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PubMed2005

Steady-state effects of temperature acclimation on the transcriptome of the rainbow trout heart.

Cold-acclimated (CA) phenotype of trout heart was induced by 4-wk acclimation at 4 degrees C and was characterized by 32.7% increase in relative heart mass and 49.8% increase in ventricular myocyte size compared with warm-acclimated (WA; 18 degrees C) fish (P < 0.001). Effect of temperature acclimation on transcriptome of the rainbow trout heart was examined using species-specific microarray chips containing 1,380 genes. After 4 wk of temperature acclimation, 8.8% (122) of the genes were differently expressed in CA and WA hearts, and most of them (82%) were upregulated in the cold (P < 0.01). Transcripts of genes engaged in protein synthesis and intermediary metabolism were most strongly upregulated, whereas genes contributing to the connective tissue matrix were clearly repressed. Extensive upregulation of the genes coding for ribosomal proteins and translation elongation and initiation factors suggest that the protein synthesis machinery of the trout heart is enhanced in the cold and is an essential part of the compensatory mechanism causing and maintaining the hypertrophy of cardiac myocytes. The prominent depression of collagen genes may be indicative of a reduced contribution of extracellular matrix to the remodeling of the CA fish heart. Temperature-related changes in transcripts of metabolic enzymes suggest that at mRNA level, glycolytic energy production from carbohydrates is compensated in the heart of CA rainbow trout, while metabolic compensation is absent in mitochondria. In addition, the analysis revealed three candidate genes: muscle LIM protein, atrial natriuretic peptide B, and myosin light chain 2, which might be central for induction and maintenance of the hypertrophic phenotype of the CA trout heart. These findings indicate that extensive modification of gene expression is needed to maintain the temperature-specific phenotype of the fish heart.

Acclimatization↗

PubMed2006

Gill Na+-K+-ATPase activity correlates with basolateral membrane lipid composition in seawater- but not freshwater-acclimated Arctic char (Salvelinus alpinus).

The successful migration of euryhaline teleost fish from freshwater to seawater requires the upregulation of gill Na+-K+-ATPase, an ion transport enzyme located in the basolateral membrane (BLM) of gill chloride cells. Following 39 days of seawater exposure, Arctic char had similar plasma sodium and chloride levels as individuals maintained in freshwater, indicating they had successfully acclimated to seawater. This acclimation was associated with an eightfold increase in gill Na+-K+-ATPase activity but only a threefold increase in gill Na+-K+-ATPase protein number, suggesting that other mechanisms may also modulate gill Na+-K+-ATPase activity. We therefore investigated the influence of membrane composition on Na+-K+-ATPase activity by examining the phospholipid, fatty acid, and cholesterol composition of the gill BLM from freshwater- and seawater-acclimated Arctic char. Mean gill BLM cholesterol content was significantly lower ( approximately 22%) in seawater-acclimated char. Gill Na+-K+-ATPase activity in individual seawater Arctic char was negatively correlated with BLM cholesterol content and positively correlated with %phosphatidylethanolamine and overall %18:2n6 (linoleic acid) content of the BLM, suggesting gill Na+-K+-ATPase activity of seawater-acclimated char may be modulated by the lipid composition of the BLM and may be especially sensitive to those parameters known to influence membrane fluidity. Na+-K+-ATPase activity of individual freshwater Arctic char was not correlated to any membrane lipid parameter measured, suggesting that different lipid-protein interactions may exist for char living in each environment.

Acclimatization↗

PubMed2003

Humid heat acclimation does not elicit a preferential sweat redistribution toward the limbs.

