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PubMed2004

Thirst sensations and AVP responses at rest and during exercise-cold exposure.

PURPOSE: The purpose of this study was to 1) determine the effect of hypohydration (HYPO) on thirst sensations during moderate exercise in the cold and 2) determine a possible mechanism for a cold-induced decline in thirst. METHODS: In the first phase of the study, eight males walked on four occasions, in T-shirts, shorts, and shoes, at 50% VO2max, for 60 min in either a 4 degrees C (cold) or 27 degrees C (temperate) environment in a state of HYPO or euhydration (EU). In the second phase, nine males in states of EU or HYPO randomly performed four trials consisting of 30 min standing at 27 degrees C, followed by 30 min of standing and 30 min of treadmill exercise at 50% of VO2max, in either 4 degrees C or 27 degrees C air. RESULTS: In phase 1, thirst sensations were lower throughout 60 min of exercise (P < 0.05) in both HYPO and EU conditions during the cold trials. In phase 2, despite elevated plasma osmolality (P < 0.05), perception of thirst and plasma arginine vasopressin [AVP] similarly decreased (P < 0.05) after 30-min standing rest and 30-min exercise in the HYPO-cold trial, compared with the HYPO-temperate, EU-cold, and EU-temperate trials. CONCLUSIONS: When either euhydrated or hypohydrated, cold exposure attenuated thirst by up to 40% at rest and during moderate-intensity exercise. The attenuated thirst when hypohydrated during cold exposure was associated with lower plasma [AVP] despite an elevated plasma osmolality. This decline in thirst and AVP in the cold may be the result of peripheral vasoconstriction, mediating an increase in central blood volume and stimulation of central volume receptors.

Arginine Vasopressin↗
PubMed2006

American College of Sports Medicine position stand: prevention of cold injuries during exercise.

It is the position of the American College of Sports Medicine that exercise can be performed safely in most cold-weather environments without incurring cold-weather injuries. The key to prevention is use of a comprehensive risk management strategy that: a) identifies/assesses the cold hazard; b) identifies/assesses contributing factors for cold-weather injuries; c) develops controls to mitigate cold stress/strain; d) implements controls into formal plans; and e) utilizes administrative oversight to ensure controls are enforced or modified. The American College of Sports Medicine recommends that: 1) coaches/athletes/medical personnel know the signs/symptoms and risk factors for hypothermia, frostbite, and non-freezing cold injuries, identify individuals susceptible to cold injuries, and have the latest up-to-date information about current and future weather conditions before conducting training sessions or competitions; 2) cold-weather clothing be chosen based on each individual's requirements and that standardized clothing ensembles not be mandated for entire groups; 3) the wind-chill temperature index be used to estimate the relative risk of frostbite and that heightened surveillance of exercisers be used at wind-chill temperatures below -27 degrees C (-18 degrees F); and 4) individuals with asthma and cardiovascular disease can exercise in cold environments, but should be monitored closely.

Adaptation, Physiological↗
PubMed1998

The role of zinc lozenges in treatment of the common cold.

