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PubMed1990

Heat loss responses in rats acclimated to heat loaded intermittently.

The present study examined the heat loss response of heat-acclimated rats to direct body heating with an intraperitoneal heater or to indirect warming by elevating the ambient temperature (Ta). The heat acclimation of the rats was attained through exposure to Ta of 33 or 36 degrees C for 5 h daily during 15 consecutive days. Control rats were kept at Ta of 24 degrees C for the same acclimation period. Heat acclimation lowered the body core temperature at Ta of 24 degrees C, and the core temperature level was lowered as acclimation temperature increased. When heat was applied by direct body heating, the threshold hypothalamic temperature (Thy) for the tail skin vasodilation was also lower in heat-acclimated rats than in the control rats. However, the amount of increase in Thy from the resting level to the threshold was the same in all three groups. When heat was applied by indirect warming, threshold Thy was slightly higher in heat-acclimated than in control rats. The amount of increase in Thy from the resting level to the threshold was significantly greater in heat-acclimated rats. In addition, Ta and the skin temperature at the onset of skin vasodilation were significantly higher in heat-acclimated rats. The results indicate that heat-acclimated rats were less sensitive to the increase in skin temperature in terms of threshold Thy. The gain constant of nonevaporative heat loss response was assessed by plotting total thermal conductance against Thy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed2003

Time course of the response of mitochondria from oxidative muscle during thermal acclimation of rainbow trout, Oncorhynchus mykiss.

The time course of changes in the properties of mitochondria from oxidative muscle of rainbow trout was examined during warm (15 degrees C) and cold (5 degrees C) acclimation. Mitochondrial oxidative capacities showed a biphasic response during thermal acclimation: at a given assay temperature, capacities first increased and then decreased during warm acclimation and showed the inverse pattern during cold acclimation. This was most apparent for maximal rates of state 3 oxygen consumption expressed per mg mitochondrial protein. Rates expressed per nmol ADP-ATP translocase (ANT) showed this pattern during cold acclimation. A biphasic pattern was also apparent for state 4 and oligomycin-inhibited (state 4(ol)) rates of oxygen uptake expressed per mg protein. Changes in states 4 and 4(ol) were smaller during cold than warm acclimation. Warm acclimation reduced the proportion of cytochrome c oxidase and citrate synthase needed during mitochondrial substrate oxidation. Phospholipid concentrations per mg mitochondrial protein changed little with thermal acclimation. Mitochondrial properties changed more quickly during warm than cold acclimation. While the biochemical modifications during thermal acclimation may eventually compensate for the thermal change, compensation did not occur at its onset. Rather, the initial changes of mitochondrial oxidative capacity in response to temperature change accentuated the functional impact of the thermal change, and prolonged exposure to the new temperature was required to attain a degree of thermal compensation.

Acclimatization↗

PubMed2005

Two-dimensional gel analysis of the heat-shock response in marine snails (genus Tegula): interspecific variation in protein expression and acclimation ability.

