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PubMed1993

Human circulatory and thermoregulatory adaptations with heat acclimation and exercise in a hot, dry environment.

1. Heat acclimation was induced in eight subjects by asking them to exercise until exhaustion at 60% of maximum oxygen consumption rate (VO2) for 9-12 consecutive days at an ambient temperature of 40 degrees C, with 10% relative humidity (RH). Five control subjects exercised similarly in a cool environment, 20 degrees C, for 90 min for 9-12 days; of these, three were exposed to exercise at 40 degrees C on the first and last day. 2. Acclimation had occurred as seen by the increased average endurance from 48 min to 80 min, the lower rate of rise in the heart rate (HR) and core temperature and the increased sweating. 3. Cardiac output increased significantly from the first to the final heat exposure from 19.6 to 21.4 l min-1; this was possibly due to an increased plasma volume and stroke volume. 4. The mechanism for the increased plasma volume may be an isosmotic volume expansion caused by influx of protein to the vascular compartment, and a sodium retention induced by a significant increase in aldosterone. 5. The exhaustion coincided with, or was elicited when, core temperature reached 39.7 +/- 0.15 degrees C; with progressing acclimation processes it took progressively longer to reach this level. However, at this point we found no reduction in cardiac output, muscle (leg) blood flow, no changes in substrate utilization or availability, and no recognized accumulated 'fatigue' substances. 6. It is concluded that the high core temperature per se, and not circulatory failure, is the critical factor for the exhaustion during exercise in heat stress.

Acclimatization↗

PubMed1995

Shifts of thermoeffector thresholds in heat-acclimated rats.

1. Heat-acclimated (HA) rats, kept under a 12:12 h light-dark regime, were subjected to an ambient temperature (Ta) of 33 degrees C for 5 h in the last half of the dark phase for 3 weeks. Control rats were kept under a 12:12 h light-dark regime at a constant Ta of 24 degrees C. 2. After the acclimation period, the rats were then placed in a metabolic chamber at a Ta of 26.5 degrees C, and body core temperature was gradually increased and decreased using an intravenous thermode. Thermoeffector thresholds were determined by the hypothalamic temperature (T(hy)) at the onset of warm-induced tail skin vasodilatation and cold-induced thermogenesis measured by oxygen consumption. 3. Each rat was subjected to the experiment twice, once in the first half and once in the last half of the dark phase, on different days in random order. 4. In HA rats, T(hy) at the onset of both skin vasodilatation and thermogenesis were significantly lower in the last half of the dark phase compared with the first half. In control rats, however, there were no such differences between the two halves. 5. The results suggest that in rats acclimated to daily heat exposure, thermoeffector thresholds shift to lower temperatures only during the period of day when the rats had previously been exposed to heat.

Adaptation, Physiological↗

PubMed1988

Effect of inorganic nutrients on the acclimation period preceding mineralization of organic chemicals in lake water.

The addition of phosphate, nitrate, or sulfate (each at 10 mM) decreased the acclimation period for the mineralization of low concentrations of p-nitrophenol (PNP) in lake water. Added phosphate shortened the acclimation period for biodegradation of 2 ng to 2 micrograms of PNP per ml in various lake water samples and of 2,4-dichlorophenoxyacetate at 100 ng/ml. Added P enhanced the rate of growth of PNP-mineralizing microorganisms in waters containing 200 ng or 2 micrograms of PNP per ml. We suggest that the effect of P on the acclimation period results from an increase in the growth rate of the initially small population of microorganisms able to mineralize the synthetic chemicals.

Acclimatization↗

PubMed1989

Reductive dehalogenation of dichloroanilines by anaerobic microorganisms in fresh and dichlorophenol-acclimated pond sediment.