OBJECTIVE: To summarize and critique the medical literature on the use of zinc lozenges for treatment of the common cold. DATA SOURCES: MEDLINE searches (January 1966-June 1997) identified human clinical trials on the use of zinc lozenges for the treatment of the common cold. Bibliographies were also reviewed for relevant articles. STUDY SELECTION: Double-blind, placebo-controlled trials of zinc lozenges in adults for the treatment of the common cold, with the clinical end points of reduction in duration and/or severity of cold symptoms. DATA EXTRACTION: All double-blind placebo-controlled, human clinical trials on the use of zinc lozenges for the treatment of the common cold were included. DATA SYNTHESIS: The use of zinc lozenges in the treatment of the common cold has been suggested to reduce the duration and severity of cold symptoms. Of eight double-blind, placebo-controlled trials, four found zinc lozenges to be effective, while the other four reported no difference between zinc and placebo therapy. Potential reasons for the discrepancy between the results of these trials include inadequate placebo control, formulation of the lozenge, and the dose of zinc used. Common adverse effects include unpleasant taste, mouth irritation, and nausea. CONCLUSIONS: Treatment of the common cold with zinc gluconate lozenges, using adequate doses of elemental zinc, may be effective in reducing duration and severity of cold symptoms. The benefit appears to be maximal if the lozenges are started immediately after the onset of symptoms. The formulation of the lozenges also appears to be important because the addition of citric acid or tartaric acid may reduce efficacy due to chelation of zinc ion. Although zinc gluconate lozenges have dominated clinical trials thus far, further studies are needed to demonstrate the efficacy of zinc acetate lozenges and to determine whether their adverse effect profile is more favorable to that of zinc gluconate lozenges. Patients should play an important role in the decision-making process and must decide whether the benefit gained from treatment with zinc lozenges outweighs the potential adverse effects.

Common Cold↗
PubMedDate not supplied

Is there a common cold constitution?

OBJECTIVE: Constitutional factors might play a role in the susceptibility to clinical illness during the common cold. This study seeks to determine if the likelihood of developing frequent common colds persists during childhood. DESIGN: The Tucson Children's Respiratory Study involves 1246 children enrolled at birth and followed prospectively since 1980 and 1984. Parents reported the occurrence of frequent (> or =4) colds during the past year by questionnaire at 2, 3, 6, 8, 11, and 13 years of age. Blood for ex vivo interferon-gamma responses was obtained at 9 months and 11 years of age. RESULTS: After adjustment for potential confounding variables, children with frequent colds at year 2 or 3 were twice as likely to experience frequent colds at year 6 (relative risk [RR], 2.8; 95% confidence interval [CI], 2.1-3.9), year 8 (RR, 2.6; 95% CI, 2.1-3.3), year 11 (RR, 2.4; 95% CI, 1.8-3.1), and year 13 (RR, 2.1; 95% CI, 1.4-3.3) compared with children who had infrequent colds at years 2 and 3. At 9 months of age, children who ultimately experienced persistent frequent colds had lower interferon-gamma titers than children without persistent frequent colds (3.05 +/- 1.61 vs 3.74 +/- 1.39, P =.016); this finding persisted at 11 years of age. CONCLUSION: These data suggest the existence of a common cold constitution, whereby some children are more susceptible to infection and/or the expression of clinical symptoms when infected than are other children.

Adolescent↗
PubMed2006

Neural substrate of cold-seeking behavior in endotoxin shock.

Systemic inflammation is a leading cause of hospital death. Mild systemic inflammation is accompanied by warmth-seeking behavior (and fever), whereas severe inflammation is associated with cold-seeking behavior (and hypothermia). Both behaviors are adaptive. Which brain structures mediate which behavior is unknown. The involvement of hypothalamic structures, namely, the preoptic area (POA), paraventricular nucleus (PVH), or dorsomedial nucleus (DMH), in thermoregulatory behaviors associated with endotoxin (lipopolysaccharide [LPS])-induced systemic inflammation was studied in rats. The rats were allowed to select their thermal environment by freely moving in a thermogradient apparatus. A low intravenous dose of Escherichia coli LPS (10 microg/kg) caused warmth-seeking behavior, whereas a high, shock-inducing dose (5,000 microg/kg) caused cold-seeking behavior. Bilateral electrocoagulation of the PVH or DMH, but not of the POA, prevented this cold-seeking response. Lesioning the DMH with ibotenic acid, an excitotoxin that destroys neuronal bodies but spares fibers of passage, also prevented LPS-induced cold-seeking behavior; lesioning the PVH with ibotenate did not affect it. Lesion of no structure affected cold-seeking behavior induced by heat exposure or by pharmacological stimulation of the transient receptor potential (TRP) vanilloid-1 channel ("warmth receptor"). Nor did any lesion affect warmth-seeking behavior induced by a low dose of LPS, cold exposure, or pharmacological stimulation of the TRP melastatin-8 ("cold receptor"). We conclude that LPS-induced cold-seeking response is mediated by neuronal bodies located in the DMH and neural fibers passing through the PVH. These are the first two landmarks on the map of the circuitry of cold-seeking behavior associated with endotoxin shock.

