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PubMed2001

Plasma copper clearance and biliary copper excretion are stimulated in copper-acclimated trout.

Nonacclimated and Cu-acclimated rainbow trout (Oncorhynchus mykiss) exhibited equally rapid clearance of a single bolus of injected (64)Cu (3,780 nmol/kg) from the plasma (32-40 min to half- concentration). Eight hours after Cu injection, approximately 80% of the injected Cu was found in the liver. However, when Cu labeled with (64)Cu was presented intravascularly via continuous infusion at a rate of 158 nmol x kg(-1) x h(-1) for 72 h, Cu-acclimated fish cleared plasma Cu more effectively than nonacclimated fish. The use of chronically implanted cystic bile duct cannulas revealed a fourfold increase in hepatobiliary Cu excretion in Cu-acclimated fish during infusion, demonstrating the important homeostatic role of the liver in Cu metabolism. Extrahepatobiliary Cu excretion, likely through the gills and apparently exceeding biliary Cu excretion, was evident from appearance of (64)Cu in the ambient water but was not altered by Cu acclimation. Cu accumulation in white muscle also played an important a role in copper homeostasis.

Adaptation, Physiological↗

PubMed1976

Carbohydrate metabolism of heat-acclimated hamsters. V. Control of gluconeogenesis.

The rate of gluconeogenesis was similar in liver of both fed heat-acclimated and control hamsters. Twenty-four hours of fasting calsed 6 times elevation in hepatic gluconeogenesis of the control animals whereas only 4 times enhancement of this pathway was found in heat-acclimated animals. Thus, significant difference existed between the two experimental groups in fasting. Triiodothyronine stimulated the rate of gluconeogenesis only in fed heat-acclimated hamsters whereas dibutyryl cyclic AMP caused elevation of this pathway in liver slices of fed control hamsters only. The results suggest that a decrease in hepatic gluconeogenesis in heat acclimation occurs only in fasted animals and it is controlled by thyroid hormones.

Acclimatization↗

PubMed1977

Lipolysis in brown adipose tissue of cold- and heat-acclimated hamsters.

Rates of release of free fatty acids (FFA) and glycerol to the incubation medium by brown adipose tissue (BAT) slices isolated from heat-acclimated (H), cold-acclimated (C), and control (N) hamsters in the absence or presence of epinephrine (E) were studied. Rates of FFA and glycerol release by tissue slices isolated from H and N animals were similar. In tissue slices isolated from C animals rate of release of FFA and glycerol was three times as high. Addition of E to the incubation medium (200 microgram/ml) had no effect on the rate of FFA and glycerol release of slices from C animals, but tripled the rates of slices from N, resulting in similar values for the two groups. In slices from H animals the rate of release was lower than in the other two groups, increasing only 1.5-fold. Pretreatment of N animals with triiodothyronine (T3; 0.8 microgram/100 g daily for 7 days) doubled the rates of FFA and glycerol release. Addition of E to the medium affected both pretreated and nontreated slices similarly. Two possible mechanisms by which temperature acclimation controls the lipolytic rate of BAT are suggested by 1) the concentration of specific enzymes and 2) cellular metabolites and hormones which activate existing systems. It seems that both operate in temperature-acclimated hamsters.

Acclimatization↗

PubMed1979

Influence of air velocity and heat acclimation on human skin wettedness and sweating efficiency.

Before and after heat acclimation, four male resting subjects were exposed to humid heat that caused levels of skin wettedness ranging from 50 to 100%. The physical experimental conditions were chosen so that the same skin wettedness was attained with modification of only the ambient water vapor pressure, at two wind speeds (0.6 and 0.9 m . s-1). The esophageal temperature (Tes), mean skin temperature (Tsk), sweating rate (msw), and dripping sweat rate (mdr) were recorded; the amounts of local drippage in the same thermal conditions before and after acclimation were also determined. The relationship between the evaporative efficiency of sweating (eta sw) and the skin wettedness (w) is reported, as is the influence of the subject's acclimation to humid heat on adjustments of skin wettedness. The effects of the air velocity on the coefficient of evaporation and on sweating efficiency are discussed. Beneficial increases in evaporation were achievable by increasing skin wettedness only when there was a consistent drippage, which differed from one body area to another and from one subject to another. The relation of drift in body temperature to skin wettedness changed with the acclimation of the subjects.

Acclimatization↗

PubMed1980

In vitro hepatic deiodination of L-thyroxine to 3,5,3'-triiodothyronine in cold-acclimated rats.

