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PubMed1996

Effect of chronic cold exposure on Na-dependent D-glucose transport along small intestine in ducklings.

In conditions of chronic cold exposure, ducklings develop a nonshivering thermogenesis that requires a high energy expenditure. Therefore, energy supply becomes essential to cold-acclimated ducklings, which increase their intake of carbohydrate-rich food. The aim of this work was to investigate the effect of cold acclimation on the activity of the intestinal brush-border Na(+)-D-glucose cotransport, which is the first major step controlling glucose entrance into an organism. Cotransport activity was determined by measuring D-glucose uptake in brush-border membrane vesicles isolated from different parts of the small intestine of thermoneutral control (25 degrees C) or cold-acclimated (4 degrees C) ducklings (Cairina moschata). Two D-glucose transport sites were described in ducklings: a high-affinity/low-capacity site and a low-affinity/high-capacity site. The former was mainly located in the ileum and the latter in the duodenum. These two transport sites were altered differently by cold exposure. Major alterations occur in the ileum where 1) a reduction in the Michaelis-Menten constant and maximal transport rate of the high-affinity site was observed, and 2) the occurrence of low-affinity site activity was noted in cold-acclimated ducklings, although it was not detected in the thermoneutral control group. Cold effect on the high-affinity site could be related to the changes in the ileal brush-border membrane vesicle lipids, whereas cold effect on the low-affinity site could be due, at least in part, to the higher glycosyl content found in this segment. The small intestine appears then able to react to cold exposure by increasing both its mucosa mass in proximal segments and D-glucose uptake capacity in ileum to respond to the higher energy demand induced by thermoregulatory requirements.

Acclimatization↗
PubMed1999

Cold exposure regulates the norepinephrine uptake transporter in rat brown adipose tissue.

The neuronal uptake of norepinephrine (NE) in sympathetically innervated tissues is mediated by a high-affinity NE uptake transporter (NET). Rat interscapular brown adipose tissue (ISBAT) is densely innervated by the sympathetic nervous system for the control of cold- and diet-induced thermogenesis. To determine if cold exposure regulates the NET, kinetic parameters for [3H]NE uptake and [3H]nisoxetine (Nis) binding were determined in ISBAT from 7-day cold-exposed (CE) and control rats. Uptake of [3H]NE in ISBAT slices was of high affinity (1.6 microM). After 7 days of cold exposure the affinity for [3H]NE uptake was not altered; however, the uptake capacity was decreased (38%) in ISBAT slices from CE rats. Kinetic parameters for [3H]Nis binding demonstrated a single high-affinity site in ISBAT from CE and control rats with similar affinity. The density of [3H]Nis sites in ISBAT was decreased (38%) following cold exposure. A time course (2 h-7 days) for cold exposure demonstrated downregulation of [3H]Nis binding density by day 3, which remained through day 7. The affinity for [3H]Nis binding was transiently decreased at 2 h of cold exposure. Similarly, ISBAT NE content was decreased at 2 h of cold exposure. Pair feeding CE rats to food intake of controls normalized plasma NE content; however, [3H]Nis binding density in ISBAT remained decreased in pair-fed rats. These results demonstrate that the ISBAT NET is downregulated following cold exposure. Reductions in ISBAT NE content precede alterations in NET density; however, plasma NE content is not related to regulation of the NET.

Adipose Tissue, Brown↗
PubMed1988

Lipoprotein lipase in adipose tissues of rats running during cold exposure.