Animals↗
PubMed1979

Motility, acrosome morphology and fertilizing capacity of cold-shocked hamster spermatozoa.

When fresh epididymal spermatozoa were cold shocked for 10 or 30 min, then warmed to 24 degrees C, sperm motility was normal, but cold shocking ejaculated or capacitated spermatozoa caused a significant decrease in the percentage of motile spermatozoa and, for capacitated spermatozoa, in the rate of motility. The acrosomes of motile fresh epididymal and ejaculated spermatozoa became crenulated after cold shock, and the percentage of spermatozoa with crenulated acrosomes increased with longer periods of cold shock and was higher when spermatozoa were cold shocked in serum than in saline. When epididymal spermatozoa were cold shocked after incubation for 4 h at 37 degrees C, the acrosomes on spermatozoa which had not undergone an acrosome reaction became swollen and elevated instead crenulated. Epididymal spermatozoa which were cold shocked and then incubated for 4 h at 37 degrees C exhibited acrosome reactions and activation of motility, but had reduced fertilizing capacity when tested in vitro. Spermatozoa incubated in serum and cold shocked were able to penetrate zone-free ova even though their tails had been bent through 180 degrees. It is suggested that cold shock decreases the fertilizing capacity of hamster spermatozoa by interfering with the ability of spermatozoa to bind to and/or penetrate the zone pellucida.

Acrosome↗
PubMed2003

Pravastatin protection from cold stress in myocardium of rats.

The aim of this research was to evaluate the possible protective effect of pravastatin on ultrastructural alterations induced by cold stress in the myocardium of rats. Sixteen EPM-Wistar rats (Rattus norvegicus albinus) were used and distributed into four groups: 1) control; 2) pravastatin; 3) cold stress, and 4) pravastatin + cold stress. A daily oral dose of 10 mg/kg of weight of pravastatin was administered to each rat in groups 2 and 4 for 15 days. The stress induced by cold was obtained by keeping the group 3 and 4 rats in a freezer at -8 degrees C for 4 hours. The animals were killed and the heart and fragments of the left ventricles (LV) were removed and processed prior to conducting electron microscopic analysis. The ultrastructural alterations in cardiomyocytes were quantified through the number of mitochondrial cristae pattern (cristalysis). The group subjected only to cold stress showed a significant increase in cristalysis (391.9) when compared with control group (42.0). In the cold stress and pravastatin pretreatment group, a statistically significant (96.9)*, P<0.05 cristalysis reduction was observed when compared with cold stress group. The mitochondrial cristalysis profiles of the control and pravastatin groups were 42.0 and 65.7, respectively. Cold stress induced a significant increase in the rate of mitochondrial cristalysis. In the group that received pravastatin and was exposed to cold stress, the drug protected the LV cardiomyocytes. This fact was confirmed by a reduction mitochondrial cristalysis pattern.

Animals↗
PubMed2005

Cold injuries.