An in vitro model has been employed to evaluate the effect of cold acclimation on peripheral outer ring deiodination of thyroxine (T4) to triiodothyronine (T3) by 9,000 g supernatants of fresh liver homogenates. Hepatic T3 generation from T4 in male rats exposed to 4 +/- 1 degree C for 12 wk was 41 and 24% higher than control after 30- and 60-min incubation periods, respectively. This was associated with a 49% increase in serum T3 concentration in the cold-acclimated rats, whereas serum T4 concentration did not differ from the control. Thus, hepatic deiodination of T4 appears to serve as an important source for production of T3 during cold acclimation. It is suggested that the increased beta-adrenergic activity observed previously in cold-acclimated rats stimulates this change.

Acclimatization↗

PubMed1983

Hypohydration and exercise: effects of heat acclimation, gender, and environment.

This study examined the effects of heat acclimation and subject gender on treadmill exercise in comfortable (20 degrees C, 40% rh), hot-dry (49 degrees C, 20% rh), and hot-wet (35 degrees C, 79% rh) environments while subjects were hypo- or euhydrated. Six male and six female subjects, matched for maximal aerobic power and percent body fat, completed two exercise tests in each environment both before and after a 10-day heat acclimation program. One exercise test was completed during euhydration and one during hypohydration (-5.0% from baseline body weight). In general, no significant (P greater than 0.05) differences were noted between men and women at the completion of exercise for rectal temperature (Tre), mean skin temperature (Tsk), or heat rate (HR) during any of the experimental conditions. Hypohydration generally increased Tre and HR values and decreased sweat rate values while not altering Tsk values. In the hypohydration experiments, heat acclimation significantly reduced Tre (0.19 degrees C) and HR (13 beats X min-1) values in the comfortable environment, but only HR values were reduced in hot-dry (21 beats X min-1) and hot-wet (21 beats X min-1) environments. The present findings indicated that men and women respond in a physiologically similar manner to hypohydration during exercise. They also indicated that for hypohydrated subjects heat acclimation decreased thermoregulatory and cardiovascular strain in a comfortable environment, but only cardiovascular strain decreased in hot environments.

Acclimatization↗

PubMed1983

Hypohydration and heat acclimation: plasma renin and aldosterone during exercise.

This study was designed to assess the effects of hydration, acclimation, environment, and exercise on plasma levels of renin and aldosterone. Sixteen subjects exercised (1.34 m X s-1), both pre- and postacclimation, when euhydrated or hypohydrated (-5% of body wt) in a comfortable (20 degrees C, rh = 40%), hot-wet (35 degrees C, rh = 79%), or hot-dry (49 degrees C, rh = 20%) environment. Although light exercise in a thermoneutral environment had no effects on plasma levels of renin activity (PRA) or aldosterone (ALD), exercise in both hot environments resulted in significantly increased levels of both. Increments in both PRA and ALD were greater when hypohydrated, and PRA effects were significantly moderated by heat acclimation in both the euhydration and hypohydration experiments. Although PRA and ALD responses were generally correlated, acclimation did not consistently attenuate ALD increments. We concluded that hydration state, acclimation level, and environmental conditions all affected the responses of PRA and ALD to light exercise.

Acclimatization↗

PubMed1984

Heat exchange following atropine injection before and after heat acclimation.

The effect of saline and atropine injection (2 mg, im) on eight healthy male subjects before and after heat acclimation was studied while each subject walked on a treadmill (1.34 m X s-1) in a hot-dry environment (ambient temperature = 48.4 degrees C, dew-point temperature = 20.5 degrees C). Partitional calorimetric analysis was done for the periods in which maximum sweat inhibition occurred (30 min). Mean skin temperature, rectal temperature, and heart rate were continuously observed. Evaporative loss from the skin was calculated by changes in body weight (Sauter balance); heat transfer coefficients were defined by Nishi equations. A prediction of sweat inhibition based on an analysis of heat storage and its effect on a theoretical temperature, which can be graphed on a psychrometric chart, was developed. A rational effective temperature (ET) defined as the operative temperature at the intersection of the 50% rh, which encompasses total heat exchange, was used to compare the effects of atropine before and after heat acclimation. The results show that heat acclimation reduced ET by approximately 2.5 degrees C when compared with the unacclimated state after atropine injection. Thus heat acclimation reduces the hazards of heatstroke caused by exercise in the heat with atropine injection.

