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Effect of cold acclimation on bulk tissue electrical impedance: I. Measurements with birdsfoot trefoil at subfreezing temperatures.

The resistive and reactive components of electrical impedance were measured for birdsfoot trefoil (Lotus corniculatus L.) stems at freezing temperatures to -8 degrees C. As temperature decreased the specific resistance at frequencies between 49 hertz and 1.11 megahertz of stems from cold acclimated plants increased more rapidly than from nonacclimated plants. This temperature dependence of specific resistance could be characterized by an Arrhenius activation energy; cold acclimated stems had a larger Arrhenius activation energy than nonacclimated stems. The low frequency resistance is believed to characterize the extracellular region of the stems and the high frequency resistance is believed to characterize the intracellular region of the stems. Cold acclimation increased the intracellular but not the extracellular resistance at nonfreezing temperatures. Cold acclimated stems were not injured by freezing to -8 degrees C and thawing, but nonacclimated stems were injured by freezing to temperatures between -2.2 and -5.6 degrees C and thawing. Injury to nonacclimated stems at freezing temperatures below -2.2 degrees C was indicated by a decrease in the ratio of resistance at 49 Hz to that at 1.11 megahertz.

Journal Article↗

Effect of Cold Acclimation on Bulk Tissue Electrical Impedance: II. Measurements with Alfalfa and Birdsfoot Trefoil at Nonfreezing Temperatures.

Stem and electrode electric impedance at 14 frequencies were monitored during cold acclimation of alfalfa (Medicago sativa L.) and birdsfoot trefoil (Lotus corniculatus L.). Cold acclimation significantly increased high frequency (e.g. 1.11 megahertz) resistance and reactance but not low frequency (49 hertz) resistance and reactance of both species. High frequency resistance of living stems was equivalent to the average resistance at all frequencies of dead stems and the resistance of dead stems (y) was related to stem water content (x):y = 9.28 - 4.11x + 0.47x(2), R = 0.92. The low-high frequency (49 hertz/1.11 megahertz) resistance ratio decreased during cold acclimation. A time constant believed to be a function of membrane resistance and capacitance was not affected by cold acclimation.

Journal Article↗

Arabidopsis transcriptome profiling indicates that multiple regulatory pathways are activated during cold acclimation in addition to the CBF cold response pathway.

Many plants, including Arabidopsis, increase in freezing tolerance in response to low, nonfreezing temperatures, a phenomenon known as cold acclimation. Previous studies established that cold acclimation involves rapid expression of the CBF transcriptional activators (also known as DREB1 proteins) in response to low temperature followed by induction of the CBF regulon (CBF-targeted genes), which contributes to an increase in freezing tolerance. Here, we present the results of transcriptome-profiling experiments indicating the existence of multiple low-temperature regulatory pathways in addition to the CBF cold response pathway. The transcript levels of approximately 8000 genes were determined at multiple times after plants were transferred from warm to cold temperature and in warm-grown plants that constitutively expressed CBF1, CBF2, or CBF3. A total of 306 genes were identified as being cold responsive, with transcripts for 218 genes increasing and those for 88 genes decreasing threefold or more at one or more time points during the 7-day experiment. These results indicate that extensive downregulation of gene expression occurs during cold acclimation. Of the cold-responsive genes, 48 encode known or putative transcription factors. Two of these, RAP2.1 and RAP2.6, were activated by CBF expression and thus presumably control subregulons of the CBF regulon. Transcriptome comparisons indicated that only 12% of the cold-responsive genes are certain members of the CBF regulon. Moreover, at least 28% of the cold-responsive genes were not regulated by the CBF transcription factors, including 15 encoding known or putative transcription factors, indicating that these cold-responsive genes are members of different low-temperature regulons. Significantly, CBF expression at warm temperatures repressed the expression of eight genes that also were downregulated by low temperature, indicating that in addition to gene induction, gene repression is likely to play an integral role in cold acclimation.

Acclimatization↗

Interpreting rejections of the beneficial acclimation hypothesis: when is physiological plasticity adaptive?

Although many studies testing the beneficial acclimation hypothesis have rejected it, what these rejections imply about the adaptive value of physiological change remains unclear. Uncertainty arises because the hypothesis focuses on the relative performance of organisms exposed to one environment versus another, whereas the raw material available to evolution is variation in acclimation responses of individual traits. This mismatch is problematic when organisms are exposed to poor environments. In poor environments, the adaptive or maladaptive value of changes in individual traits may be obscured by long-term decrements in organismal condition. A better match between the evolutionary pressures shaping acclimation and the tests used to examine them can be achieved by focusing on the fitness consequences of acclimation changes in individual traits.