We investigated the transformation of 2,4-dichloroaniline (2,4-DiCA) and 3,4-DiCA to monochloroanilines (CA) in anaerobic pond sediment. Dechlorination of 3,4-DiCA to 3-CA started after a lag period of 3 weeks and was complete after an additional 5 weeks. Although 2,4-DiCA disappeared over 8 weeks, the appearance of a CA product could not be detected. In contrast, anaerobic bacteria in pond sediment acclimated to dehalogenate 2,4-dichlorophenol (2,4-DiCP) or 3,4-DiCP rapidly dechlorinated 2,4-DiCA and 3,4-DiCA without any lag time. By comparison, anaerobic sediment bacteria acclimated to 3,4-DiCA rapidly degraded 3,4-DiCP without a lag. In all cases, the CA products were stable for the duration of the experiments. It is concluded that cross-acclimation occurred.

Acclimatization↗

PubMed1997

Induction of the heat shock protein ClpB affects cold acclimation in the cyanobacterium Synechococcus sp. strain PCC 7942.

The heat shock protein ClpB is essential for acquired thermotolerance in cyanobacteria and eukaryotes and belongs to a diverse group of polypeptides which function as molecular chaperones. In this study we show that ClpB is also strongly induced during moderate cold stress in the unicellular cyanobacterium Synechococcus sp. strain PCC 7942. A fivefold increase in ClpB (92 kDa) content occurred when cells were acclimated to 25 degrees C over 24 h after being shifted from the optimal growth temperature of 37 degrees C. A corresponding increase occurred for the smaller ClpB' (78 kDa), which arises from a second translational start within the clpB gene of prokaryotes. Shifts to more extreme cold (i.e., 20 and 15 degrees C) progressively decreased the level of ClpB induction, presumably due to retardation of protein synthesis within this relatively cold-sensitive strain. Inactivation of clpB in Synechococcus sp. increased the extent of inhibition of photosynthesis upon the shift to 25 degrees C and markedly reduced the mutant's ability to acclimate to the new temperature regime, with a threefold drop in growth rate. Furthermore, around 30% fewer delta clpB cells survived the shift to 25 degrees C after 24 h compared to the wild type, and more of the mutant cells were also arrested during cell division at 25 degrees C, remaining attached after septum formation. Development of a cold thermotolerance assay based on cell survival clearly demonstrated that wild-type cells could acquire substantial resistance to the nonpermissive temperature of 15 degrees C by being pre-exposed to 25 degrees C. The same level of cold thermotolerance, however, occurred in the delta clpB strain, indicating ClpB induction is not necessary for this form of thermal resistance in Synechococcus spp. Overall, our results demonstrate that the induction of ClpB contributes significantly to the acclimation process of cyanobacteria to permissive low temperatures.

Adaptation, Physiological↗

PubMed2004

Involvement of the SppA1 peptidase in acclimation to saturating light intensities in Synechocystis sp. strain PCC 6803.

The sll1703 gene, encoding an Arabidopsis homologue of the thylakoid membrane-associated SppA peptidase, was inactivated by interposon mutagenesis in Synechocystis sp. strain PCC 6803. Upon acclimation from a light intensity of 50 to 150 microE m(-2) s(-1), the mutant preserved most of its phycobilisome content, whereas the wild-type strain developed a bleaching phenotype due to the loss of about 40% of its phycobiliproteins. Using in vivo and in vitro experiments, we demonstrate that the DeltasppA1 strain does not undergo the cleavage of the L(R)(33) and L(CM)(99) linker proteins that develops in the wild type exposed to increasing light intensities. We conclude that a major contribution to light acclimation under a moderate light regime in cyanobacteria originates from an SppA1-mediated cleavage of phycobilisome linker proteins. Together with changes in gene expression of the major phycobiliproteins, it contributes an additional mechanism aimed at reducing the content in phycobilisome antennae upon acclimation to a higher light intensity.

Acclimatization↗

PubMed1996

Heat strain in protective clothing following hot-wet or hot-dry heat acclimation.