We tested the hypothesis that local sweat rates would not display a systematic postadaptation redistribution toward the limbs after humid heat acclimation. Eleven nonadapted males were acclimated over 3 wk (16 exposures), cycling 90 min/day, 6 days/wk (40 degrees C, 60% relative humidity), using the controlled-hyperthermia acclimation technique, in which work rate was modified to achieve and maintain a target core temperature (38.5 degrees C). Local sudomotor adaptation (forehead, chest, scapula, forearm, thigh) and onset thresholds were studied during constant work intensity heat stress tests (39.8 degrees C, 59.2% relative humidity) conducted on days 1, 8, and 22 of acclimation. The mean body temperature (Tb) at which sweating commenced (threshold) was reduced on days 8 and 22 (P < 0.05), and these displacements paralleled the resting thermoneutral Tb shift, such that the Tb change to elicit sweating remained constant from days 1 to 22. Whole body sweat rate increased significantly from 0.87 +/- 0.06 l/h on day 1 to 1.09 +/- 0.08 and 1.16 +/- 0.11 l/h on days 8 and 22, respectively. However, not all skin regions exhibited equivalent relative sweat rate elevations from day 1 to day 22. The relative increase in forearm sweat rate (117 +/- 31%) exceeded that at the forehead (47 +/- 18%; P < 0.05) and thigh (42 +/- 16%; P < 0.05), while the chest sweat rate elevation (106 +/- 29%) also exceeded the thigh (P < 0.05). Two unique postacclimation observations arose from this project. First, reduced sweat thresholds appeared to be primarily related to a lower resting Tb, and more dependent on Tb change. Second, our data did not support the hypothesis of a generalized and preferential trunk-to-limb sweat redistribution after heat acclimation.

Acclimatization↗

PubMed1994

Cold acclimation increases carnitine palmitoyltransferase I activity in oxidative muscle of striped bass.

The effect of thermal acclimation on the activity of carnitine palmitoyltransferase I (CPT I), the rate-limiting enzyme for beta-oxidation of long-chain fatty acids, was determined in oxidative red muscle of striped bass (Morone saxatilis) acclimated at 5 or 25 degrees C. As observed in mammalian tissues, malonyl-CoA potently inhibited CPT I activity of mitochondria. Inhibition by malonyl-CoA required inclusions of both bovine serum albumin (BSA) and palmitoyl-CoA in the reaction media. Because BSA binds long-chain fatty acyl-CoAs, this observation suggests that free fatty acyl-CoAs may disrupt mitochondrial membranes and affect the CPT I protein. Cold acclimation increased citrate synthase activity 1.6-fold and total CPT activity 2-fold in homogenates of red muscle; free carnitine increased 62%, and specific activity of CPT I in mitochondria increased 2-fold. No differences were observed between cold- and warm-acclimated fish in substrate-binding properties of CPT I at an assay temperature of 15 degrees C, as judged by the Michaelis constant (Km) for carnitine (0.11 +/- 0.02 vs. 0.13 +/- 0.02 mM) or inhibition of CPT I, as determined by the half-maximal inhibition concentration (IC50) for malonyl-CoA (0.14 +/- 0.05 vs. 0.09 +/- 0.03 microM). Thermal sensitivity of CPT I (Q10 = 2.91 +/- 0.12 vs. 3.02 +/- 0.20) and preference of CPT I for different long-chain fatty acyl-CoA substrates (16:1-CoA = 16:0-CoA > 18:1-CoA) were not altered by thermal acclimation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1998

Influence of acclimation temperature on mitochondrial DNA, RNA, and enzymes in skeletal muscle.

Skeletal muscle fibers typically undergo modifications in their mitochondrial content, concomitant with alterations in oxidative metabolism that occur during the development of muscle fiber and in response to physiological stimuli. We examined how cold acclimation affects the mitochondrial properties of two fish skeletal muscle fiber types and how the regulators of mitochondrial content differed between tissues. After 2 mo of acclimation to either 4 or 18 degrees C, mitochondrial enzyme activities in both red and white muscle were higher in cold-acclimated fish. No significant differences were detected between acclimation temperatures in the abundance of steady-state mitochondrial mRNA (cytochrome-c oxidase 1, subunit 6 of F0F1-ATPase), rRNA (16S), or DNA copy number. Steady-state mRNA for nuclear-encoded respiratory (adenine nucleotide translocase 1) and glycolytic genes showed high interindividual variability, particularly in the cold-acclimated fish. Although mitochondrial enzymes were 10-fold different between the two muscle types, mitochondrial DNA copy number differed only 4-fold. The relative abundance of mitochondrial mRNA and nuclear mRNA in red and white muscle reflected the differences in copy number of their respective genes. These data suggest that the response to physiological stimuli and determination of tissue-specific mitochondrial properties likely result from the regulation of nuclear-encoded genes.

Acclimatization↗

PubMed1999

Core temperature and sweating onset in humans acclimated to heat given at a fixed daily time.