Acclimatization↗

Local cold acclimation of the hand impairs thermal responses of the finger without improving hand neuromuscular function.

AIM: To investigate the effects of cold acclimation on the thermal response and neuromuscular function of the hand. METHODS: Ten healthy subjects [three female, seven male, age (mean +/- SD): 27.9 +/- 7.9 years] immersed their right hand in 8 degrees C water for 30 min, 5 days a week for 3 weeks. On the first and the last day, neuromuscular function of the first dorsal interosseus (FDI) muscle was tested. RESULTS: There was no significant change in maximal voluntary contraction strength or evoked contractile characteristics of the FDI after cold acclimation. Minimum finger temperature decreased significantly from 10.6 +/- 1.2 to 9.3 +/- 0.8 degrees C after 3 weeks (P < 0.01), with most of the decrease occurring after a single exposure. Mean finger temperature dropped significantly from 14.2 +/- 1.9 to 11.7 +/- 1.4 degrees C following cold acclimation (P < 0.05), with 90% of this adaptation occurring after 5 days. Onset time of cold-induced vasodilatation increased from 446 +/- 171 to 736 +/- 384 s (P < 0.05) and the amplitude decreased from 5.3 +/- 3.2 to 2.5 +/- 2.1 degrees C (P < 0.05). This was significantly different from the control group, who immersed their right hand on the first and last days only. CONCLUSION: These data suggest that cold acclimation does not enhance hand temperature or function but may put the hands at a greater risk of cold injury when exposed to the cold.

Acclimatization↗

Cold acclimation increases physiological responsiveness to intraventricular injection of beta-endorphin in pentobarbital anaesthetized rats. 1. Cardiovascular functions.

Intraventricular injection of beta-endorphin (3, 7, 10 and 30 nmol/kg) into the third ventricular of pentobarbital-anaesthetized male Sprague-Dawley rats resulted in a dose-dependent increase in mean arterial pressure (MAP) while injection of the same volume of 0.9% NaCl solution did not cause significant changes in MAP. Naloxone, which did not produce any significant change in MAP, antagonized the vasopressor effect of beta-endorphin, indicating that the response is mediated via the naloxone sensitive opiate receptors. Rats acclimated to cold (5 degrees) for 3 weeks showed a potentiated and prolonged increase in MAP following beta-endorphin injection, indicating an increased responsiveness to the peptide. This increased responsiveness in the cardiovascular system is probably of adaptive value in cold acclimation. Naloxone itself did not alter MAP either, but abolished the cardiovascular response to beta-endorphin completely in cold acclimated rats, indicating an increased effectiveness in its antagonistic effect following cold acclimation as well.

Animals↗

Synaptosomal and brain mitochondrial lipids in hibernating and cold-acclimated golden hamsters.

Synaptosomes and mitochondria were isolated from the brains of warm-adapted, hibernating, and cold-acclimated golden hamsters (Mesocricetus auratus). Lipid extracts of these subcellular fractions were prepared and assayed for plasmenylethanolamine (ethanolamine plasmalogen) and cholesterol levels. The ganglioside composition of synaptosomes was also determined. Samples from the hibernating animals showed characteristic changes in lipid composition. These changes include decreases in plasmenylethanolamine levels and a shift in the ganglioside composition toward a higher percentage of the more polar gangliosides. Those animals which were exposed to cold and did not hibernate (cold-acclimated) showed no such changes. Fatty acid analyses of synaptosomal and mitochondrial ethanolamine glycerophospholipids demonstrated a similar trend. Samples from hibernators showed decreases in 16:0, 18:0, and 22:6 (n-3), and increases in 16:1, 18:1, and 20:4 (n-6) fatty acids. No changes were detectable in samples from cold-acclimated animals, indicating that hibernating and cold-acclimated hamsters represent chemically distinct populations.

Acclimatization↗

Comparison of the effects of physical exercise, cold acclimation and repeated injections of isoprenaline on rat muscle enzymes.