The purpose of the present study was to compare the heat strain while wearing nuclear, biological, and chemical (NBC) protective clothing following a hot-wet (HW) or hot-dry (HD) heat acclimation protocol. Twenty-two males were assigned to groups HW (n = 7), HD (n = 8), or control (C, n = 7). Subjects were evaluated during continuous treadmill walking while wearing lightweight combat clothing and during intermittent exercise while wearing the NBC protective clothing. While wearing Combat clothing, greater decreases in rectal temperature (Tre), mean skin temperature (Tsk), and heart rate were observed for both acclimation groups. For the NBC clothing trials, lower Tre, Tsk, and heart rates were observed only for group HW. The time required for Tre to increase 1.0 degrees C and 1.5 degrees C was significantly delayed for groups HW and HD. Sweat evaporation increased for HW, whereas no change was found for HD. The most significant changes in Tre, Tsk, and heart rate while wearing the NBC protective clothing occur following heat acclimation that involves wearing the clothing during exercise.

Acclimatization↗

PubMed1977

Increased lipoprotein lipase activity of skeletal muscle in cold-acclimated rats.

The activity of lipoprotein lipase (LPL) in the heart, diaphragm, and soleus muscles was markedly increased in cold-acclimated rats and it was even greater in rats treated with oxytetracycline (OTC) while exposed to cold. Other skeletal muscles studied had low and variable activities which were not significantly increased by cold acclimation or by cold plus OTC treatment. It appears therefore that, apart from the heart and the muscles involved in respiratory movements, LPL activity is primarily associated with those muscles which contain a predominance of slow-twitch oxidative fibers, and that the enzyme in muscle, heart, and diaphragm responds to cold acclimation and cold plus OTC treatment in a parallel fashion in these tissues.

Acclimatization↗

PubMed1982

Growth of interscapular brown adipose tissue in cold-acclimated hypophysectomized rats maintained on thyroxine and corticosterone.

Brown adipose tissue (BAT) of rats is known to grow in response to acclimation to cold. The growth is accompanied by changes in mitochondrial polypeptide composition (an increase in the relative proportion of a polypeptide of molecular weight 32,000, known to be associated with the thermogenic proton conductance pathway). The mediator of the change in mitochondrial polypeptide composition is unknown. The objective of these experiments was to find out whether any of the pituitary hormones might be the mediator. Treatment of rats with growth hormone failed to alter BAT size or mitochondrial polypeptide composition. BAT grew and the change in BAT mitochondrial polypeptide composition occurred in cold-acclimated hypophysectomized rats, maintained on thyroxine and corticosterone to ensure their survival in the cold. It is concluded that none of the pituitary hormones is the mediator for the cold-induced change in BAT mitochondrial polypeptide composition or is required to exert a direct effect on BAT for cold-induced BAT growth to occur. It also seems unlikely that more than a maintenance amount of glucocorticoids is required for normal cold-induced growth of BAT; these hormones are thus also unlikely to mediate the change in BAT mitochondrial polypeptide composition. The requirement for no more than a maintenance amount of thyroxine for BAT growth and for the cold-induced change in BAT mitochondrial polypeptide composition confirms previous conclusions drawn from studies on cold-acclimated thyroidectomized rats.

Acclimatization↗

PubMed1976

Norepinephrine thermogenesis in seasonally acclimatized and cold acclimated red-backed voles in Alaska.

The calorigenic response (millilitres O2 per gram pre hour) to injected norepinephrine (NE) was compared as an index of nonshivering thermogenesis (NST) in the following groups of the Alaska red-backed vole (Clethrionomys rutilus): (1) summer, (2) fall acclimatized, (3) winter acclimatized, (4) 20 degrees C acclimated and (5) 5 degrees C acclimated. The metabolic response was tested at thermoneutrality (25 degrees C) and during cold exposure (5 degrees C). Winter acclimatized voles showed a significantly greater metabolic response to NE than summer voles at both 25 degrees C and 5 degrees C. In summer or winter voles the total metabolic rate after NE (Mne) was similar at 25 degrees C and 5 degrees C but the fraction of the total caused by exogenous NE was lower at 5 degrees C. Thus, thermogenesis during cold exposure and resulting from exogenous NE appear to be based on the same mechanism, and NE has thermoregulatory significance in these voles. The magnitude of the NE response in winter voles was comparable to he highest values reported for bats and exceeded levels reported for other adult small mammal species. Summer acclimatized voles and those acclimatized to 20 degrees C in the laboratory were comparable in their response to NE but winter acclimatized voles were significantly more sensitive to NE than voles acclimated to 5 degrees C. The seasonal winter peak in MNE coincided with peaks previously found for maximum metabolic capacity (MMAX), maximum brown fat, and the period of coldest temperature in December-January. the ratio of MNE to Mmax was similar throughout the year. The results suggest that small arctic-subarctic rodents have a greater capacity for NE stimulated NST than rodents from temperate latitudes probably because they are acclimatized to colder seasonal condtions.