The thermoregulatory functions of rats acclimated to heat given daily at a fixed time are altered, especially during the period in which they were previously exposed to heat. In this study, we investigated the existence of similar phenomena in humans. Volunteers were exposed to an ambient temperature (Ta) of 46 degrees C and a relative humidity of 20% for 4 h (1400-1800) for 9-10 consecutive days. In the first experiment, the rectal temperatures (Tre) of six subjects were measured over 24 h at a Ta of 27 degrees C with and without heat acclimation. Heat acclimation significantly lowered Tre only between 1400 and 1800. In the second experiment, six subjects rested in a chair at a Ta of 28 degrees C and a relative humidity of 40% with both legs immersed in warm water (42 degrees C) for 30 min. The Tre and sweating rates at the forearm and chest were measured. Measurements were made in the morning (0900-1100) and afternoon (1500-1700) on the same day before and after heat acclimation. Heat acclimation shortened the sweating latency and decreased the threshold Tre for sweating. However, these changes were significant only in the afternoon. The results suggest that repeated heat exposure in humans, limited to a fixed time daily, alters the core temperature level and thermoregulatory function, especially during the period in which the subjects had previously been exposed to heat.

Acclimatization↗

PubMed1975

Rabbit's ear in cold acclimation studied on the change in ear temperature.

The role of the rabbit's ear in cold acclimation was studied by varying the temperature of a climatic room in the range from -10 to +30 degrees C; The skin temperature in a nonanesthetized rabbit's ear showed a characteristic response to changes in ambient temperatures; plotting the ear temperature against the ambient temperature yielded an S-shaped curve. The mean ambient temperature corresponding to the inflection point on the S-shaped curve shifted significantly from about 13 degrees C to about 8 degrees C after cold acclimated of a group fed for 7 wk at -10 degrees C. The shift of the S-shaped curve after cold acclimation may not be due to the change in the norepinephrine sensitivity of the vascular beds of the ear: the effect of norepinephrine on the pressure-flow curve in the isolated rabbit's ear was almost unchanged between the control and the cold-acclimated groups. It is proposed that the shift of the inflection point gives a qualitative index of the acclimated state of the rabbit at a particular temperature.

Acclimatization↗

PubMed1976

Fever: exchange of shivering by nonshivering pyrogenesis in cold-acclimated guinea pigs.

The pyrogenic response of adult, unanesthetized guinea pigs to 2 mug/kg iv of Salmonella enteritidis endotoxin was measured at 27 and 7 degrees C ambient temperatures, both before and after an 8-wk exposure to 7 degrees C. There were no significant differences between the onset, maximum height, and total duration of the fevers produced before and after cold acclimation in both thermal environments. However, in 27 degrees C, before cold acclimation, fever production was associated with vigorous shivering activity; two temperature maxima typically developed. After cold acclimation, visible shivering was not detectable during pyrogenesis; moreover, only a single maximum occurred, culminating during the interval between the two rises previously. In 7 degrees C, shivering occurred in both the non-cold- and cold-acclimated endotoxin-treated guinea pigs, but the increase in oxygen consumption was significantly greater in the latter. These results indicated, therefore, that nonshivering (NST) replaces shivering thermogenesis (ST) in a thermoneutral, while ST is added onto NST in a cold, environment in cold-acclimated guinea pigs in supplying the necessary heat for fever production, and that these effects involve alterations in the character of the febrile course.

Adipose Tissue, Brown↗

PubMed1979

Effect of training and heat acclimation on exercise responses of sedentary females.

In an attempt to explain why females experience greater strain than males during exercise in the heat, we studied the responses of nine females to moderate exercise (40% VO2 max) on a cycle ergometer in a cool (16--20 degrees C, 30% rh) and a hot (45 degrees C, 30% rh) environment. Venous blood was sampled during rest, at the 40th min of exercise, and 25 min after exercise. Test runs were then performed during a 4-wk training program (phase 2) and during heat acclimation (phase 3). Except for K+, changes in plasma constituents during exercise were not altered by training or acclimation. A greater mean decrease in plasma volume occurred during exercise in a hot (11.9%) than in a cool (3.9%) environment. Plasma osmolality and protein concentration increased due to the loss of plasma water. The most striking response to training was a significant expansion of resting plasma volume (9.7%) and total protein content (11.6%). During acclimation, sweat rates increased and mean skin temperatures significantly decreased. Hemodilution reported in heat-acclimated men was not seen. The factor primarily responsible for improved cardiovascular fitness in these women during acclimation may have been the maintenance of a larger central blood volume.

