins (CIPs) and cold acclimatization proteins (CAPs), respectively. Only recently, the B. subtilis two-component system encoded by the desKR operon has been demonstrated to be essential for the cold-induced expression of the lipid-modifying desaturase Des, which is required for efficient cold adaptation of the membrane in the absence of isoleucine. At present, one of the most intriguing questions in this research field is whether DesKR plays a global role in cold signal perception and transduction in B. subtilis. In this report, we present the first genomewide transcriptional analysis of a cold-exposed bacterium and demonstrate that the B. subtilis two-component system DesKR exclusively controls the desaturase gene des and is not the cold-triggered regulatory system of global relevance. In addition to this, we identified a set of genes that might participate as novel players in the cold shock adaptation of B. subtilis. Two cold-induced genes, the elongation factor homolog ylaG and the sigma(L)-dependent transcriptional activator homolog yplP, have been examined by construction and analysis of deletion mutants.

Bacillus subtilis↗
PubMed1997

Early increases in ischaemic heart disease mortality dissociated from and later changes associated with respiratory mortality after cold weather in south east England.

STUDY OBJECTIVE: To identify the time courses and magnitude of ischaemic heart (IHD), respiratory (RES), and all cause mortality associated with common 20-30 day patterns of cold weather in order to assess links between cold exposure and mortality. DESIGN: Daily temperatures and daily mortality on successive days before and after a reference day were regressed on the temperature of the reference day using high pass filtered data in which changes with a cycle length < 80 days were unaffected (< 2%), but slower cyclical changes and trends were partly or completely suppressed. This provided the short term patterns of both temperature and mortality associated with a one day displacement of temperature. The results were compared with simple regressions of unfiltered mortality on temperature at successive delays. STUDY POPULATION AND SETTING: Population of south east England, including London, over 50 years of age from 1976-92. MAIN RESULTS: Colder than average days in the linear range 15 to 0 degrees C were associated with a "run up" of cold weather for 10-15 days beforehand and a "run down" for 10-15 days afterwards. The increases in deaths were maximal at 3 days after the peak in cold for IHD, at 12 days for RES, and at 3 days for all cause mortality. The increase lasted approximately 40 days after the peak in cold. RES deaths were significantly delayed compared with IHD deaths. Excess deaths per million associated with these short term temperature displacements were 7.3 for IHD, 5.8 for RES, and 24.7 for all cause, per one day fall of 1 degree C. These were greater by 52% for IHD, 17% for RES, and 37% for all cause mortality than the overall increases in daily mortality per degree C fall, at optimal delays, indicated by regressions using unfiltered data. Similar analyses of data at 0 to -6.7 degrees C showed an immediate rise in IHD mortality after cold, followed by a fall in both IHD and RES mortality rates which peaked 17 and 20 days respectively after a peak in cold. CONCLUSION: Twenty to 30 day patterns of cold weather below 15 degrees C were followed:(1) rapidly by IHD deaths, consistent with known thrombogenic and reflex consequences of personal cold exposure; and (2) by delayed increases in RES and associated IHD deaths in the range 0 to 15 degrees C, which were reversed for a few degrees below 0 degree C, and were probably multifactorial in cause. These patterns provide evidence that personal exposure to cold has a large role in the excess mortality of winter.

Aged↗
PubMed1990

Increased nonshivering thermogenesis, brown fat cytochrome-c oxidase activity, GDP binding, and uncoupling protein mRNA levels after short daily cold exposure of Phodopus sungorus.

In their natural environment, burrowing rodents experience rather fluctuating ambient temperatures and are acutely cold exposed only for short periods outside their burrows. The effect of short daily cold exposure on basal metabolic rate, nonshivering thermogenesis, brown fat thermogenesis, and uncoupling protein mRNA was studied in the Djungarian hamster, Phodopus sungorus. They were kept at 23 degrees C and exposed to 5 degrees C daily either for one 4-h period or twice for 2 h (in 12-h intervals). At the same time control hamsters were kept continuously either at thermoneutrality (23 degrees C) or at 5 degrees C. Two 2-h cold exposures daily were sufficient to increase basal metabolic rate and nonshivering thermogenesis to the same level as continuous cold exposure, whereas one 4-h cold period per day did not result in a significant increase of both parameters. Brown fat thermogenesis (as measured by cytochrome-c oxidase activity and GDP binding to the mitochondrial uncoupling protein) increased to the same extent by both treatments with short daily cold exposure. However, this increase was less than in the chronically cold-exposed hamsters. A similar result was found for uncoupling protein mRNA: both short-term cold-exposed hamsters increased uncoupling protein mRNA levels to a similar extent, but less than after chronic cold treatment. It is concluded that short daily cold exposures are sufficient to cause adaptive increases of the capacity of metabolic heat production as well as brown fat thermogenic properties.

Adipose Tissue↗
PubMed1990

Alterations in adipocyte response to lipolytic hormones during cold acclimation.