Exposure to cold can produce a variety of injuries that occur as a result of man's inability to adapt to cold. These injuries can be divided into localized injury to a body part, systemic hypothermia, or a combination of both. Body temperature may fall as a result of heat loss by radiation, evaporation, conduction, and convection. Hypothermia or systemic cold injury occurs when the core body temperature has decreased to 35 degrees C (95 degrees F) or less. The causes of hypothermia are either primary or secondary. Primary, or accidental, hypothermia occurs in healthy individuals inadequately clothed and exposed to severe cooling. In secondary hypothermia, another illness predisposes the individual to accidental hypothermia. Hypothermia affects multiple organs with symptoms of hypothermia that vary according to the severity of cold injury. The diagnosis of hypothermia is easy if the patient is a mountaineer who is stranded in cold weather. However, it may be more difficult in an elderly patient who has been exposed to a cold environment. In either case, the rectal temperature should be checked with a low-reading thermometer. The general principals of prehospital management are to (1) prevent further heat loss, (2) rewarm the body core temperature in advance of the shell, and (3) avoid precipitating ventricular fibrillation. There are two general techniques of rewarming--passive and active. The mechanisms of peripheral cold injury can be divided into phenomena that affect cells and extracellular fluids (direct effects) and those that disrupt the function of the organized tissue and the integrity of the circulation (indirect effects). Generally, no serious damage is seen until tissue freezing occurs. The mildest form of peripheral cold injury is frostnip. Chilblains represent a more severe form of cold injury than frostnip and occur after exposure to nonfreezing temperatures and damp conditions. Immersion (trench) foot, a disease of the sympathetic nerves and blood vessels in the feet, is observed in shipwreck survivors or in soldiers whose feet have been wet, but not freezing, for long periods. Patients with frostbite frequently present with multisystem injuries (e.g., systemic hypothermia, blunt trauma, substance abuse). The freezing of the corneas has been reported to occur in individuals who keep their eyes open in high wind-chill situations without protective goggles (e.g., snowmobilers, cross-country skiers).

Chilblains↗
PubMed1992

Importance of sympathetic nerves for the stimulatory effect of cold exposure on glucose utilization in brown adipose tissue.

The effects of cold exposure on glucose transport system in brown adipose tissue (BAT) and the role of sympathetic nerves in this response were studied in rats. The rate constant of glucose uptake in BAT increased 10-, 13-, and 14-fold after 6 h, 1 d, and 2 d of cold exposure, respectively, as compared with controls. After 2 d of cold exposure, the number of glucose transporters in the plasma membranes increased from 10.2 +/- 1.1 to 16.7 +/- 1.4 pmol/mg protein and the transporter number in the microsomal membranes decreased from 15.1 +/- 1.0 to 9.0 +/- 1.1 pmol/mg protein, as measured by cytochalasin B binding. However, the increase in glucose utilization in BAT preceded the recruitment of glucose transporters to the plasma membranes. Thus, the glucose utilization markedly increased 6 h after cold exposure without significant increase in the glucose transporter number. The apparent dissociation constant (Kd) for cytochalasin B was unchanged. The stimulatory effect of cold exposure on glucose utilization in BAT was prevented by sympathetic denervation. In denervated BAT, cold exposure conversely decreased the number of glucose transporters in the plasma membranes. These results indicate that: (1) cold exposure increases glucose utilization in BAT and promotes translocation of glucose transporters from the microsomes to plasma membranes; (2) the effects of cold exposure depend entirely upon sympathetic innervation of BAT; (3) the recruitment or redistribution of glucose transporters accounts only partly for the large increase in glucose utilization in BAT after acute cold exposure.

Adipose Tissue, Brown↗
PubMed1999

Changes in forearm blood flow during single and intermittent cold application.

STUDY DESIGN: Two-factor repeated measures design. OBJECTIVES: To compare the effects of a 20-minute cold application to the effects of a 20-minute cold application followed by 20 additional minutes of intermittent cold on forearm blood flow over a 60-minute period. BACKGROUND: The appropriate duration of cold application as a therapeutic modality following soft tissue trauma is an important clinical question because the goal of using this modality is to limit edema, decrease pain, and produce effective muscle relaxation without causing cold-induced reactive vasodilatation or nerve damage. METHODS AND MEASURES: Thirteen subjects (mean age, 21.46 +/- 4.01 years) volunteered to participate in this study. A bilateral tetrapolar impedance plethysmograph was used with venous occlusion to measure changes in local limb blood volume at the forearm for a period of 60 minutes under 2 conditions: Condition 1: Prolonged intermittent cold application (20 minutes ice application; 10 minutes off; 10 minutes ice on; 10 minutes off; 10 minutes ice on); Condition 2: Cold followed by application of a room-temperature pack of equal weight to the ice bag (20-minute ice application; 10 minutes off; 10 minute room-temperature pack on; 10 minutes off; 10-minute room-temperature pack on). RESULTS: A significantly lower blood flow was noted during the last 10 minutes of Condition 1 compared with Condition 2. CONCLUSIONS: The findings of this study indicate that blood flow is reduced when a prolonged intermittent cold application (Condition 1) is used compared to a single cold application (Condition 2).