Adult↗

PubMed1980

Body fluid and hematologic adjustments during resting heat acclimation in rhesus monkey.

The purpose of this study was to examine body fluid adjustments during prolonged resting heat exposure in primates. Rhesus monkeys were acclimated for 35 days at 35 degrees C and 30% rh. Red cell mass, extracellular fluid volume (ECF), and total body water (TBW) were determined with 51Cr, 35SO4, and 3H2O, respectively, prior to and at intervals during heat exposure. Heat acclimation was characterized by a fluid shift from the interstitial compartment. In relation to TBW, interstitial fluid volume and ECF decreased 10.3 and 8.3%, respectively, while plasma volume (PV) and intracellular fluid were increased an average of 5.8 and 3.8%. TBW increased 4.8% during heat exposure. Hematocrit and hemoglobin decreased significantly on day 3 (7.9 and 6.5%) followed by a return toward control values. PV in relation to TBW remained elevated throughout the exposure. An increased drinking (25.0%) was associated with a decrease in caloric intake (30.7%) during heat acclimation. This study has provided a complete body fluid compartment analysis during resting heat acclimation in the rhesus monkey. Our results are consistent with the hypothesis that heat acclimation in primates is characterized by a protein and fluid shift from the interstitial fluid compartment to the cardiovascular system and to the intracellular compartment.

Adaptation, Physiological↗

PubMed1986

Plasma aldosterone and sweat sodium concentrations after exercise and heat acclimation.

This investigation was designed to determine the relationship between the levels of plasma aldosterone and eccrine sweat gland sodium excretion following exercise and heat acclimation. Ten subjects exercised at 45% of their maximal O2 uptake in a hot (40 degrees C), moderately humid (45% relative humidity) environment for 2 h/day on ten consecutive days. Acclimation was verified by significant reductions in exercise heart rate, rectal temperature, and heat storage, as well as significant elevation of resting plasma volume (12%, P less than 0.05) and exercise sweat rate on day 10 compared with day 1 of acclimation. During exercise, the concentration and total content of sodium in sweat as well as plasma aldosterone were significantly decreased from day 1 to day 10. The ratio of sweat sodium reabsorbed to plasma aldosterone concentration was significantly increased from day 1 to day 10 after both 1 and 2 h of exercise. These data indicate that plasma aldosterone concentrations decrease following heat acclimation; and eccrine gland responsiveness to aldosterone, as represented by sweat sodium reabsorption, may be augumented through exercise and heat acclimation.

Acclimatization↗

PubMed1994

Thyroid hormone changes in a cold air environment after local cold acclimation.

Serum thyroid hormones (TH) and internal temperatures were investigated in 8 euthyroid men during a general standard cold air test (SCAT) (dry bulb temperature = 1 degree C, 2 h, nude, at rest) performed both before and after a local cold acclimation. Serum total thyroxin (TT4), total triiodothyronine (TT3), free thyroxin (FT4), free triiodothyronine (FT3), and thyrotropin (TSH) were studied during the SCT. The TH values were corrected following the plasmatic volume reduction (delta PV) calculated with Dill and Costill's formula. During SCAT, delta PV reached -9 to -11% (P < 0.05) without any effect of local cold acclimation. Slight TH changes were observed according to delta PV: TT4, TT3, and TSH increased during SCAT (P < 0.05) only before correction. FT4 and FT3 did not vary before correction but increased after correction (P < 0.05). After acclimation, a slightly decreased TT3 was observed both before and after correction (-18% and -11.7%, respectively; P < 0.05). Decreased internal temperatures after local cold acclimation suggested a hypothermic general cold adaptation. It was concluded that TH changes during SCAT differed if correction due to delta PV was applied and that the slight decrease in TT3 observed after local cold acclimation could suggest the presence of a "T3 polar syndrome."

Acclimatization↗

PubMed1995

Thermoregulatory responses of rats acclimated to heat given daily at a fixed time.

Body core temperature of rats acclimated to heat given daily at a fixed time falls during the previous heat exposure time. In the present study, thermoregulatory responses of heat-acclimated rats were examined during the specific period. Heat-acclimated rats were subjected to an ambient temperature of 32 degrees C for approximately 5 h in the first half or last half of the dark phase for 14 days while control rats were kept at 24 degrees C. Then the rats were placed in a direct calorimeter and were warmed for 30 min with an intraperitoneal electric heater. Measurements were made twice in the first and last halves of the dark phase. Body warming significantly increased body core temperature in all rats. In the heat-acclimated rats, heat production (M) was significantly depressed during the previous heat exposure time but not during the other period. Body warming had little effect on M in the control rats during either period. The results suggest that rats acclimated to heat given at a fixed time daily respond to an acute heat load with a pronounced reduction of M. However, such a response was observed only during the period when the rats had been previously exposed to heat.