Acclimatization↗

PubMed1977

Reduced hyperglycemic action of glucagon in cold-acclimated rats, especially in venous drainage from brown adipose tissue.

Glucagon infusion at a rate of 2 microgram/min for 30 min into warm-acclimated rats induced a marked rise of glucose concentration in venous blood both in the external jugular vein and in Sulzer's vein from the interscapular brown adipose tissue. In cold-acclimated rats the increase in the concentration of glucose was significantly reduced in the former vein and abolished in the latter one. These results suggest an enhanced use of glucose in the brown adipose tissue in cold-acclimated animals under the influence of glucagon.

Acclimatization↗

PubMed1980

Noradrenaline-induced calorigenesis in warm- and cold-acclimated rats: relations between concentration of noradrenaline in arterial plasma, blood flow to differently located masses of brown adipose tissue, and calorigenic response.

Barbital-sedated, warm-acclimated (WA) or cold-acclimated (CA) rats were infused intravenously with noradrenaline (NA) at doses that elicited graded calorigenic responses. Blood flow (Q) to the various bodies of brown adipose tissue (BAT), the major sites of the NA-induced calorigenesis, was measured with labeled microspheres. The O2 content of arterial blood and of venous blood from interscapular BAT and the concentration of NA in arterial plasma (ANA) were also determined. ANA was linearly related to the dose of NA. Calorigenic response and the Q of total BAT and of separate bodies of BAT were sigmoid functions of ANA. The threshold for calorigenic response or for increased flow to BAT was an ANA of about 2 ng/mL (12 nM), except for some bodies of BAT in CA rats where it was closer in 4 ng/mL. Delivery of O2 to total BAT and calorigenic response were related linearly. The bodies of BAT were heterogeneous in Q per gram in CA rats the hierarchy in Q per gram changed markedly as ANA and calorigenic response increased. The analysis of these results takes into account that calorigenesis in BAT normally is not mediated by circulating NA, that in NA-infused rats neuronal and extraneuronal uptakes of NA would effect a lower concentration of NA at the adrenoceptors of BAT than in circulation, and that many factors such as organization and density of adrenergic innervation and the number of efficacy of receptors must have contributed to determining the measured responses of BAT. It is concluded that the differently located bodies of BAT in rats may have significant differences in composition and structure and that they may undergo differential development during cold acclimation.

Acclimatization↗

PubMed1980

Noradrenaline-induced calorigenesis in warm- or cold-acclimated rats. In vivo estimation of adrenoceptor concentration of noradrenaline effecting half-maximal response.

Desmethylimipramine (DMI, 1 mg DMI . HCl kg-1) and normetanephrine (NMN, 1 microgram min-1 g-0.74) were used to inhibit, respectively, neuronal and extraneuronal uptakes of noradrenaline (NA) during calorigenesis induced in barbital-sedated warm-acclimated (WA) or cold-acclimated (CA) rats by infusion of NA, a procedure which mimics the effects of NA released within calorigenic tissues in response to cold exposure. The doses of the inhibitors were selected for maximal effectiveness in potentiating calorigenic response and for minimal side effects. For rats of either acclimation group treated with DMI and NMN, with DMI only, or with neither inhibitor the doses of NA required to evoke approximately half-maximal calorigenic responses were, respectively, 0.5, 1.0, and 3.5 ng min-1 g-0.74. The corresponding steady-state concentrations of NA in arterial plasma averaged 14.3, 21.7, and 43.2 nM in the three groups of WA rats and 10.0, 14.8, and 31.9 nM in the three groups of CA rats. Reduction by NA uptake inhibitors of the circulating levels of NA necessary to stimulate calorigenesis, half-maximally, presumably in brown adipose tissue, indicates a reduction in the steepness of the NA concentration gradient between capillary plasma and synaptic clefts in that tissue. The steady-state concentration of NA in blood plasma of rats treated with DMI and NMN and infused with NA at a dose of 0.5 ng min-1 g-0.74 (approximately 1 x 10(-8) M) is a good estimate of the NA concentration required at calorigenic adrenoceptors to effect half-maximal activation. Presumably, this concentration is also an estimate of that resulting from NA released at nerve endings during cold-induced activation of nonshivering thermogenesis at half-maximal rates in brown adipose tissue.