The effects of cold exposure (7 days, 5 degrees C) and cold acclimation (21 days, 5 degrees C) on the regulation of lipolysis were investigated in adipocytes isolated from epididymal fat pads of rats. Catecholamines stimulated lipolysis in an affinity sequence typical of the beta 1-adrenoceptor subtype: one-half maximum velocity (1/2 Vmax) isoproterenol (35 nM) much greater than 1/2 Vmax norepinephrine (150 nM) approximately 1/2 Vmax epinephrine (200 nM). Cold exposure markedly decreased the sensitivity (1/2 Vmax) and the responsiveness (Vmax) of the adipocytes to the lipolytic action of catecholamines. Addition of adenosine deaminase to fat cells isolated from cold-exposed rats did not normalize the lipolytic activity, suggesting that extracellular adenosine was not responsible for the obtunded lipolysis. This effect of cold exposure was transient as the lipolytic response to catecholamines was normal in fully cold-acclimated animals. Remarkably, the responsiveness of adipocytes to the lipolytic action of glucagon (200 nM) and adrenocorticotropic hormone (ACTH, 1 microM) progressively increased during cold acclimation. Adipocyte lipolytic response to dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) and theophylline was normal in cold-exposed rats, indicating that the lipolytic defect resides at an early step in the lipolytic cascade (pre-cAMP). On the other hand, the antilipolytic effect of insulin on norepinephrine-induced lipolysis significantly decreased during cold acclimation, particularly at physiological levels of insulin (nanomolar level). These results demonstrate that the transient decrease in the lipolytic action of catecholamines observed during cold acclimation is compensated by 1) an increased responsiveness of adipocytes to glucagon and ACTH and 2) by a decreased effectiveness of insulin to induce antilipolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1993

Role of angiotensin II in brown adipose thermogenesis during cold acclimation.

The role of angiotensin II (ANG II) in increased sympathetic neuroeffector mechanisms observed in cold-induced thermogenesis of brown adipose tissue (BAT) was examined. Cold exposure (4 degrees C) for 7 days resulted in an increase in interscapular fat (ISF) ANG II content expressed per gram wet weight or per lobe of ISF, without concomitant changes in plasma components of the renin-angiotensin system. Additionally, in ISF slices preloaded with [3H]norepinephrine (NE), ANG II (10 nM) resulted in an increase (3-fold) in evoked 3H overflow from ISF slices from cold-exposed rats compared with ambient temperature controls. However, although basal 3H outflow was increased (2-fold) in ISF slices from cold-exposed rats, evoked 3H overflow was not different between ISF slices from cold-exposed and control rats. Specific neuronal uptake of [3H]NE in ISF slices from cold-exposed rats was decreased by 64%. Administration of the non-peptide AT1-receptor antagonist losartan to cold-exposed rats resulted in complete inhibition of ANG II-mediated presynaptic facilitation of evoked 3H overflow from ISF slices. However, losartan administration had no effect on cold-induced increases in ANG II content, protein content, and decreases in neuronal [3H]NE uptake in ISF. Results from these studies suggest that cold-induced thermogenesis of BAT results in alterations in presynaptic ANG II facilitation of NE release and defects in removal of NE from the synaptic cleft (neuronal uptake), both of which would enhance sympathetic nervous system-mediated thermogenesis. Furthermore, these results demonstrate a role for ANG II in enhanced sympathetic activity of cold-induced thermogenesis in BAT.

Acclimatization↗
PubMed1986

Gastric motility is a major factor in cold restraint-induced lesion formation in rats.

These studies were performed to characterize the pattern of gastric contractility associated with cold restraint-induced lesion formation. Gastric motility in the rat was examined with extraluminal transducers at three sites of the stomach. The motility was monitored in the 24-h-fasted state, the postprandial state, and during cold-water immersion restraint. Gastric acid secretion was also monitored in a separate group of animals placed in cold restraint. Both feeding and cold restraint resulted in an equivalent increase in the amplitude of gastric contractions. Prolonged cold restraint, however, resulted in a distinct contractile pattern in which contractions were 56% less frequent and 300-400% longer in duration than those stimulated by feeding. All cold-restrained animals developed multiple gastric erosions. Cold restraint was not associated with increased acid secretion. A single subcutaneous injection of papaverine HCl (50 or 100 mg/kg) suppressed cold restraint-induced high-amplitude contractions and the cold restraint-induced lesion formation without altering acid secretion. These studies suggest that the stimulation of high-amplitude, prolonged duration contractions are more important than changes in gastric acid secretion in the formation of cold restraint-induced gastric lesions.

Animals↗
PubMed1989

Postprandial gastrointestinal blood flow and oxygen consumption during environmental cold stress.