Acclimatization↗

PubMed1998

Heat acclimation, aerobic fitness, and hydration effects on tolerance during uncompensable heat stress.

The purpose of the present study was to determine the separate and combined effects of aerobic fitness, short-term heat acclimation, and hypohydration on tolerance during light exercise while wearing nuclear, biological, and chemical protective clothing in the heat (40 degrees C, 30% relative humidity). Men who were moderately fit [(MF); <50 ml . kg-1 . min-1 maximal O2 consumption; n = 7] and highly fit [(HF); >55 ml . kg-1 . min-1 maximal O2 consumption; n = 8] were tested while they were euhydrated or hypohydrated by approximately 2.5% of body mass through exercise and fluid restriction the day preceding the trials. Tests were conducted before and after 2 wk of daily heat acclimation (1-h treadmill exercise at 40 degrees C, 30% relative humidity, while wearing the nuclear, biological, and chemical protective clothing). Heat acclimation increased sweat rate and decreased skin temperature and rectal temperature (Tre) in HF subjects but had no effect on tolerance time (TT). MF subjects increased sweat rate but did not alter heart rate, Tre, or TT. In both MF and HF groups, hypohydration significantly increased Tre and heart rate and decreased the respiratory exchange ratio and the TT regardless of acclimation state. Overall, the rate of rise of skin temperature was less, while DeltaTre, the rate of rise of Tre, and the TT were greater in HF than in MF subjects. It was concluded that exercise-heat tolerance in this uncompensable heat-stress environment is not influenced by short-term heat acclimation but is significantly improved by long-term aerobic fitness.

Acclimatization↗

PubMed1999

Heat acclimation does not alter rat mesenteric artery response to norepinephrine.

Previous studies have shown that heat acclimation raises the temperature threshold for heat-induced splanchnic vasoconstriction in the rat (W. Haddad and M. Horowitz. Thermal Balance in Health and Disease, Advances in Pharmacological Sciences. Basel: Birkhauser, 1994, p. 203-208; M. Shochina, W. Haddad, U. Meiri, and M. Horo-witz. J. Therm. Biol. 21: 289-295, 1996). We tested the hypothesis that heat acclimation alters splanchnic resistance artery sensitivity to norepinephrine (NE). Male Sprague-Dawley rats (n = 5) were acclimated to 35 degreesC ambient temperature for 5-8 wk. Control rats (n = 5) were maintained at 22-23 degreesC ambient temperature for 5-7 wk. Small mesenteric artery segments (2- to 3-mm length, 100- to 340-micrometer ID) were isolated, cannulated at both ends, and pressurized to 50 mmHg. Artery luminal diameter was measured in response to cumulative doses of NE (10(-9) to 10(-5) M) by using video microscopy. NE dose response was measured at 37 and 43 degreesC bath temperatures. There were no differences in constriction responses to NE between acclimated and control rat arteries at either 37 or 43 degreesC. We conclude that acclimation does not alter rat mesenteric artery sensitivity to NE.

Acclimatization↗

PubMed2000

Heat storage in horses during submaximal exercise before and after humid heat acclimation.