This study evaluated the individual and combined effects of exercise training and intermittent cold exposure of similar energy cost on serum lipids and lipoprotein lipase (LPL) activity on epididymal white (WAT) and interscapular brown (BAT) adipose tissues of the rat. The animals were subjected daily to 2 h of treadmill running at 24 degrees C or for the same period of time at -5 degrees C, with or without exercise, for 28 days. Exercise training lowered serum triglycerides (P less than 0.01), whereas serum cholesterol was reduced by cold exposure (P less than 0.05). Cholesterol lowering occurred in the lipoproteins of lower densities. WAT weight was diminished by both treatments. Exercise training had an overall lowering effect on WAT total LPL activity (P less than 0.05), whereas cold exposure did not affect enzyme activity significantly. Exercise and intermittent cold interacted on BAT weight. Cold increased total BAT LPL activity (P less than 0.03), whereas simultaneous exercise in the cold greatly diminished this effect. Serum insulin levels were not affected by either treatment. Thus, in WAT, intermittent exposure to cold did not have any lasting effect on LPL activity, whereas exercise training decreased the latter. In contrast, exercise did not influence LPL in BAT of rats not exposed to cold but prevented the stimulation of enzyme activity induced by repeated cold exposure. These results support the notion that the regulation of LPL is tissue specific.

Adipose Tissue↗
PubMed1989

Effects of hypoxia on metabolic rate of conscious adult cats during cold exposure.

Oxygen consumption (VO2) and shivering movements were recorded in adult, conscious cats in a thermoneutral (24-27 degrees C) and in a cold (3-8 degrees C) environment during normoxia, hypoxia, or hyperoxia for 55 min. In the cold environment, VO2 correlated with shivering index (SI) under conditions of normoxia or ambient hypoxia (FIO2 = 0.12). During normoxia, VO2 was 63% higher in the cold than the thermoneutral environment. Ambient hypoxia acutely reduced VO2 in cold and thermoneutral environments, the decrement being greater for the former than the latter. Similarly, the variation in VO2 for unit change in SI was greater in hypoxia than normoxic conditions, suggesting that hypoxia influenced nonshivering as well as shivering components of cold-induced VO2. Hypoxia induced by CO (FICO = 0.002) also reduced VO2 and SI, a result that is consistent with previous results indicating that carotid body chemoreceptors do not mediate the suppression of shivering by ambient hypoxia. Hyperoxia increased VO2 and SI in the cold, and the effects of both hypoxia and hyperoxia in the cold were antagonized by increasing FICO2 to 0.03. The results demonstrate that hypoxia suppresses VO2 in the cold by reducing the intensity of shivering and, probably, by an action on metabolic rate that is unrelated to cold-induced calorigenesis.

Animals↗
PubMed1991

Role of the sympathetic nervous system in cold-induced hypertension in rats.

Hypertension develops in rats exposed chronically to cold [6 +/- 2 degrees C (SE)] and includes both an elevation of mean arterial pressure and cardiac hypertrophy. Previous studies suggest that cold-exposed animals, at least initially, have a large sustained increase in the activity of their sympathetic nervous system, suggesting a failure of the baroreceptor system to provide sufficient negative feedback to the central nervous system. The present study was designed to investigate whether alterations in the activity of the sympathetic nervous system, including the baroreceptor reflex, occur during exposure to cold and whether they contribute to cold-induced hypertension. Twenty male rats were prepared with indwelling catheters in the femoral artery and vein. Ten of the rats were exposed to cold (6 +/- 2 degrees C) chronically, while the remaining 10 were kept at 26 +/- 2 degrees C. Withdrawal of arterial blood samples (less than 5 ml/kg), measurement of direct arterial pressures, and measurement of baroreflex function were carried out at 0800 h at intervals throughout the experiment. Norepinephrine and epinephrine concentrations in plasma were also determined at intervals throughout the experiment. Systolic, diastolic, and mean blood pressures of cold-exposed rats were increased to levels significantly above those of controls. The sensitivity of the baroreflex (delta heart period/delta mean arterial pressure) was decreased in the cold-treated group. The concentration of norepinephrine in plasma increased after 24 h of exposure to cold and remained elevated throughout the experiment, whereas the concentration of epinephrine in plasma increased initially but returned to control levels after 19 days of exposure to cold.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Metabolic and thermal adaptations from endurance training in hot or cold water.