Acclimatization↗

PubMed1981

Effects of adrenaline and noradrenaline on the heat production of warm- and cold-acclimated sheep.

The heat production (HP), heart rate (HR), respiration rate, rumen motility, and body temperature responses to 2.5-h adrenaline (A) and noradrenaline (NA) intrajugular infusions at 0.00, 0.15, 0.30, 0.60, and 0.90 micrograms.kg-1.min-1 were studied in 10 shorn wethers which had been chronically (3-8 weeks) exposed to warm (19-24 degrees C) or moderately cold (8-13 degrees C) temperatures. Heat production, as estimated from respired gas analysis, increased 40-45% with all doses of A and the effect was potentiated by chronic cold exposure. Only the higher dose rates of NA induced an increase in HP. The maximum HP increase due to NA was 30% and the effect was not influenced by chronic cold exposure. Thermoneutral HP was greater by 16-19% in cold-acclimated as compared with warm-acclimated sheep. Corresponding to the HP effects of A and NA, all doses of A and the highest dose of NA resulted in slight increases in rectal temperature. Respiration rate increased with increased dose rate of NA but only the highest dose of a resulted in an increase in respiration rate. HR, rectal temperature, and respiration rate responses to A and NA were not influenced by cold acclimation.

Acclimatization↗

PubMed1991

Adipose tissue lipolytic activity and urinary catecholamine excretion in cold-acclimated piglets.

This study was designed to investigate the effect of chronic cold exposure (12 degrees C for 3 weeks) on catecholamine production and noradrenaline-induced lipolytic rate to further describe thermoregulatory mechanisms in 5- to 8-week-old pigs. Lipolytic activity in white adipose tissue was assessed in vitro while catecholamine production was estimated by measuring noradrenaline, adrenaline, and dopamine levels in 24-h urine samples. Animals were fed ad libitum and food intake was 20% greater in the cold. In control piglets maintained in a 23 degrees C environment, the addition of increasing amounts of noradrenaline (10(-6), 10(-5), 10(-4) M) stimulates lipolysis (p less than 0.05) and enhances the basal lipolytic rate (5.4 mu equiv. fatty acids.120 min-1.g-1 tissue) by 2.5-, 2.7-, and 3.9-fold, respectively. Three weeks of cold acclimation had no effect on basal lipolytic rate but increased significantly noradrenaline responsiveness: incubation of subcutaneous white fat in the presence of 10(-4) M noradrenaline does increase the basal lipolytic rate by sixfold. Noradrenaline effects were maximally activated by theophylline. Daily dopamine and noradrenaline excretions (3-10 micrograms/24 h) were increased significantly (up to eightfold) after 10 days of cold acclimation. By contrast, adrenaline excretion was quite low (0.6-1.6 micrograms/24 h) and showed no significant variation with time. It is likely that these hormonal and biochemical modifications play a prominent part in the mechanism of cold acclimation in the piglet. Their significance in the development of shivering and nonshivering thermogenesis is discussed in relation to the supply of energy substrates to the fatty acid utilizing tissues and to the possible uncoupling effect of free fatty acids.

Acclimatization↗

PubMed1993

Sarcoplasmic reticulum Ca(2+)-ATPase and ryanodine receptor in cold-acclimated ducklings and thermogenesis.