The degree to which temperature acclimation modifies the acute synthesis of the entire heat-shock protein (Hsp) complement is still unknown, but it may constitute an important mechanism for understanding the differences in acclimation ability among closely related ectothermic species that occupy widely varying thermal environments. In general, eurythermal (heat-tolerant) species modify physiological function in response to an increase in acclimation temperature to a greater extent than stenothermal (heat-sensitive) species. In the present work I used 35S-labelled amino acids and two-dimensional gel electrophoresis to test this assumption for how acclimation affects acute Hsp expression (referred to as phenotypic plasticity) in two heat-sensitive, low-intertidal to subtidal zone turban snails, Tegula brunnea and T. montereyi, in comparison to a heat-tolerant, mid- to low-intertidal zone congener, T. funebralis. I was able (i) to detect the synthesis of over 30 proteins in gill tissue, primarily in the 70 kDa range, in response to an increase in temperature (13 degrees C, 24 degrees C, 27 degrees C and 30 degrees C), (ii) to assess the effect of acclimation (13 degrees C vs 22 degrees C) on acute Hsp synthesis, and (iii) to compare this effect among the three Tegula congeners. After increasing acclimation temperature from 13 degrees C to 22 degrees C, synthesis of the most highly expressed Hsps decreased more in T. brunnea and T. montereyi than in T. funebralis. Two highly expressed proteins of molecular mass 71 and 74 kDa, however, were also synthesized constitutively at 13 degrees C and changed with increasing acclimation temperature in all three species. Although similar in phenotypic plasticity, T. brunnea and T. montereyi synthesized either a 76 or a 72 kDa cluster of proteins, respectively, and differed in how acclimation affected the acute synthesis of several 77 kDa proteins. Thus, in Tegula, the effect of acclimation on Hsp expression is (i) Hsp-specific, (ii) dependent on a protein's expression pattern (constitutive and inducible vs only inducible), (iii) and is actually limited in the more eurythermal mid- to low-intertidal congener. These results contradict the general assumption that greater heat tolerance correlates with an increased ability to modify physiological function in response to acclimation.

Acclimatization↗

PubMed1985

Properties of the chloride conductance associated with temperature acclimation in muscle fibres of green sunfish.

Characteristics of the anion conductance of muscle fibres from green sunfish have been determined. The membrane conductance of fibres from sunfish acclimated to 25 and 7 degrees C was linearly related to the extracellular chloride concentration. The chloride conductance exhibited a pH dependence which was adequately described by the titration of an acidic site with a pKa of 5.3 in 25 degrees C-acclimated fibres and 6.4 in 7 degrees C-acclimated fibres. The anion current-voltage (I-V) relationship of warm-acclimated fibres exhibited constant-field rectification, while the I-V relationship of cold-acclimated fibres was linear. In Ringer solutions containing elevated calcium concentrations (33 and 115 mmol 1(-1)), the I-V relationship of warm-acclimated fibres was similar to the control situation. However, the I-V relationship of cold-acclimated fibres showed a calcium concentration-dependent curvature in the direction expected for constant-field rectification. The voltage-dependence of the time constant of chloride current inactivation was shifted along the voltage axis by about 40 mV in the negative direction in 7 degrees C-acclimated fibres as compared to 25 degrees C-acclimated fibres. The results can be adequately described by a model of constant-field rectification with the inclusion of a term for the membrane surface potential. A simple hypothesis which can qualitatively account for many of these observations is that temperature acclimation alters the density of fixed negative surface charges in the vicinity of chloride channels.

Animals↗

PubMed1985

Force-velocity characteristics and metabolism of carp muscle fibres following temperature acclimation.

Common carp (Cyprinus carpio L.), 1 kg body weight, were acclimated for 1-2 months to water temperatures of either 7-8 degrees C (cold-acclimated group) or 23-24 degrees C (warm-acclimated group). Single fast fibres and small bundles of slow fibres were isolated from the myotomal muscles and chemically skinned. Force-velocity (P-V) characteristics were determined at 7 degrees C and 23 degrees C. The contractile properties of carp muscle fibres are dependent on acclimation temperature. In the warm-acclimated group maximum isometric tensions (P0, kN m-2) are 47 +/- 6 and 64 +/- 5 for slow muscle fibres and 76 +/- 10 and 209 +/- 21 for fast muscle fibres at 7 degrees C and 23 degrees C, respectively. Maximum contraction velocities (Vmax, muscle lengths-1), are 0.4 +/- 0.05 and 1.5 +/- 0.1 at 7 degrees C (slow fibres) and 0.6 +/- 0.04 and 1.9 +/- 0.4 at 23 degrees C (fast fibres). All values represent mean +/- S.E. P0 and Vmax at 7 degrees C are around 1.5-2.0 times higher for slow and fast muscle fibres isolated from the cold-acclimated group. Fibres from 7 degrees C-acclimated carp fail to relax completely following maximal activations at 23 degrees C. The resulting Ca-insensitive force component (50-70% P0) is associated with the development of abnormal crossbridge linkages and very slow contraction velocities. Activities of enzymes associated with energy metabolism were determined at a common temperature of 15 degrees C. Marker enzymes of the electron transport system (cytochrome oxidase), citric acid cycle (citrate synthase), fatty acid metabolism (carnitine palmitoyl transferase, beta-hydroxyacyl CoA dehydrogenase) and aerobic glucose utilization (hexokinase) have 30-60% higher activities in slow muscle from cold-acclimated than from warm-acclimated fish. Activities of cytochrome oxidase and citrate synthase in fast muscle are also elevated following acclimation to low temperature. It is concluded that thermal compensation of mechanical power output by carp skeletal muscle is matched by a concomitant increase in the potential to supply aerobically-generated ATP at low temperatures.