The metabolic effects on rat cardiac and skeletal muscle of a strenous program of swimming, of cold acclimation and of isoprenaline treatment (0.3 mg/kg daily for 5 five-day weeks) were compared. Exercised and cold-exposed rats gained less body weight than did controls or isoprenaline-treated rats. In all treated groups the heart and the intercapular brown adipose tissue hypertrophied. The size of the adrenals increased only in isoprenaline-treated animals. Cold-acclimation and physical training increased and isoprenaline treatment reduced or did not affect the activities of succinate dehydrogenase, malate dehydrogenase and citrate synthase of cardiac muscle. In the skeletal muscle all treatments resulted in increased activities of these enzymes. Of the anaerobic enzymes analysed, only the activity of hexokinase increased in response to the treatements used. This increase was the same in cardiac as in skeletal muscle, but it was significantly greater with isoprenaline-treatment than with training or with cold-acclimation. The activities of lactate dehydrogenase and phosphofructokinase did not differ significantly. All treatments improved cold resistance, but only swimming exercise and cold acclimation significantly increased tolerance to exercise. It is concluded that prolonged stimulation of adrenergic beta-receptors by catecholamines is responsible for the metabolic changes observed.

Acclimatization↗

The role of brown adipose tissue in the calorigenic effect of adrenaline and noradrenaline in cold-acclimated rats.

1. Removal of the interscapular brown adipose tissue of the cold-acclimated rat has no immediate effect on the calorigenic response of the rat to adrenaline or noradrenaline.2. There is a progressive loss of the enhanced response to adrenaline and to noradrenaline during the 4 days following removal of the interscapular brown adipose tissue from cold-acclimated rats. There is no loss of response in sham-operated cold-acclimated rats.3. Removal of the interscapular brown adipose tissue from rats living at room temperature has no effect on the calorigenic response to adrenaline or noradrenaline, neither immediately afterwards nor 2-4 days later.4. It is concluded that interscapular brown adipose tissue is not the major site of oxygen consumption in the enhanced calorigenic response to adrenaline or noradrenaline in cold-acclimated rats. However, it does play an important role in this enhanced metabolic response, probably as an endocrine gland whose secretory product modifies the ability of other tissues to respond calorigenically to catecholamines.

Acclimatization↗

Chlorophyll fluorescence analysis of cyanobacterial photosynthesis and acclimation.

Cyanobacteria are ecologically important photosynthetic prokaryotes that also serve as popular model organisms for studies of photosynthesis and gene regulation. Both molecular and ecological studies of cyanobacteria benefit from real-time information on photosynthesis and acclimation. Monitoring in vivo chlorophyll fluorescence can provide noninvasive measures of photosynthetic physiology in a wide range of cyanobacteria and cyanolichens and requires only small samples. Cyanobacterial fluorescence patterns are distinct from those of plants, because of key structural and functional properties of cyanobacteria. These include significant fluorescence emission from the light-harvesting phycobiliproteins; large and rapid changes in fluorescence yield (state transitions) which depend on metabolic and environmental conditions; and flexible, overlapping respiratory and photosynthetic electron transport chains. The fluorescence parameters FV/FM, FV'/FM',qp,qN, NPQ, and phiPS II were originally developed to extract information from the fluorescence signals of higher plants. In this review, we consider how the special properties of cyanobacteria can be accommodated and used to extract biologically useful information from cyanobacterial in vivo chlorophyll fluorescence signals. We describe how the pattern of fluorescence yield versus light intensity can be used to predict the acclimated light level for a cyanobacterial population, giving information valuable for both laboratory and field studies of acclimation processes. The size of the change in fluorescence yield during dark-to-light transitions can provide information on respiration and the iron status of the cyanobacteria. Finally, fluorescence parameters can be used to estimate the electron transport rate at the acclimated growth light intensity.

Acclimatization↗

Improved cold tolerance and its mechanism in cold-acclimated rats by high fat diet feeding.

Cold tolerance and metabolic responses to cold were studied in cold-acclimated rats on high fat diet (CAHF). Cold tolerance at-5 degrees C was assessed by fall of colonic temperature of clipped rats after 18 h of fasting. Rate of fall in colonic temperature was greatest in warm-acclimated control rats (WAST), slowest in cold-acclimated rats on standard diet (CAST), and remained unchanged in CAHF during cold exposure for 240 min. Increment in blood free fatty acid (FFA) concentration 80 min after cold exposure was greatest in WAST, less in CAST, and least in CAHF. Blood glucose decreased similarly in WAST and CAST after cold exposure, while it remained unchanged in CAHF. Blood beta-hydroxybutyrate also increased similarly in WAST and CAST, while it did not change in CAHF. Nonshivering thermogenesis tested by noradrenaline was greatest in CAHF, followed by CAST and WAST. Shivering induced by cold exposure was less pronounced in CAST than in WAST and did not develop in CAHF; changes in colonic temperature were inversely related to the extent of shivering during cold exposure for 90 min. These results suggest that an integrating effect of cold and high fat diet could improve cold tolerance much more than cold acclimation itself, possibly through enhanced nonshivering thermogenesis caused by metabolic modifications such as increased lipid use and gluconeogenesis.