Adult↗
PubMed1995

Effect of cold exposure on profiles of metabolic and endocrine responses and on responses to feeding and arginine injection in sheep.

The effect of cold exposure (0 degrees C) on profiles of total heat production (HP), energy metabolism, and blood metabolite and hormone concentrations were measured in nine shorn Suffolk rams. Blood metabolite and hormone responses to feeding and to i.v. arginine injection (.625 mmol/kg BW) and postprandial changes in HP were also measured. Heat production was greater (P < .05) during cold exposure than in the thermoneutral environment due to enhanced (P < .05) nonprotein oxidation. Protein oxidation and nitrogen balance remained unchanged during cold exposure. Plasma glucagon concentrations increased (P < .05) during the initial period of cold exposure. Heat production increased (P < .01) after the initiation of feeding in both environments. Heat production returned gradually to prefeeding values in the thermoneutral environment, but it remained close to the higher levels during cold exposure. Plasma insulin and glucagon concentrations increased (P < .05), and plasma growth hormone concentrations decreased (P < .10) after the initiation of feeding in both environments. Plasma glucagon responses to feeding (P < .05) and plasma insulin responses to arginine injection (P < .01) were reduced by cold exposure. We suggest that 1) enhanced HP in sheep exposed to cold is maintained by enhanced nonprotein oxidation and 2) endocrine responses to stimulants are influenced by cold exposure, even though profiles after cold exposure change little.

Acetates↗
PubMed1982

Cold exposure and absorption of colostral immunoglobulins by neonatal pigs.

To investigate the effect of cold exposure on absorption of colostral immunoglobulins, 56 piglets were weaned at birth and placed in either a thermoneutral (35 C) or cold (21 C) environmental chamber. Thermoneutral piglets had a survival rate of 62% at 48 h, but survival among cold-exposed piglets was only 36% (P less than .10). Cold aid reduced (P less than .01) rectal temperature by more than 6 C after 24 h of exposure. A constant amount of bovine colostrum was administered orally at 4 h after initiation of thermal treatments. Bovine immunoglobulin G1 (IgG1) was readily absorbed and reached a serum level of 17 mg/ml after 24 h. Bovine IgM also was absorbed and increased to approximately 2 mg/ml at 24 h. However, absorption of colostral IgG1 and IgM was not affected by cold exposure. Cold air increased (P less than .05) incidence of diarrhea by over five fold after 72 h, and severity of diarrhea was nearly doubled (P less than .01). Hematocrit was also higher (P less than .05) in cold-exposed piglets. These data demonstrate that a cold stressor sufficient to induce hypothermia does not impair absorption of colostral macromolecules in piglets. However, cold exposure was related to increase incidence and severity of diarrhea.

Animals↗
PubMed1975

Changes in metabolite concentration in the plasma, liver and muscle of feed restricted Japanese quail exposed to cold.