Acclimatization↗

PubMed1990

Effect of cold acclimation on the broiler chicks' resistance to acute aflatoxicosis.

The effect of acclimation to environmental temperatures of 10 to 12, 14 to 16, or 28 to 30 C on the resistance of broiler chicks to acute aflatoxicosis was studied in a series of four experiments. Chicks acclimated to 10 to 12 C were more resistant to a single oral dose of aflatoxin (8 mg per kg of BW) after 10 and 20 days than chicks acclimated to 28 to 30 C. However, chicks acclimated to 14 to 16 C required 20 days of acclimation before an increase in resistance was observed. Acclimation to 10 to 12 C for 14 days followed by acclimation to 28 to 30 C for 7 days resulted in no increase in the resistance of the chicks to an aflatoxin dose (8 mg per kg of BW) at 21 days, indicating that the resistance conveyed by cold acclimation was temporary. Sodium-pentobarbital sleeping time was significantly decreased and the cytochrome P-450 content was significantly increased after acclimating broiler chicks to 10 to 12 C. These observations suggest that stimulation of the microsomal mono-oxygenase system after cold acclimation may be responsible for the increased resistance of the broiler chick to acute aflatoxicosis.

Acclimatization↗

PubMed1987

Temperature acclimation and metabolism in ectotherms with particular reference to teleost fish.

As body temperature decreases, changes in the physical chemistry of the cell produce a reduction in metabolic activity. In temperate fish, cold water temperatures either lead to dormancy or else trigger a range of homeostatic responses which serve to offset the passive effects of reduced temperature. Compensatory adjustments to temperature occur with time courses ranging from less than a second to more than a month. Although swimming performance may increase with cold-acclimation, active metabolic rate remains significantly below that for warm-acclimated fish. Compensatory and dormancy responses are not mutually exclusive and sometimes occur in the same species depending on the temperature. Cold-acclimation results in significant increases in the density of mitochondria and capillaries in skeletal muscle. This serves to reduce diffusion distances and increase the capacity for aerobic ATP production relative to fish acutely exposed to low temperature. There is evidence that cold acclimation has differential effects on the synthesis and degradation rates of mitochondrial proteins leading to a net increase in their concentration. In contrast, the activities of enzymes associated with glycolysis and phosphocreatine hydrolysis show no consistent changes with thermal acclimation suggesting that flux through these pathways is modulated by factors other than enzyme concentration. Higher mitochondrial densities have also been reported for the liver, brain and gill tissue of cold compared with warm acclimated fish. In spite of their increased concentration, the activities of aerobic enzymes remain much lower at cold than warm temperatures. Acclimation temperature affects hepatosomatic index, the concentration of energy reserves, and the relative importance of glucose and fatty acid catabolism in liver. The fraction of glucose oxidized by the hexose monophosphate shunt (HMPS) pathway also increases with cold acclimation in some species. It is likely that many of the changes in liver metabolism with temperature acclimation reflect associated changes in feeding behaviour and/or diet, and other energetic demands (e.g. gametogenesis). Possible mechanisms underlying alterations in pathway utilization with temperature acclimation are discussed. They include changes in factors influencing enzyme structure and activity (e.g. pH, substrate/modulator concentrations, phosphorylation state, membrane composition), and effects of temperature on gene expression.