Metabolic and thermal adaptations resulting from endurance training in hot vs. cold water were compared. It was hypothesized that training in hot water would have greater effects on muscle glycogen use and blood lactate accumulation during exercise than training in cold water. Eighteen men exercised at 60% of maximal oxygen uptake while immersed in hot (n = 9) or cold water (n = 9) for 1 h, 5 days/wk, for 8 wk. Training in hot water (35 degrees C) potentiated body temperature increases during exercise, and training in cold water (20 degrees C) blunted body temperature increases during exercise. Before and after training, cardiorespiratory and thermoregulatory responses and muscle glycogen and blood lactate changes were assessed during a 1-h exercise trial in hot water and, on a separate day using the same intensity, in cold water. Oxygen uptake was similar for all trials, averaging 2.0 +/- 0.1 l/min. It was observed that 1) training reduced glycogen use and lactate accumulation during exercise, with no difference between cold and hot water training groups in the magnitude of this effect; 2) lactate accumulation during exercise was the same in hot water as in cold water; and 3) skin temperature decreased more rapidly during cold-water exercise after than before training, with no difference between cold and hot water training groups in the magnitude of this effect. Thus, exercise-induced body temperature increases are not an important stimulus for glycogen-sparing effects and blunted lactate accumulation associated with endurance training.

Adaptation, Physiological↗
PubMed1996

Acute cold stress induces suppressor macrophages in mice.

To elucidate mechanisms underlying acute cold stress-induced immunosuppression, functions of murine peritoneal cells of monocyte/ macrophage lineage from acute cold-stressed mice (exposed to 5 degrees C for 24 h) were investigated. Proliferative responses of spleen cells from control mice (reared at 25 degrees C) stimulated with concanavalin A (ConA) were significantly suppressed by adding peritoneal exudate cells from mice immediately after acute cold stress. The proportion of adherent cells was markedly increased in the peritoneal exudate cells from acute cold-stressed mice. These adherent cells from acute cold-stressed mice were shown to be the cells responsible for the suppressor activity for ConA responses of control spleen cells. Nonadherent cells did not suppress the ConA responses. The adherent cells in peritoneal exudate cells from control mice also suppressed the ConA responses, the inhibitory effect being considerably lower than that from acute cold-stressed mice. Addition of a nitric oxide synthase substrate analogue, NG-monomethyl-L-arginine, to the mixed cell cultures of normal spleen cells and adherent cells from acute cold-stressed mice inhibited nitric oxide release and completely abolished the suppressive effect of the adherent cells, suggesting that reactive nitrogen oxide released from the activated macrophages is apparently involved in the downregulation of proliferative responses of T cells. Thus the present findings suggest that acute cold stress induces macrophages with suppressor function and that this may contribute to the immune-suppressive state seen in spleen cells from acute cold-stressed mice.

Acute Disease↗
PubMed1996

Tolerance of the cirrhotic liver to cold ischemia: ex vivo analysis in rats.

We investigated the viability of rat cirrhotic livers preserved cold using an isolated rat liver perfusion model. Cirrhosis was induced by intravenous thioacetamide injection. Normal and cirrhotic livers were reperfused immediately or following 6 h of preservation through the portal vein with Krebs-Henseleit buffer and hyaluronic acid added. Cirrhotic livers with short cold ischemia showed higher portal venous resistance than their normal counterparts (p < 0.05), while cirrhotic livers preserved for 6 h exhibited marked elevation of the portal venous resistance as compared with their fresh counterparts or normal liver preserved cold for 6 h (p < 0.05). Similarly, the oxygen consumption of cirrhotic livers with short cold preservation was lower than that of normal livers (p < 0.05), which was further reduced by 6 h of cold preservation (p < 0.05). The bile output was not different between normal and cirrhotic livers. The sinusoidal endothelial cell function of cirrhotic livers as assessed by the clearance of hyaluronic acid was impaired even after a short period of cold ischemia. Histologically, cirrhotic livers showed severe sinusoidal endothelial cell damage, hepatocellular swelling, and marked septal edema which became more prominent by cold preservation. We conclude that the viability of the cirrhotic liver is impaired even by a short cold exposure, and that the prolongation of cold ischemia of the cirrhotic liver leads to further deterioration of the viability.