Acclimatization↗

PubMed1984

Heat acclimation in cystic fibrosis.

Cystic fibrosis (CF) patients may be at risk for heat illness because of their high sweat chloride and sodium concentrations ([Cl-], [Na+]), but it is not known if they can heat acclimate. We studied 10 CF patients and 10 normal controls on 8 consecutive days of cycle exercise in the heat (37 degrees C dry bulb, 24-29 degrees C wet bulb). Both groups acclimated. CF peak rectal temperature (Tre) was 38.2 +/- 0.3 degrees C on day 1 and 37.8 +/- 0.4 degrees C on day 8 (P less than .005), and peak heart rates (HR) were 151 +/- 24 beats/min on day 1 and 136 +/- 22 beats/min on day 8 (P less than 0.025). Control temperature (T) and HR were similar. Controls decreased sweat [Cl-] from 37.2 +/- 14.6 meq/l on day 1 and to 24.9 +/- 10.6 meq/l on day 8 (P less than 0.005). CF sweat [Cl-] was significantly higher and did not change with acclimation (day 1, 71.1 +/- 20.9 meq/l; day 8, 72.6 +/- 21.6 meq/l, NS). Before and after acclimation, exercise-heat sessions resulted in significant decreases in serum [Cl-] in CF patients (104.5 +/- 4.6 to 101.3 +/- 4.4 meq/l on day 1, P less than 0.05; 103.5 +/- 5.1 to 99.7 +/- 4.2 meq/l on day 8, P less than 0.025) but not in controls. Serum [Cl-] was significantly lower in CF than control subjects at every measurement. Both groups had significant renal Na+ conservation after exercise on both days.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1988

Thermoregulatory responses of middle-aged and young men during dry-heat acclimation.

Thermoregulatory responses during heat acclimation were compared between nine young (mean age 21.2 yr) and nine middle-aged men (mean age 46.4 yr) who were matched (P greater than 0.05) for body weight, surface area, surface area-to-weight ratio, percent body fat, and maximal aerobic power. After evaluation in a comfortable environment (22 degrees C, 50% relative humidity), the men were heat acclimated by treadmill walking (1.56 m/s, 5% grade) for two 50-min exercise bouts separated by 10 min of rest for 10 consecutive days in a hot dry (49 degrees C ambient temperature, 20% relative humidity) environment. During the first day of heat exposure performance time was 27 min longer (P less than 0.05) for the middle-aged men, whereas final rectal and skin temperatures and heart rate were lower, and final total body sweat loss was higher (P less than 0.05) compared with the young men. These thermoregulatory advantages for the middle-aged men persisted for the first few days of exercise-heat acclimation (P less than 0.05). After acclimation no thermoregulatory or performance time differences were observed between groups (P greater than 0.05). Sweating sensitivity, esophageal temperature at sweating onset, and the sweating onset time did not differ (P greater than 0.05) between groups either pre- or postacclimatization. Plasma osmolality and sodium concentration were slightly lower for the young men both pre- and postacclimatization; however, both groups had a similar percent change in plasma volume from rest to exercise during these tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1994

Muscle metabolism during exercise and heat stress in trained men: effect of acclimation.

Exercise metabolism was examined in 13 endurance athletes who exercised on three occasions for 40 min at 70% of maximal O2 uptake in an environmental chamber at either 20 degrees C and 20% relative humidity (RTT) or 40 degrees C and 20% relative humidity before (PRE ACC) or after (POST ACC) 7 days of acclimation. Exercise in the heat resulted in a lower (P < 0.05) mean O2 uptake (0.13 l/min) and higher (P < 0.01) heart rate and respiratory exchange ratio. Acclimation resulted in a lower (P < 0.01) mean heart rate and respiratory exchange ratio. Postexercise rectal temperature, muscle temperature, muscle and blood lactate, and blood glucose were higher (P < 0.01) in the PRE ACC than in the RTT trial, but all were reduced (P < 0.01) in the POST ACC compared with the PRE ACC trial. Muscle glycogenolysis and percentage of type I muscle fibers showing glycogen depletion were greater (P < 0.05) in the PRE ACC than in the RTT trial. Muscle glycogenolysis was unaffected by acclimation during exercise in the heat, although the percentage of depleted type I fibers was higher (P < 0.05) in the unacclimated state. Plasma epinephrine was higher (P < 0.01) during exercise in the heat in the unacclimated individual relative to RTT but was lower (P < 0.01) in the POST ACC than in the PRE ACC trial. The greater reliance on carbohydrate as a fuel source during exercise in the heat appears to be partially reduced after acclimation. These alterations are consistent with the observed changes in plasma epinephrine concentrations.