Quail fed ad libitum and 50% ad libitum were cold exposed for several weeks, during time control quail remained at 21 degrees C. The concentration of plasma glucose, FFA, and uric acid, tissue glycogen and carcass fat content was measured at the end of the cold exposure period. Quail fed ad libitum showed no significant change in the levels of plasma and tissue metabolites, or the carcass fat content, following cold exposure. The feed consumption by the cold exposed quail increased, and the mean body weight showed little variation from that of the controls. Feed restricted quail which were cold exposed lost significantly more weight, and had a lower ranked fat content than their controls. Whereas feed restriction caused a lowering of the liver glycogen concentration in both treatment groups, muscle glycogen levels were higher than in quail fed ad libitum. However, cold exposure was not accompanied by a change in muscle and liver glycogen levels in feed restricted quail. Feed restricted quail at 21 degrees C were hypoglycaemic and hyperlipaemic compared to quail fed ad libitum, but cold exposed feed restricted quail had a much higher plasma glucose concentration than the controls. The ranked carcass fat content was inversely related to plasma FFA level in both control and cold exposed feed restricted quail. It is suggested that both a glycolytic and lipid mobilizing response to cold is obtained in quail whose body reserves are not spared from catabolism by adequate dietary nutrient absorption, and the possibility of gluconeogenesis from precursors produced by proteolysis is indicated.

Adaptation, Physiological↗
PubMed1992

Effect of a reduction in sodium intake on cold-induced elevation of blood pressure in the rat.

Chronic exposure of rats to cold (5 degrees C) induces hypertension within 3 weeks. The objective of this study was to determine the effect of treatment with graded levels of dietary NaCl on the induction of hypertension during chronic exposure to cold. Four groups of male rats were used. The first, given a commercial sodium-deficient diet containing 0.30% NaCl, served as the warm-adapted control group. The second, third, and fourth groups were given the same diet containing 0.075%, 0.15%, and 0.30% NaCl, respectively. Because cold-exposed rats ingest approximately twice as much food as warm-adapted controls, this represented half, the same, and twice the amount of NaCl ingested by the control group. The latter three groups were placed in cold air (5 degrees C). All cold-treated groups had an elevation of systolic blood pressure that was proportional to the concentration of NaCl in the diet by the seventeenth week of exposure to cold. Cardiac hypertrophy occurred to the same extent in all cold-exposed groups and was thus unaffected by the NaCl content of the diet or by the extent of elevation of blood pressure. Hence, cardiac hypertrophy during chronic exposure to cold is supported by other factors, possibly by the increased concentration of either norepinephrine or triiodothyronine, or both, which occurs characteristically in rats under these conditions. The results of this experiment suggest that the amount of NaCl ingested daily plays a role in the cold-induced elevation of blood pressure observed in rats.

Acclimatization↗
PubMed1994

Direct blood pressure measurements in rats during abrupt exposure to, and removal from, cold air.

When male rats, each bearing an indwelling femoral arterial cannula, were exposed abruptly to cold (5 degrees C), systolic, diastolic, and mean blood pressures increased within 1 hr to levels significantly above those measured prior to exposure to cold. Blood pressures reached maximal levels within 2 hr of exposure to cold and remained elevated during the next seven days. Heart rates, measured at the same time, responded similarly. When cannulated rats that had been exposed to cold for four weeks were removed abruptly to 26 degrees C, systolic, diastolic, and mean blood pressures decreased nearly linearly for 5 hr. By two days after removal from cold, blood pressures stabilized at levels that were still elevated above those observed prior to exposure to cold. In contrast, heart rate returned to precold exposure level by the 13th day after removal from cold. The mechanisms responsible for the elevation of blood pressure during abrupt exposure of rats to cold and the decrease in blood pressure after removal from cold remain to be elucidated.

Animals↗
PubMed1996

Thermoregulation with age: restoration of beta(3)-adrenergic responsiveness in brown adipose tissue by cold exposure.