We studied the independent and combined effects of feeding and environmental cold stress by measuring pre- and postprandial gastrointestinal blood flow (QGI), oxygen consumption (GIVO2), and oxygen extraction (GIO2ex) in seven awake 3- to 4-day-old piglets while in a thermoneutral environment (control phase, 31 degrees C) and during environmental cold stress (experimental phase, 20.5 degrees C). Each animal consecutively completed both the control and experimental phases. In the control phase, measurements were made before and 30 min after feeding. In the experimental phase, measurements were made before and 30 min after induction of cold stress. A feeding was then given and measurements repeated 30 min later during continued cold stress. QGI (ml.100 g-1.min-1) increased postprandially while in a thermoneutral environment (130 +/- 11 to 152 +/- 12) but not while in a cold environment (126 +/- 15 to 121 +/- 8). Postprandial GIVO2 (ml O2.100 g-1.min-1) increased from 2.1 +/- 0.2 to 3.7 +/- 0.5 while in a warm environment. During preprandial cold stress, an unexpected increase in GIVO2 was observed (1.7 +/- 0.2 to 3.1 +/- 0.5). Feeding while in a cold environment provoked a further significant increase in GIVO2 (3.1 +/- 0.5 to 4.2 +/- 0.4). All increases in GIVO2 were associated with increased GIO2ex. This study has demonstrated that 1) postprandial GIVO2 is appropriately increased during cold stress as a function of GIO2ex and 2) that fasting GIVO2 is increased during cold stress, demonstrating an intestinal metabolic contribution to cold-induced systemic thermogenesis.

Animals↗
PubMed1975

Autonomic nervous system and adaptation to cold in man.

The responses to cold hand test (blood pressure increase and tachycardia) and to a cold face test (blood pressure increase and bradycardia) were used to study the role of the autonomic nevrous system in cold adaptation in humans. The Eskimos (men, women, children) were shown to have a very weak sympathetic response to cold but the vagal response (bradycardia) was identical to that of white people. A group of mailmen from Quebec city living outdoors approximately 30 h/wk throughout the year was also studied. A significant decline in the cold pressor response and an enhanced bradycardia (cold face test) were observed at the end of the winter. Similarly the fall in skin temperature of the cheek was not as pronounced when the measurements were made in May compared to those made in October. A group of soldiers was also studied before and after an Arctic expedition. It was found that the bradycardia of the cold face test was also more pronounced after sojourning in the cold. These results indicate that repeated exposures to severe cold in men activate some adaptive mechanisms characterized by a diminution of the sympathetic response and a concomitant enhancement of the vagal activation normally observed when the extremities and the face are exposed to cold.

Adaptation, Physiological↗
PubMed1980

Effects of gravitational profiles on the rat's thermoregulatory response to cold.

Unrestrained rats were subjected to a 1-h period of cold exposure during centrifugation to characterize their ability to regulate core temperature (Tc) and to determine if this regulation was dependent on the amplitude of the hypergravic field before the cold exposure. Tc was measured in unrestrained rats by the use of a thermistor implanted adjacent to the carotid artery. One hour of cold exposure applied over the last hour of either a 1-, 4-, 7-, 13-, 19-. 25-, or 37-h period at 3 G evoked a decrease in Tc of about 3 degrees C. This fall in Tc was significantly greater than changes in Tc in cold-exposed rats at 1 G. No significant differences were found between the measured decreases in Tc observed for the 1-h cold exposures during the first 37 h at 3 G. However, when rats were subjected concurrently to cold and acceleration after 8 days at 3 G, they exhibited a smaller fall in Tc, suggesting a partial recovery of the acceleration-induced impairment of temperature regulation. In another series of experiments, the gravitational field profile was changed in amplitude in three different ways during the 3-h period preceding the 1-h cold exposure at 3 G. Despite the different gravitation field profiles before cold, the magnitude of the fall in Tc over the 1-h period of cold exposure was the same of all cases. These results suggest that the thermoregulatory impairment has a rapid onset, it a manifestation of an ongoing effect of hypergravity, and is not dependent on the prior G profile. The inability of rats to maintain Tc when cold exposed may be transient as indicated by the partial recovery of regulation by the 8th day.

Animals↗
PubMed1994

Effect of exercise on cold tolerance and metabolic heat production in adult and aged C57BL/6J mice.

Two groups of adult (12-mo-old) and two groups of aged (24-mo-old) C57BL/6J male mice were subjected to a standardized cold stress test (3-h partial restraint at 6 degrees C). One group from each age group was tested in the morning, and the other was tested in the afternoon. Half of the mice were subjected to running exercise on a treadmill during 1 h before the cold stress test. The other half were placed on a nonoperational treadmill for 1 h before the cold stress test. One hour of exercise resulted in improvement of cold tolerance during the subsequent cold exposure in both age groups but only during afternoon testing. Improvement in cold tolerance was not accompanied by an elevation of cold-induced metabolic heat production in adult mice. Metabolic heat production in aged mice showed only modest elevation. The discrepancy between improvement in cold tolerance and lack of elevation of metabolic heat production suggests that the primary mechanism for augmentation of cold tolerance after exercise in the afternoon is an improvement in cold-induced vasoconstriction of skin vessels, which is probably normally compromised in the afternoon.

Age Factors↗