Acclimatization↗

Insulin secretion by the perfused pancreas of the cold-acclimated rat.

Rats were acclimated to cold at 4 degrees C for a period of 42 days. Pancreases of normal and cold-acclimated rats were isolated and perfused with a Krebs-Henseleit bicarbonate medium containing dextran, adenosine, glucose, and a fluorocarbon as oxygen carrier. The biphasic secretion pattern of insulin in response to glucose stimulation was evident in both groups. Both basal and glucose-induced insulin release from pancreases of cold-acclimated rats exhibited a very significant reduction in comparison with controls (p less than 0.001). These observations are interpreted as indicating that cold-acclimation, an altered steady state of metabolism, is characterized by enhanced sympathetic activity which reduces insulin availability and release. Consequently enhanced free fatty acid mobilization resulting from reduced inhibition by insulin of lipolysis in the peripheral fat depots and increased lipolysis resulting from sympathetic activation are seen.

Acclimatization↗

Influence of cold and warm acclimation on neuronal responses in the lower brain stem.

Neurons in two lower brain stem areas, the nucleus raphe magnus and the subcoeruleus region, have been shown to be part of the thermoafferent system. It is concluded from microcut experiments in unanaesthetized guinea pigs that inhibition of shivering caused by nucleus raphe magnus stimulation is mediated partly by ascending and partly by descending efferents of the nucleus raphe magnus. Electrical stimulation of the subcoeruleus area caused excitatory metabolic responses. Interruption of the ascending efferents of the subcoeruleus area did not prevent the metabolic activation. It is concluded that the excitatory responses are partly mediated by descending efferents of the subcoeruleus area. The descending pathways project mainly to motoneurone pools and to dorsal horn cells. In cold-acclimated guinea pigs, the average maximum activity of bell-shaped subcoeruleus cold-responsive units was reduced significantly in comparison with cold-responsive neurons in animals acclimated to normal room temperature. Furthermore, peak activity of warm-responsive units in the nucleus raphe magnus was larger in cold-acclimated animals than in animals acclimated to normal room temperature. These neuronal changes may contribute via descending lower loops and via ascending upper loops to long-term slope reduction of metabolic cold defence and shivering threshold displacements.

Acclimatization↗

Increase in plasma thyroid hormone levels during the previous heat exposure time in heat-acclimated rats.

The present study was conducted to investigate day-night variations of plasma thyroid hormone and energy substrate levels in rats after acclimation to heat loaded for several hours at a fixed time per day. The heat-acclimated rats were exposed to an ambient temperature of 33 degrees C for 5 h in the last half of the dark phase for 16 consecutive days, while the control rats were kept at 24 degrees C for the same period. After completing the schedule, plasma levels of triiodothyronine (T3), free T3 (FT3), thyroxine (T4), free T4 (FT4), cortisol, triglyceride, nonesterified fatty acid, total protein, and glucose were measured at 3-h intervals between 00:00 and 18:00 (dark phase, 03:00-15:00). The plasma levels of T3 and FT3 of the heat-acclimated rats were higher than those of the controls in the last half of the dark phase. Similar differences were observed for T4 and FT4 levels. The plasma cortisol level was consistently higher in the heat-acclimated rats than in the control rats. There were no particular differences in energy-substrate levels between the two groups at any time of the day. These results indicate that heat exposure at a fixed time per day alters the pattern of day-night variations of plasma thyroid hormone levels in rats. It is noteworthy that the plasma levels of thyroid hormones, especially T3 and FT3, increased during the period when the rats had been previously exposed to heat.

Acclimatization↗

Increased calcium uptake by muscle mitochondria of cold-acclimated rats.

Skeletal muscle mitochondria of cold-acclimated rats have an altered morphology that is related to the occurrence of nonshivering thermogenesis. The transport of calcium by these mitochondria was studied in a search for an alteration in an energy-dissipating mechanism which might be related to the altered morphology and to the altered mode of thermogenesis in the cold-acclimated animal. The rates of calcium uptake, of calcium-stimulated respiration, and of state 4 respiration after calcium uptake were increased in the altered mitochondria. The capacity to accumulate calcium without phosphate was increased, whereas with phosphate all the calcium was removed from the medium and no difference in total uptake was seen. Spontaneous release of calcium was greater but sodium-induced release was unchanged. No effect of cyclic AMP or prostaglandin E1 on release of calcium was seen. The increase in rate of calcium uptake occurred gradually during the first 3-5 wk of acclimation to cold. The results are considered to give some support to the hypothesis that adaptive changes in the mitochondrial calcium transport cycle in skeletal muscle occur during acclimation to cold.