Acclimatization↗

PubMed1994

Modifications of glucose and lipid metabolism in cold-acclimated lean and genetically obese rats.

Glucose turnover rate, 2-deoxy-D-[3H]glucose (2-DG) uptake, lipid synthesis in liver, white adipose tissue, and brown adipose tissue (BAT) were measured in lean FA/FA and genetically obese fa/fa rats either kept at 21 degrees C or acclimated to a cold environment (4 degrees C). After 10 days at 4 degrees C, lean rats increased their glucose turnover rate; 2-DG uptake as well as lipid synthesis in BAT were markedly stimulated. After cold acclimation, obese rats also increased glucose turnover; however, BAT glucose utilization was only slightly stimulated. Basal hyperinsulinemia and muscle insulin resistance of the obese group (as assessed by reduced 2-DG uptake in the soleus muscle) were present at room temperature and persisted at 4 degrees C. Total BAT lipid synthesis was increased to the same extent as in lean rats. Obese rat liver lipid synthesis, already much higher than normal at 21 degrees C, was further increased by cold exposure. We conclude that obese cold-acclimated fa/fa rats do not improve their muscle insulin resistance and barely improve BAT glucose utilization. We further suggest that an additional activation of hepatic lipid synthesis and oxidation thereof could participate in the heat production needed by the cold-acclimated obese rats.

Acclimatization↗

PubMed1996

Evidence for contribution of effector organ cellular responses to the biphasic dynamics of heat acclimation.

The involvement of cellular processes in the biphasic dynamics of heat acclimation was studied. Key steps in the cholinergic signal transduction pathway for water secretion were measured in the submaxillary gland of acclimating [2-day short-term heat acclimation (STHA) and 30-day long-term heat acclimation (LTHA) at 34 degrees C] or acute heat-stressed (2 h at 40 degrees C) rats in vitro. Both the carbamylcholine (CCh)-induced maximal fractional rate and the total 86Rb+ efflux, reflecting K+ efflux and water transport, transiently decreased in STHA (P < 0.001). In LTHA, the total K+ efflux increased (P < 0.001), whereas the maximal fractional rate of efflux increased only slightly. During STHA, the density of the high-affinity binding site of the muscarinic receptors (MRs) increased by 50% and their affinity for the muscarinic antagonist [3H]-N-methylscopolamine decreased transiently by 87%. Basal cytosolic Ca2+ concentration ([Ca2+]i) decreased (P < 0.05), but the peak CCh-induced [Ca2+]i increase resembled the control values. In LTHA, MR density continued to increase (100%; P < 0.05), whereas affinity resumed control values. Basal and CCh-induced [Ca2+]i increases returned to control levels. We conclude that glandular cellular processes follow a biphasic pattern with major apparent changes attributable to events distal to the [Ca2+]i rise. This was further validated by employing heat stress, which produced qualitatively different effects on the MR profile with a decrease in 86Rb+ efflux comparable to STHA. Hence, although heat-induced changes in the proximal components of the signal transduction pathway may contribute to altered regulatory span, the predominant apparent cellular effect is on the distal part of the pathway.

Acclimatization↗

PubMed2003

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats.

The effects of long-term cold exposure on muscle and liver mitochondrial oxygen consumption in hypothyroid and normal rats were examined. Thyroid ablation was performed after 8-wk acclimation to 4 degrees C. Hypothyroid and normal controls remained in the cold for an additional 8 wk. At the end of 16-wk cold exposure, all hypothyroid rats were alive and normothermic and had normal body weight. At ambient temperature (24 degrees C), thyroid ablation induced a 65% fall in muscle mitochondrial oxygen consumption, which was reversed by thyroxine but not by norepinephrine administration. After cold acclimation was reached, suppression of thyroid function reduced muscle mitochondrial respiration by 30%, but the hypothyroid values remained about threefold higher than those in hypothyroid muscle in the warm. Blockade of beta- and alpha1-adrenergic receptors in both hypothyroid and normal rats produced hypothermia in vivo and a fall in muscle, liver, and brown adipose tissue mitochondria respiration in vitro. In normal rats, cold acclimation enhanced muscle respiration by 35%, in liver 18%, and in brown adipose tissue 450% over values in the warm. The results demonstrate that thyroid hormones, in the presence of norepinephrine, are major determinants of thermogenic activity in muscle and liver of cold-acclimated rats. After thyroid ablation, cold-induced nonshivering thermogenesis replaced 3,5,3'-triiodothyronine-induced thermogenesis, and normal body temperature was maintained.