Animals↗
PubMed1991

Effect of chronic treatment with clonidine and spironolactone on cold-induced elevation of blood pressure.

The present study was designed to determine whether antihypertensive agents known to affect the renin-angiotensin-aldosterone (RAA) system might affect the elevation of blood pressure induced by chronic exposure to cold. Spironolactone, a mineralocorticoid receptor blocker, was added to the food and administered to rats chronically exposed to cold. In addition, clonidine, and alpha 2-adrenergic agonist and inhibitor of renin secretion, was administered to another group of cold-exposed rats by daily intraperitoneal injection. A warm-adapted and a cold-treated control group were also used. Chronic administration of spironolactone prevented the development of hypertension but failed to prevent other adaptive physiological changes characteristically occurring during exposure to cold and seen in the cold-treated control rats. Thus, increased weight of the heart, kidneys, adrenals and brown adipose tissue, increased dipsogenic responsiveness to angiotensin II, increased urinary outputs of norepinephrine and epinephrine, and increased food and water consumption were observed in all rats, treated and untreated, during exposure to cold. Similarly, daily injection of clonidine attenuated the elevation of blood pressure but also failed to prevent the other adaptive physiological changes characteristic of cold. These results are consistent with the hypothesis that the RAA system plays a role in the development of the cold-induced elevation of blood pressure.

Aldosterone↗
PubMed1995

Cyclosporin A reduces the severity of cold-restraint-induced gastric lesions: role of leukocytes.

The objective of this study was to determine the role of cyclosporin A (CsA) on cold-restraint-induced gastric lesions. Animals were subjected to 3 h immobilization at 4 degrees C in plastic restraining devices following a starvation period of 48 h. Gastric samples were obtained for the measurement of myeloperoxidase (MPO) activity, an index of number of peroxidase positive cells and thiobarbituric acid-reactive substances (TBARS; lipid peroxidation). Animals were pretreated with CsA which is a potent immunosuppressant and inhibits ischemia/reperfusion-induced polymorphonuclear leukocyte (PMN) infiltration. Cold-restraint administration significantly elevated the tissue MPO activity and TBARS formation. CsA pretreatment significantly reduced the severity of cold-restraint-induced gastric lesions while attenuating the elevated MPO measurements observed during cold-restraint administration. Animals rendered neutropenic with antineutrophil serum (ANS) exhibited significantly less gastric mucosal injury normally observed after cold-restraint stress. Neither CsA nor ANS treatment effected the elevated TBAR levels, indicating that PMNs are not involved in the lipid peroxidation process observed after cold-restraint stress. In conclusion, the results of this study indicate that CsA is capable of inhibiting cold-restraint-induced gastric mucosal injury and can attenuate the cold-restraint-induced increases in gastric MPO measurements. Our results also indicate that PMNs may be the important mediators of cold-restraint-induced gastric lesions.

Animals↗
PubMed1989

Exercise-induced myocardial ischemia in a cold environment. Effect of antianginal medications.

The influence of cold on the threshold for myocardial ischemia and the efficacy of antianginal drugs in a cold environment were assessed in 24 patients with stable angina and exercise-induced ST depression. Treadmill exercise tests were done according to a randomized double-blind protocol 90 minutes after administration of placebo, 80 mg propranolol, or 120 mg diltiazem, each at both -8 degrees and 20 degrees C. Eight of the patients were classified by history as cold-sensitive before the study. For the entire group, none of the exercise end points differed significantly between cold and normal temperatures with placebo. However, cold-sensitive patients developed 1 mm ST depression 30% sooner (169 +/- 41 versus 244 +/- 38 seconds, p less than 0.01) at -8 degrees C compared with 20 degrees C. At the onset of ischemia, rate-pressure product was lower in the cold (19.8 +/- 1.0 versus 22.0 +/- 1.6 x 10(-3), p less than 0.05). Both propranolol and diltiazem prolonged time to onset of 1 mm ST depression at both temperatures. The magnitude of improvement at -8 degrees C was equal to that at 20 degrees C, and differences between the two drugs were not statistically significant. Only diltiazem prolonged total exercise duration. Thus, as assessed by exercise testing, cold does not worsen ischemic threshold in most stable angina patients. However, in a subgroup identifiable by history, ischemic threshold is lower in the cold. Propranolol and diltiazem are as effective for exercise-induced ischemia in a cold environment as at normal temperatures.