Acclimatization↗

Expression of sarcoplasmic reticulum Ca2+ transport proteins in cold-acclimating ducklings.

The relationship between the cold-induced increase in sarcoplasmic reticulum (SR) Ca2+ transport proteins and the development of muscular nonshivering theermogenesis (NST) was investigated by determining the time course of expression of the sarcoplasmic or endoplasmic reticulum Ca(2+)-ATPase (SERCA), Ca2+ release channel, and calsequestrin in control and cold-acclimating ducklings. 45Ca2+ uptake and [3H]ryanodine binding measurements with skeletal muscle homogenates showed that a cold acclimation period of approximately 4 wk was required to observe a substantial increase in Ca(2+)-ATPase activity and Ca2+ release channel content, which correlates well with NST development Immunoblot analysis of muscle homogenates showed no differences in calsequestrin levels but revealed that the decrease in SERCA2a content was delayed in cold-acclimating birds and that the SERCA1 level was increased after 4 wk of cold acclimation. The persistence of SERCA2a may be related to shivering thermogenesis occurring preferentially in slow-twitch fibers. SERCA1 may account for most of the cold-induced increase in 45Ca2+ uptake activity, suggesting the preferential occurrence of a Ca(2+)-dependent NST in fast-twitch fibers.

Acclimatization↗

Lipoprotein lipase in adipose tissues of exercise-trained, cold-acclimated rats.

The combined effects of exercise training and cold acclimation on serum lipids and on the activity of lipoprotein lipase (LPL) in epididymal white (WAT) and interscapular brown adipose tissues (BAT) of the rat were evaluated. Sedentary and exercise-trained (treadmill) rats were housed and trained at either 24 or 4 degrees C for 45 days. Although neither treatment given alone influenced serum total cholesterol, exercise training in the cold resulted in a 54% increase in this variable. Serum triglycerides were lowered to 80% of control values by exercise training and to 44% of control by cold acclimation. Both treatments resulted in lower insulin and thyroxine concentrations, while triiodothyronine levels were unaffected. Total LPL activity in WAT was increased twofold by exercise training at both temperatures, whereas cold acclimation stimulated WAT LPL activity to a lesser extent. Exercise training had no overall effect on LPL activity of BAT, whereas cold acclimation increased the latter in both sedentary (217%) and trained (420%) animals. These results emphasize the potential importance of LPL-mediated lipid assimilation in the metabolic events that lead to energy production in response to environmental stresses and lend support to the notion that the regulation of LPL activity is tissue specific.

Acclimatization↗

Effect of high-altitude acclimation on NEFA turnover and lipid utilization during exercise in rats.

Relative exercise intensity (or %maximum O(2) consumption, VO(2 max)) controls fuel selection at sea level (SL) and after high-altitude acclimation (HA) in rats. In this context we used indirect calorimetry, [1-(14)C]palmitate infusions, and muscle triacylglycerol (TAG) measurements to determine 1) total lipid oxidation, 2) the relationship between circulatory nonesterified fatty acid (NEFA) flux and concentration, and 3) muscle TAG depletion after exercise in HA-acclimated rats. Aerobic capacity is decreased in trained rats after 10 wk of acclimation. Both SL and HA showed the same relative use of lipids at 60% [62 +/- 5% (HA) and 61 +/- 3% (SL) of O(2) consumption (VO(2))] and 80% [46 +/- 6% (HA) and 47 +/- 5% (SL) of VO(2)] of their respective VO(2 max). At 60% VO(2 max), plasma [NEFA] were higher in HA, but rate of appearance was essentially the same in both groups (at 30 min, 38 +/- 9 vs. 49 +/- 6 micromol. kg(-1). min(-1) in HA and SL, respectively). At this intensity SL showed no significant decrease in muscle TAG, but in HA it decreased by 64% in soleus and by 90% in red gastrocnemius. We conclude that 1) the relative contributions of total lipid are the same in SL and HA, contrary to differences in [NEFA], because the relationship between flux rate and [NEFA] is modified after acclimation, and 2) muscle TAG may play a more important role at HA.

Acclimatization↗