The effect of humid heat acclimation on thermoregulatory responses to humid and dry exercise-heat stress was studied in six exercise-trained Thoroughbred horses. Horses were heat acclimated by performing moderate-intensity exercise for 21 days in heat and humidity (HH) [34.2-35.7 degrees C; 84-86% relative humidity (RH); wet bulb globe temperature (WBGT) index approximately 32 degrees C]. Horses completed exercise tests at 50% of peak O(2) uptake until a pulmonary arterial temperature (T(pa)) of 41.5 degrees C was attained in cool dry (CD) (20-21.5 degrees C; 45-50% RH; WBGT approximately 16 degrees C), hot dry (HD 0) [32-34 degrees C room temperature (RT); 45-55% RH; WBGT approximately 25 degrees C], and HH conditions (HH 0), and during the second hour of HH on days 3, 7, 14, and 21, and in HD on the 18th day (HD 18) of heat acclimation. The ratios of required evaporative capacity to maximal evaporative capacity of the environment (E(req)/E(max)) for CD, HD, and HH were approximately 1.2, 1.6, and 2.5, respectively. Preexercise T(pa) and rectal temperature were approximately 0.5 degrees C lower (P < 0. 05) on days 7, 14, and 21 compared with day 0. With exercise in HH, there was no effect of heat acclimation on the rate of rise in T(pa) (and therefore exercise duration) nor the rate of heat storage. In contrast, exercise duration was longer, rate of rise in T(pa) was significantly slower, and rate of heat storage was decreased on HD 18 compared with HD 0. It was concluded that, during uncompensable heat stress in horses, heat acclimation provided modest heat strain advantages when E(req)/E(max) was approximately 1.6, but at higher E(req)/E(max) no advantages were observed.

Acclimatization↗

PubMed2006

Acclimatory-phase specificity of gene expression during the course of heat acclimation and superimposed hypohydration in the rat hypothalamus.

The induction of the heat-acclimated phenotype involves reprogramming the expression of genes encoding both constitutive and inducible proteins. In this investigation, we studied the global genomic response in the hypothalamus during heat acclimation, with and without combined hypohydration stress. Rats were acclimated for 2 days (STHA) or for 30 days (LTHA) at 34 degrees C. Hypohydration (10% decrease in body weight) was attained by water deprivation. 32P-labeled RNA samples from the hypothalamus were hybridized onto cDNA Atlas array (Clontech no. 1.2) membranes. Clustering and functional analyses of the expression profile of a battery of genes representing various central regulatory functions of body homeostasis demonstrated a biphasic acclimation profile with a transient upregulation of genes encoding ion channels, transporters, and transmitter signaling upon STHA. After LTHA, most genes returned to their preacclimation expression levels. In both STHA and LTHA, genes encoding hormones and neuropeptides, linked with metabolic rate and food intake, were downregulated. This genomic profile, demonstrating an enhanced transcription of genes linked with neuronal excitability during STHA and enhanced metabolic efficiency upon LTHA, is consistent with our previously established integrative acclimation model. The response to hypohydration was characterized by an upregulation of a large number of genes primarily associated with the regulation of ion channels, cell volume, and neuronal excitability. During STHA, the response was transiently desensitized, recovering upon LTHA. We conclude that hypohydration overrides the heat acclimatory status. It is notable that STHA and hypohydration gene profiles are analogous with the physiological profile described in the response to various types of brain injury.

Acclimatization↗

PubMed2003

HIF-1 is required for heat acclimation in the nematode Caenorhabditis elegans.

Chronic exposure to environmental heat improves tolerance via heat acclimation (AC). Our previous data on mammals indicate that reprogramming the expression of genes coding for stress proteins and energy-metabolism enzymes plays a major role. Knowledge of pathways leading to AC is limited. For their identification, we established a Caenorhabditis elegans AC model and tested mutants in which signaling pathways pertinent to acclimatory responses are mutated. AC attained by maintaining adult C. elegans at 25 degrees C for 18 h enhanced heat endurance of wild-type worms subjected to heat stress (35 degrees C) and conferred protection against hypoxia and cadmium. Survival curves demonstrated that both daf-2 (insulin receptor pathway) showing enhanced heat tolerance and daf-16 loss-of-function (a transcription factor mediating DAF-2 signaling) mutants benefit from AC, suggesting that the insulin receptor pathway does not mediate AC. In contrast, the hif-1 (hypoxia inducible factor) loss-of-function strain did not show acclimation, and non-acclimated vhl-1 and egl-9 mutants (overexpressing HIF-1) had greater heat endurance than the wild type. Like mammals, HIF-1 and HSP72 levels increased in the wild-type AC nematodes. HSP72 upregulation in AC hif-1 mutants was also observed; however, it was insufficient to improve heat/stress tolerance, suggesting that HIF-1 upregulation is essential for acclimation, whereas HSP72 upregulation in the absence of HIF-1 is inadequate. We conclude that HIF-1 upregulation is both an evolutionarily conserved and a necessary component of heat acclimation. The known targets of HIF-1 imply that metabolic adaptations are essential for AC-dependent tolerance to heat and heavy metals, in addition to their known role in hypoxic adaptation.

Acclimatization↗