The beta(3)-adrenergic-stimulated thermogenic response in brown adipose tissue (BAT) is impaired in senescent rats, whereas cold-induced thermogenesis is not. To determine if cold exposure can restore beta(3)-adrenergic receptor responsiveness in senescent rats, we examined BAT mitochondrial GDP binding in young and old rats, and UCP mRNA levels in young rats following stimulation by the beta(3)-adrenergic agonist CGP-12177 with and without prior cold exposure. F-344 male rats were maintained at thermoneutrality or exposed to 8 degrees C for 48 hr, followed by a 24-hr period of rewarming before administration of 0.75 mg/kg CGP-12177 or vehicle solution. During the rewarming period, GDP binding remained elevated but UCP mRNA levels with a half-life of 11 hr returned to levels observed in the thermoneutral controls. In young rats, both cold exposure and administration of the beta(3)-adrenergic agonist to thermoneutral controls increased GDP binding 2-fold and UCP mRNA levels 4-fold. However, in cold-exposed young rats, there was no further increase with beta(3)-agonist treatment. In senescent control rats, CGP-12177 did not increase GDP binding, but cold exposure did. However, in cold-exposed old rats, the beta(3)-agonist was now able to increase GDP binding. The induction of UCP mRNA by CGP-12177 was also investigated and found to be 25% less in senescent compared with young rats. These observations indicate that cold exposure restores the impaired beta(3)-adrenergic signal transduction in BAT from senescent rats. One possibility is that cold exposure induces the synthesis of one or more components in the beta(3)-adrenergic pathway in senescent rats.

Adipose Tissue, Brown↗
PubMed2003

Bacterial cold shock responses.

As a measure for molecular motion, temperature is one of the most important environmental factors for life as it directly influences structural and hence functional properties of cellular components. After a sudden increase in ambient temperature, which is termed heat shock, bacteria respond by expressing a specific set of genes whose protein products are designed to mainly cope with heat-induced alterations of protein conformation. This heat shock response comprises the expression of protein chaperones and proteases, and is under central control of an alternative sigma factor (sigma 32) which acts as a master regulator that specifically directs RNA polymerase to transcribe from the heat shock promotors. In a similar manner, bacteria express a well-defined set of proteins after a rapid decrease in temperature, which is termed cold shock. This protein set, however, is different from that expressed under heat shock conditions and predominantly comprises proteins such as helicases, nucleases, and ribosome-associated components that directly or indirectly interact with the biological information molecules DNA and RNA. Interestingly, in contrast to the heat shock response, to date no cold-specific sigma factor has been identified. Rather, it appears that the cold shock response is organized as a complex stimulon in which post-transcriptional events play an important role. In this review, we present a summary of research results that have been acquired in recent years by examinations of bacterial cold shock responses. Important processes such as cold signal perception, membrane adaptation, and the modification of the translation apparatus are discussed together with many other cold-relevant aspects of bacterial physiology and first attempts are made to dissect the cold shock stimulon into less complex regulatory subunits. Special emphasis is placed on findings concerning the nucleic acid-binding cold shock proteins which play a fundamental role not only during cold shock adaptation but also under optimal growth conditions.

Adaptation, Physiological↗
PubMed2002

Cold exposure and musculoskeletal disorders and diseases. A review.

The aim of this study was to investigate how cold exposure may be associated with musculoskeletal problems either on symptomatic or disease level based on available relevant scientific literature. The data collection resulted in ten scientific articles, from which nine were epidemiological and one a case report consisting of three cases. The results indicated that musculoskeletal symptoms are more frequent in cold store work and in related conditions than in normal temperature work and symptoms seems to be increased when the working time in cold environment increases. In cold store work low back pain and knee pain are more frequent problems than in normal temperature working environment. The association between cold exposure and shoulder pain is still unclear and has been poorly studied. Meteorological conditions, principally low ambient temperature may have an effect of reported low back pain in a remarkable part of population. In the etiology of tenosynovitis cold exposure has a specific role either as a causative or a contributing factor. The risk for carpal tunnel disease is 2.2-fold in repetitive wrist movements compared with no repetition and 9.4-fold when cold exposure added. Cold exposure in work seems to be is associated with a little increased risk (Odds ratio 2.2) for degenerative discopathies of lower back in men. However, this risk is small and seems to be associated with other physical factors in the background. In conclusion, the associations between cold exposure and musculoskeletal complaints or diseases are shown in some studies and the need of further research is apparent.

Cold Temperature↗