Adipose Tissue, Brown↗

PubMed2003

Effect of acclimation on resting energy expenditure measurements.

BACKGROUND: Development of an acclimation protocol for use when measuring resting energy expenditure (REE) would simplify and standardize data collection. The purpose of this study was to determine if our 2 metabolic carts could be used interchangeably and to determine if excluding the first 3 or 5 minutes of data collected as an acclimation period would significantly improve the coefficients of variation (CVs) for oxygen consumed (VO(2)) and carbon dioxide produced (VCO(2)) when performing REE assessments with our metabolic cart systems. METHODS: Thirteen healthy, nonsmoking adults ranging in age from 32 to 45 years, with activity levels ranging from sedentary to highly active, participated. Indirect calorimetry was performed twice in the morning after 30 minutes of supine resting. Subjects had fasted for 12 hours, and did not exercise within the last 24 hours. The system order for testing was randomized for the first measurement. When the first measurement was completed, subjects were crossed over for measurement using a second metabolic cart. RESULTS: The CVs for VO(2) and VCO(2) were significantly lower when excluding the first 3 (VO(2), p = .0005), (VCO(2), p = .0024) or 5 minutes (VO(2), p = .0001, VCO(2), p = .0021) of data compared with no exclusions. No significant differences in CVs between the 3- and 5-minute exclusions were found for VO(2) (p = .3224) or VCO(2) (p = .2255). CONCLUSIONS: Clearly, our machines cannot be used interchangeably within a study. An acclimation period improves CVs of VO(2) and VCO(2.) The similarities in CVs led us to adopt a 3-minute acclimation period for measuring REE.

Journal Article↗

PubMed2003

Regulation of branchial Na(+)/K(+)-ATPase in common carp Cyprinus carpio L. acclimated to different temperatures.

Isogenic carp Cyprinus carpio L. were acclimated to water temperatures of 15, 22 and 29 degrees C for at least 8 weeks. The acclimations consistently resulted in slightly, but significantly, different plasma osmolality, sodium, potassium and chloride concentrations between the groups studied. Plasma total and ionic calcium levels were unaffected, indicating successful adaptation. The apparent changes in set point for plasma ion levels are explained by altered sodium pump activity and hormonal control of branchial permeability to water and ions. It appears that in 15 degrees C-acclimated fish, a lower apparent Na(+)/K(+)-ATPase activity is compensated by strongly enhanced Na(+)/K(+)-ATPase expression (determined biochemically and immunohistochemically). In 29 degrees C-acclimated fish, the higher ambient temperature activates the enzyme. Arrhenius plots for branchial Na(+)/K(+)-ATPase preparations of the three groups of fish suggest the occurrence of different enzyme isoforms or protein (in)stability as explanations for differences in apparent enzyme activities, rather than temperature-dependent changes in membrane fluidity. As for hormonal control over permeability, prolactin mRNA expression (and anticipated production and release) is lower in fish kept at 29 degrees C, suggesting that control over branchial permeability to water and ions needs to be downregulated at higher temperatures. In so doing, enhanced sodium pump activity is balanced by a controlled passive ion loss to fine-tune plasma sodium levels. Basal plasma cortisol levels did not correlate positively with Na(+)/K(+)-ATPase expression, but doubling plasma cortisol levels in control fish by administering exogenous cortisol (for 7 days, using implanted minipumps and thus stress-free) enhanced Na(+)/K(+)-ATPase expression. This effect must be the result of a glucocorticoid action of the steroid: in fish, mineralocorticoid receptors have higher affinity for cortisol than glucocorticoid receptors. At a lower ambient temperature, branchial Na(+)/K(+)-ATPase expression is upregulated to counteract the temperature-inhibited activity of the sodium pump, perhaps via a mineralocorticoid receptor.

Acclimatization↗

PubMed2003

Influences of thermal acclimation and acute temperature change on the motility of epithelial wound-healing cells (keratocytes) of tropical, temperate and Antarctic fish.