Adaptation, Physiological↗

PubMed1976

The effects of temperature and thermal acclimation upon the osmotic properties and nonelectrolyte permeability of liver and gill mitochondria from rainbow trout (Salmo gairdneri).

Thermal acclimation of rainbow trout (Salmo gairdneri) taken from 20 degrees C to 7 degrees C resulted in adaptation of mitochondrial function, as evidenced by increases in the specific activities of NADH- and succinate-cytochrome c reductase of 1.93- and 2.7-fold respectively. Mitochondria from both gill and liver obeyed the Boyle-van't Hoff relationship in the range from 400 to 60 mosM. Thermal acclimation had no effect on the osmotic properties of liver mitochondria, whereas gill mitochondria from cold-acclimated trout were more sensitive to osmotic swelling than mitochondria from warm-acclimated individuals. The non-electrolyte permeability of liver mitochondria was assessed by optically monitoring mitochondrial swelling rates in isosmotic solutions of urea, glycerol, mannitol and glucose. Two parameters of mitochondrial swelling were determined: (a) initial swelling rates, d(1/A)dt, and (b) swelling constants, ks, derived from the time required to swell a fixed volume. Regardless of the assay temperature or the permeant employed, liver mitochondria from cold-acclimated trout exhibited greater initial swelling rates than mitochondria from warm-acclimated trout, indicating properties of temperature-compensated permeability. The apparent ranking of nonelectrolyte permeabilities was urea greater than glycerol greater than mannitol greater than glucose. ks values for urea and glycerol from cold-acclimated trout were greater than values typical of warm-acclimated populations; however ks values for glucose and mannitol were not influenced by thermal acclimation. Regardless of the permeant considered, activation energies for ks values were 3- to 5-fold greater than those for initial swelling rates. The time course of mitochondrial swelling consists of two components, an initial rapid swelling phase characterized by a half-life of 3-12 seconds, and a slower swelling phase characterized by a half life of 1-6 minutes. Initial swelling rates, which approximate the rapid swelling component, are considered to be the least ambiguous index of permeability, whereas ks values are more complex and strongly influenced by the slower swelling component.

Acclimatization↗

PubMed1979

Fatty acid and sterol synthesis by hepatocytes of thermally acclimated rainbow trout (Salmo gairdneri).

Incorporation of tritium from tritiated water into lipid fractions was measured in isolated hepatocytes from rainbow trout (Salmo gairdneri) acclimated to 5 degrees C and 20 degrees C. Hepatocytes from cold-acclimated trout exhibited significantly higher rates of tritium incorporation into both fatty acid and sterol fractions at assay temperatures of 15 degrees C and 20 degrees C than did hepatocytes from warm-acclimated trout. Tritium incorporation into the fatty acid fraction was nearly temperature independent in hepatocytes from warm-acclimated trout (Q10 = 1.39) but markedly temperature dependent (Q10 = 2.63) in hepatocytes from cold-acclimated trout; in contrast, rates of sterol synthesis were more temperature dependent in warm-acclimated trout. At 5 degrees C, fatty acid lipogenesis comprised a significantly greater percentage of the total tritium incorporation in hepatocytes from warm-acclimated trout and the percentage of total lipogenesis attributable to fatty acids decreased significantly in warm-acclimated trout as the assay temperature increased; the opposite trends were observed in cold-acclimated trout.

Adaptation, Physiological↗

PubMed1986

Attenuated cardiovascular effects of prostaglandin I2 and prostaglandin F2 alpha in cold acclimated American bullfrogs, Rana catesbeiana.