Angina Pectoris↗
PubMed1994

The cold hemiplegic arm.

BACKGROUND AND PURPOSE: Vasomotor changes occur in the arm after hemiplegic stroke. Previous studies have provided conflicting results, with most showing an increase in skin temperature of the hemiplegic arm. However, a number of patients complain of distressing coldness of the hemiplegic arm. METHODS: Eleven patients with symptomatic coldness and 10 patients with hemiplegia but no coldness were recruited. The severity of the symptom of coldness was compared by questionnaire with other common symptoms after stroke. A thermographic camera was used to record the finger skin temperature response to cold stress. Blood flow to both hands was also measured simultaneously by means of two plethysmographs. In all patients there were no symptoms in the unaffected arm, and this was used as a control. RESULTS: The symptom of coldness rated highly compared with other symptoms. In the symptomatic group the finger temperature on the hemiplegic side was lower at rest (median difference at rest, 0.65 degrees C; P < .0001) and at all times after cold stress. In the asymptomatic group the fingers on the hemiplegic side were colder at rest and after initial cooling (median temperature difference, 0.2 degrees C) but at no other time. Hand blood flow on the hemiplegic side was also decreased in the symptomatic group by 35%. This was not seen in the asymptomatic group. CONCLUSIONS: Coldness of the hand may be a severe and distressing symptom in some patients after hemiplegia. Symptomatic patients have lower finger skin temperatures at rest and after standard cold stress. These symptomatic patients also had reduced blood flow to the hemiplegic hand.

Aged↗
PubMed1996

Interaction between cold and hypoxia on pulmonary circulation in COPD.

This study was designed to investigate the interaction of mild and localized cold exposure and hypoxia on pulmonary hemodynamics in chronic obstructive pulmonary disease (COPD). Nineteen patients with COPD were studied at sea level and seven at an altitude of 2,640 m. For all patients, pulmonary hemodynamic measurements were performed 10 min after insertion of a catheter in a femoral vein and following 10 min of cold exposure. Cold exposure was restricted to the forehead, and subjects breathed air at ambient temperature. Flow and temperature of air (1.5 L.s(-1), 5 degrees C) to the forehead were chosen to cool down the forehead skin to approximately 20 degrees C without discomfort for the subject. For the seven patients studied at high altitude, the same measurements were also performed after 5 min of oxygen supplementation with and without cold exposure. At sea level, an increase in pulmonary vascular resistance (PVR) during cold exposure was inversely related to the initial PaO2. In six severe hypoxic subjects (PaO2 < 50 mm Hg), PVR increased by 24%. At high altitude, PVR was significantly increased by 15%. After O2 supplementation, cold exposure did not induce an increase in PVR. We concluded that mild and localized cold exposure to the forehead only induced an increase in PVR in COPD patients with severe hypoxia. Moreover, in cold exposure responders, O2 supplementation negated the effect of cold exposure on pulmonary hemodynamics.

Cold Temperature↗
PubMed2006

Rapid cold-hardening increases the freezing tolerance of the Antarctic midge Belgica antarctica.