The ability to heal superficial wounds is an important element in an organism's repertoire of adaptive responses to environmental stress. In fish, motile cells termed keratocytes are thought to play important roles in the wound-healing process. Keratocyte motility, like other physiological rate processes, is likely to be dependent on temperature and to show adaptive variation among differently thermally adapted species. We have quantified the effects of acute temperature change and thermal acclimation on actin-based keratocyte movement in primary cultures of keratocytes from four species of teleost fish adapted to widely different thermal conditions: two eurythermal species, the longjaw mudsucker Gillichthys mirabilis (environmental temperature range of approximately 10-37 degrees C) and a desert pupfish, Cyprinodon salinus (10-40 degrees C), and two species from stable thermal environments, an Antarctic notothenioid, Trematomus bernacchii (-1.86 degrees C), and a tropical clownfish, Amphiprion percula (26-30 degrees C). For all species, keratocyte speed increased with increasing temperature. G. mirabilis and C. salinus keratocytes reached maximal speeds at 25 degrees C and 35 degrees C, respectively, temperatures within the species' normal thermal ranges. Keratocytes of the stenothermal species continued to increase in speed as temperature increased above the species' normal temperature ranges. The thermal limits of keratocyte motility appear to exceed those of whole-organism thermal tolerance, notably in the case of T. bernacchii. Keratocytes of T. bernacchii survived supercooling to -6 degrees C and retained motility at temperatures as high as 20 degrees C. Mean keratocyte speed was conserved at physiological temperatures for the three temperate and tropical species, which suggests that a certain rate of motility is advantageous for wound healing. However, there was no temperature compensation in speed of movement for keratocytes of the Antarctic fish, which have extremely slow rates of movement at physiological temperatures. Keratocytes from all species moved in a persistent, unidirectional manner at low temperatures but at higher temperatures began to take more circular or less-persistent paths. Thermal acclimation affected the persistence and turning magnitude of keratocytes, with warmer acclimations generally yielding more persistent cells that followed straighter paths. However, acclimation did not alter the effect of experimental temperature on cellular speed. These findings suggest that more than one temperature-sensitive mechanism may govern cell motility: the rate-limiting process(es) responsible for speed is distinct from the mechanism(s) underlying directionality and persistence. Keratocytes represent a useful study system for evaluating the effects of temperature at the cellular level and for studying adaptive variation in actin-based cellular movement and capacity for wound healing.

Acclimatization↗

PubMed2004

Effects of temperature acclimation on lactate dehydrogenase of cod (Gadus morhua): genetic, kinetic and thermodynamic aspects.

The aim of this study was to determine the effects of seasonal temperature variation on the functional properties of lactate dehydrogenase (LDH) from white muscle and liver of Norwegian coastal cod (Gadus morhua) and the possible relevance of LDH allelic variability for thermal acclimation. Two groups of fishes were acclimated to 4 degrees C or 12 degrees C for one year. Polymorphism was observed in only one (Ldh-B) of the three Ldh loci expressed in cod liver and/or muscle. Isozyme expression remained unchanged regardless of acclimation temperature (T(A)). The products of locus Ldh-B comprise only 14-19% (depending on the tissue) of total LDH activities and, consequently, differences between phenotypes are negligible in terms of their effect on LDH total performance. No kinetic (, V(max)) or thermodynamic (E(a), DeltaG) differences were found among Ldh-B phenotypes. Clear kinetic differences were observed between LDH isoforms in the two tissues. However, the Arrhenius activation energy (E(a)) for pyruvate reduction was the same for both tissues (E(a)=47 kJ mol(-1)) at T(A)=12 degrees C. Factors T(A), tissue and phenotype did not reveal a significant effect on the Gibbs free energy change (DeltaG) of the reaction (55.5 kJ mol(-1)). However, at T(A)=4 degrees C, the E(a) was increased (E(a)=53-56 kJ mol(-1)) and the temperature dependence of the constant of substrate inhibition for pyruvate () decreased in both muscle and liver. In conclusion, the strategies of LDH adjustment to seasonal temperature variations in cod involve changes in LDH concentration (quantitative), adjustment of thermodynamic (E(a)) and kinetic () properties of the LDH (modulative) but not the expression of alternative isoforms (qualitative). We assume that the observed increase in E(a) and the decrease of temperature dependence of at low T(A) is the result of structural changes of the LDH molecule (temperature-driven protein folding). We propose a new mechanism of metabolic compensation of seasonal temperature variations - cold acclimation results in changes in the kinetic and thermodynamic properties of LDH in a way that favours aerobic metabolism through reduction of the competition of LDH for pyruvate in normoxic conditions.

Acclimatization↗