In birds, prolonged cold exposure induces the development of a nonshivering thermogenesis (NST) of muscular origin. NST is characterized by an increased heat production, which may be achieved by an increased ATP-dependent cycling of Ca2+ between the sarcoplasmic reticulum (SR) and cytosolic compartments in muscle. In this study, the effects of prolonged cold exposure on SR function were assessed by determining the contents of the SR Ca(2+)-ATPase and Ca2+ release channel (ryanodine receptor) in the gastrocnemius muscle of ducklings (Cairina moschata) kept at thermoneutrality (25 degrees C) or cold acclimated (4 degrees C, 5 wk). Measurement of oxalate-supported 45Ca2+ uptake by whole muscle homogenates revealed that the SR Ca(2+)-ATPase activity, and fraction of vesicles containing a ryanodine-sensitive Ca2+ release channel were increased by 30-50% in response to prolonged cold exposure. Sodium dodecyl sulfate-polyacrylamide gel and immunoblot analysis, 45Ca2+ uptake, Ca(2+)-ATPase activity and [3H]ryanodine binding measurements with unfractionated and "heavy" SR membrane fractions also indicated an elevated Ca(2+)-ATPase and Ca2+ release channel content in cold-acclimated ducklings. These results showed that the contents of two components directly involved in Ca2+ cycling by the SR are increased by cold acclimation, and we suggest that this is related to NST.

Acclimatization↗

PubMed1988

Adaptive changes in individual acyl-CoA esters from hamster BAT during cold acclimation.

Long-chain fatty acyl-CoA esters (LCFACoAE) were extracted from freeze-clamped powdered brown adipose tissue (BAT) obtained from thermoneutral control and cold-acclimated hamsters and the CoA esters individually separated by high-performance liquid chromatography. LCFACoAE of carbon chain length C12 to C20 were identified by increasing column retention time in the following order: C12:0, C14:1, C14:0, C16:1, C18:2, C16:0, C18:1, C18:0, and C20:4. The mean total LCFACoAE concentrations were 235 +/- 40 nmol/g protein for the control hamsters and 648 +/- 105 nmol/g protein for the 22-day cold-acclimated hamsters. A rapid fourfold increase in the levels of C16:0, C18:0, and C18:1 occurred within hours after initiation of the cold temperature, whereas the concentrations of the other six LCFACoAE either increased only slightly or remained unchanged. Almost 50% of the total LCFACoAE in the BAT of cold-acclimated hamsters was made up of C16:0, C18:0, and C18:1. These results, which demonstrate some dynamic changes in adipose tissue LCFACoAE, are consistent with their proposed role in the initiation and maintenance of BAT thermogenesis.

Acclimatization↗

PubMed2004

Salinity acclimation affects the somatotropic axis in rainbow trout.

In this study, we set out to examine the role of the somatotropic axis in the ion-regulation process in rainbow trout. Specifically, our objective was to examine whether plasma insulin-like growth factor-binding proteins (IGFBPs) are modulated by gradual salinity exposure. To this end, freshwater (FW)-adapted rainbow trout were subjected to gradual salinity increases, up to 66% seawater, over a period of 5 days. During this acclimation process, minimal elevations in plasma Ca2+ and Cl- were seen in the salinity-acclimated groups compared with FW controls. There were no changes in plasma Na+ levels, and only a minor transient change in plasma cortisol levels was seen with salinity exposure. The salinity challenged animals responded with elevations in plasma growth hormone (GH) and IGF-I levels and gill Na+-K+-ATPase activity. We identified IGFBPs of 21, 32, 42, and 50 kDa in size in the plasma of these animals, and they were consistently higher with salinity. Despite the overall increase in IGFBPs with salinity, transient changes in individual BPs over the 5-day period were noted in the FW and salinity-exposed fish. Specifically, the transient changes in plasma levels of the 21-, 42-, and 50-kDa IGFBPs were different between the FW and salinity groups, while the 32-kDa IGFBP showed a similar trend (increases with sampling time) in both groups. Considered together, the elevated plasma IGFBPs suggest a key role for these binding proteins in the regulation of IGF-I during salinity acclimation in salmonids.

Acclimatization↗