Rapid cold-hardening (RCH) is well known to increase the tolerance of chilling or cold shock in a diverse array of invertebrate systems at both organismal and cellular levels. Here, we report a novel role for RCH by showing that RCH also increases freezing tolerance in an Antarctic midge, Belgica antarctica (Diptera, Chironomidae). The RCH response of B. antarctica was investigated under two distinct physiological states: summer acclimatized and cold acclimated. Summer-acclimatized larvae were less cold tolerant, as indicated by low survival following exposure to -10 degrees C for 24 h; by contrast, nearly all cold-acclimated larvae survived -10 degrees C, and a significant number could survive -15 degrees C. Cold-acclimated larvae had higher supercooling points than summer larvae. To evaluate the RCH response in summer-acclimatized midges, larvae and adults, maintained at 4 degrees C, were transferred to -5 degrees C for 1 h prior to exposures to -10, -15 or -20 degrees C. RCH significantly increased survival of summer-acclimatized larvae frozen at -10 degrees C for 1 h compared with larvae receiving no cold-hardening treatment, but adults, which live for only a week or so in the austral summer, lacked the capacity for RCH. In cold-acclimated larvae, RCH significantly increased freeze tolerance to both -15 and -20 degrees C. Similarly, RCH significantly increased cellular survival of fat body, Malpighian tubules and gut tissue from cold-acclimated larvae frozen at -20 degrees C for 24 h. These results indicate that RCH not only protects against non-freezing injury but also increases freeze tolerance.

Acclimatization↗
PubMed2006

Mitochondrial mechanisms of cold adaptation in cod (Gadus morhua L.) populations from different climatic zones.

Adjustments in mitochondrial properties and capacities are crucial in acclimatization to seasonal cold as well as in evolutionary cold adaptation of marine ectotherms. To examine whether gene expression mechanisms contribute to different settings of aerobic capacities in populations of cod (Gadus morhua) along a latitudinal cline, maximum activities of key enzymes of mitochondrial metabolism and their respective mRNA levels were compared in white muscle and liver of cold (4 degrees C) and warm (10 degrees C) acclimated individuals from cod populations of the North Sea and the Barents Sea, respectively. In white muscle, cold acclimation caused a parallel increase in citrate synthase (CS) and in cytochrome c oxidase (COX) activities, but with a much larger effect in the cold eurythermal Arctic population. In liver, cold acclimation was accompanied by increments in CS activities, but differences between populations were minor. Overall COX activities in liver were not affected by cold acclimation, but were higher in the cold adapted population. In both populations increments in muscle CS capacities were tightly correlated with elevated mRNA levels, suggesting transcriptional control of citrate synthase levels in muscle. In liver, CS mRNA levels differed between populations but were not affected by cold acclimation, so that post-transcriptional control may contribute to elevated functional levels in this tissue. Mitochondrial-encoded COX2 mRNA levels were not limiting for functional activities in both tissues, in favour of post-transcriptional control or limitations by other transcripts of the COX complex. Altogether, the differentiation in gene expression between both populations was more strongly expressed at 4 degrees C. The comparison of functional levels and transcript levels may reflect genetic differentiation at functional sites, in line with genetic differences between the two populations previously established by non-coding genetic markers.

Acclimatization↗
PubMed2006

Sarcolemmal ion currents and sarcoplasmic reticulum Ca2+ content in ventricular myocytes from the cold stenothermic fish, the burbot (Lota lota).

The burbot (Lota lota) is a cold stenothermic fish species whose heart is adapted to function in the cold. In this study we use whole-cell voltage-clamp techniques to characterize the electrophysiological properties of burbot ventricular myocytes and to test the hypothesis that changes in membrane currents and intracellular Ca2+ cycling associated cold-acclimation in other fish species are routine for stenothermic cold-adapted species. Experiments were performed at 4 degrees C, which is the body temperature of burbot for most of the year, and after myocytes were acutely warmed to 11 degrees C, which is in the upper range of temperatures experienced by burbot in nature. Results on K+ channels support our hypothesis as the relative density of K-channel conductances in the burbot heart are similar to those found for cold-acclimated cold-active fish species. I(K1) conductance was small (39.2+/-5.4 pS pF(-1) at 4 degrees C and 71.4+/-1.7 pS pF(-1) at 11 degrees C) and I(Kr) was large (199+/-27 pS pF(-1) at 4 degrees C and 320.3+/-8 pS pF(-1) at 11 degrees C) in burbot ventricular myocytes. We found high Na+-Ca2+ exchange (NCX) activity (35.9+/-6.3 pS pF(-1) at 4 degrees C and 58.6+/-8.4 pS pF(-1) at 11 degrees C between -40 and 20 mV), suggesting that it may be the primary pathway for sarcolemmal (SL) Ca2+ influx in this species. In contrast, the density (I(Ca), 0.81+/-0.13 pA pF(-1) at 4 degrees C, and 1.35+/-0.18 pA pF(-1) at 11 degrees C) and the charge (Q(Ca), 0.24+/-0.043 pC pF(-1) at 4 degrees C and 0.21+/-0.034 pC pF(-1) at 11 degrees C) carried by the L-type Ca2+ current was small. Our results on sarcolemmal ion currents in burbot ventricular myocytes suggest that cold stenothermy and compensative cold-acclimation involve many of the same subcellular adaptations that culminate in enhanced excitability in the cold.