American bullfrogs, Rana catesbeiana respond to prostaglandins with changes in heart rate and blood pressure. These studies compare responses of warm (22 degrees C) and cold acclimated (5 degrees C) bullfrogs to prostaglandins. Gas chromatographic analysis determined equivalent fatty acid profiles in total lipids of heart and artery tissue from warm and cold acclimated animals. Arachidonic acid was the fatty acid precursor found in greatest abundance in both groups. For cardiovascular experiments, bullfrogs were cannulated by using a T-cannula implanted in the right sciatic artery. In warm acclimated bullfrogs, preinfusion systemic arterial pressure (SAP) was 14.7 +/- 0.5 mm Hg, and heart rate was 33.0 +/- 1.7 beats/min. Cold acclimated bullfrogs had SAP values of 8.0 +/- 0.8 mm Hg, and heart rate was 6.9 +/- 0.3 beats/min. Arachidonic and eicosapentaenoic acid infusions (2,000 micrograms/kg body weight [bw]) were hypertensive in cold acclimated and hypotensive in warm acclimated animals. These effects were blocked by indomethacin (4 mg/kg bw). In both warm and cold acclimated bullfrogs, prostaglandin F2 alpha (3-100 micrograms/kg bw) was hypertensive, while prostaglandin I2 (0.03-3 micrograms/kg bw) was hypotensive, with both prostaglandins stimulating a greater absolute response in warm acclimated animals. In addition, both prostaglandins increased heart rate in warm but not in cold acclimated bullfrogs. The results suggest diminished cardiovascular sensitivity to prostaglandins at low environmental temperatures.

Acclimatization↗

PubMed2005

Effects of prolonged acclimation to intermediate photoperiod and photo-schedule reversal in photosensitive golden hamsters.

We investigated the effect of prolonged acclimation to 12 hr of light and photo-schedule reversal during the time of photosensitivity in golden hamsters (Mesocricetus auratus). Before the experiments, animals were housed under natural photoperiod and then transferred to 12L:12D (light 12 hr:dark 12 hr) in autumn for 12 weeks. After 4 weeks of acclimation, photo-schedule was reversed (12D:12L). First experiments were done after 4 weeks of acclimation to an ambient temperature (T(a)) of 23 degrees C and a 12L:12D photo-schedule. We examined the daily variations in brown adipose tissue (BAT) capacity for nonshivering thermogenesis (NST). Noradrenaline (NA) injections were given every 4 hr while BAT temperature (T(BAT)) and preferred ambient temperature (PT(a)) were monitored continuously and simultaneously in a thermal gradient system. Then, we investigated the effect of light-dark cycle reversal on a daily rhythm of NST. The hamsters were acclimated to the photo-schedule reversed by 12 hr and the same T(a). After 4 and 8 weeks of acclimation to a reversed photo-schedule, the experiments were repeated. We found that the daily rhythm of the response to NA was entrained to the new light-dark cycle after 4 weeks of acclimation to a reversed photo-schedule. Maximum effect of NA was always recorded during the light phase and in the latter part of the dark phase of the day. NA-induced increase in T(BAT) was correlated with the decrease in PT(a), and was also inversely correlated with pre-injection T(BAT). These data imply that the daily rhythm of the capacity for NST opposes the daily rhythm of body temperature (T(b)). After 8 weeks of acclimation to the reversed photo-schedule, the rhythmicity of the response to NA disappeared, and the daily fluctuations in T(BAT) were the smallest. This lack of rhythm may be a physiological adaptation to winter conditions when the daily amplitude of T(b) rhythm is markedly reduced and, as a consequence, NST capacity does not vary within the day. Moreover, after 8 weeks of acclimation to reversed photo-schedule, NST capacity decreased while response to saline increased. During the experiments, hamsters were photosensitive and were changing to their winter status. However, because of the lack of cold during acclimation, the capacity for NST did not increase. Increased responsiveness to saline, indicating an increase in stress-induced thermogenesis, might be advantageous for "fight or flight" reaction.