Acclimatization↗
PubMed1988

Thermal, metabolic, and cardiovascular changes in men and women during cold stress.

Our understanding of the responses of men and women to cold stress is extremely limited. Various scientists have suggested that there could be gender differences in thermoregulatory responses due to sexual dimorphism in body fatness and its distribution, in body surface area, and in mass. In addition, there are also several lines of evidence supporting the hypothesis that there are gender-specific physiological responses to body cooling. In cold water studies, women cool more rapidly than men when at rest; this potentially greater stimulus does not result in a greater metabolic response by the women. If both groups increase their metabolism by performing a prescribed amount of exercise, there are no differences in body cooling. However, if they exercise spontaneously, the women select a lower metabolic rate and experience greater body cooling. Thus, it appears that women are less thermally sensitive to cold water. In cold air stress women have a lower mean skin temperature than men, but this is not observed in peripheral skin sites. In contrast to cold water, women do not experience greater drops in deep body temperature than men in cold air. Furthermore, men may be more metabolically sensitive than women to cold air stress. Men also respond to cold air with a bradycardia and increased stroke volume, while women show no change in these parameters. Similarly, men show a greater blood pressure response than women to local cooling of a hand or the face. Many of these gender-specific responses cannot be explained fully by differences in body morphology and support the concept that men and women respond differently to the cold.

Adaptation, Physiological↗
PubMed2003

Physical activity and the common cold in men administered vitamin E and beta-carotene.

BACKGROUND AND PURPOSE: It has been proposed that moderate regular aerobic training may enhance immunocompetence, whereas excessive training may cause immunosuppression. We evaluated whether physical activity at work, or at leisure, is associated with the risk of the common cold, and whether the antioxidants vitamin E and beta-carotene affect common cold risk in physically active people. METHODS: A cohort of 14,401 men aged 50-69 yr and working at study entry was drawn from the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, which examined the effect of vitamin E, 50 mg.d(-1), and beta-carotene, 20 mg.d(-1), on lung cancer in smokers using a 2 x 2 factorial design. The trial was conducted in southwestern Finland in 1985-1993; the intervention lasted for 6.1 yr (median). Physical activity at work, and the type and frequency of leisure-time exercise were recorded at study entry. The subjects were questioned about common cold episodes 3x yr-1. We modeled the cumulative incidence of colds during a 2-yr follow-up period with Poisson regression, adjusting for potential confounders. RESULTS: Physical activity at work and at leisure had no association with common cold risk. In subjects with physically load-bearing jobs, neither vitamin E nor beta-carotene affected significantly the risk of common cold. In subjects carrying out heavy exercise at leisure, vitamin E and beta-carotene increased the risk of colds when compared with placebo. CONCLUSIONS: Contrary to previous suggestions, moderate physical activity is not associated with lower risk of common cold in middle-aged male smokers. It has been previously proposed that antioxidant supplementation might be beneficial for subjects carrying out heavy exercise, but in our study vitamin E and beta-carotene increased the risk of colds in subjects carrying out heavy exercise at leisure.

Aged↗