Acclimatization↗

PubMed1993

Characterization of chilling-acclimation-related proteins in soybean and identification of one as a member of the heat shock protein (HSP 70) family.

Through a 5-d exposure at 14 degrees C/8 degrees C (day/night), soybean (Glycine max [L.] Merr.) was acclimated to a lower temperature of 8 degrees C. In order to assess changes in protein synthesis related to chilling acclimation, proteins were labeled in vivo with [35S]methionine, separated by two-dimensional gel electrophoresis, and the derived autoradiograms were subjected to computer analysis. Two sets of chilling-acclimation-related proteins were characterized following exposure and labeling at 8 degrees C. One set corresponded to proteins whose synthesis was stimulated in acclimated plants in comparison with non-acclimated plants after transfer to 8 degrees C for 2 d. The other set also displayed an enhanced synthesis in the acclimated plants versus the non-acclimated plants but after 7 d of exposure at 8 degrees C. Most of these chilling-acclimation-related proteins were not increased during the acclimation period at 14 degrees C. Using microsequence analysis, one of these proteins was shown to have a high sequence homology with members of the heat-shock protein (HSP 70) family.

Acclimatization↗

PubMed1993

Central and peripheral contributions to control of heart rate during heat acclimation.

The contributions of the autonomic nervous system and the cardiac pacing cells in the development of heat-acclimation-induced bradycardia were analyzed, and the effect of heat acclimation on the chronotropic response of the heart to heat stress (40 degrees C) was studied. Rats were acclimated at 34 degrees C for 0, 5, 14, 30 and 60 days. Heart rate (HR) was measured in conscious animals, using chronic subcutaneous electrodes. Sympathetic and parasympathetic influences were studied by IP administration of 0.1 and 1 mg/100 g body weight atropine and propranolol respectively, while intrinsic HR (HRi) was measured following administration of both drugs simultaneously. The effects of carbamylcholine and norepinephrine on the beating rate of isolated rat atria were investigated to study pacemaker responsiveness to neutrotransmitters. Up to day 14 of heat acclimation, bradycardia was attained by tonic parasympathetic acceleration (18%) and temporal sympathetic withdrawal (0.8% on day 14), to compensate for the gradually augmented HRi (2.5% and 8% on days 5 and 14, respectively). Following long-term acclimation HRi declined below pre-acclimation rate. This was associated with resumed sympathetic activity (16% and 10% on days 30 and 60 respectively) while parasympathetic activity continued to be high (18%). Tachycardia, known to occur with severe uncontrolled body hyperthermia, was attenuated following heat acclimation by 42%. It was concluded that during the initial phase of heat acclimation bradycardia is achieved primarily by changes in autonomic influences, while following long-term acclimation, changes in the intrinsic properties of the pacing cells (HRi) and the autonomic system both play a role.

Acclimatization↗

PubMed1994

Effects of training and acclimation on heat tolerance in exercising men wearing protective clothing.

This study examined the effectiveness of endurance training and heat acclimation in reducing the physiological strain imposed by exercising in the heat while wearing protective clothing. Seven young men underwent 8 weeks of physical training [60-80% maximal aerobic power (VO2max) for 30-45 min.day-1, 3-4 days.week-1 at < 25 degrees C] followed by 6 days of heat acclimation (45-55% VO2max for 60 min.day-1 at 40 degrees C, 30% relative humidity). Nine other young men underwent corresponding periods of control observation and heat acclimation. Before and after each treatment, subjects completed a treadmill walk (4.8 km.h-1, 2% grade) in a climatic chamber (40 degrees C, 30% relative humidity), wearing in turn normal combat clothing or clothing protecting against nuclear, biological, and chemical (NBC) agents. Criteria for halting this test were: (1) a rectal temperature (T(re)) of 39.3 degrees C; (2) a heart rate (fc) > or = 95% of the subject's observed maximum, maintained for 3 min; (3) unwillingness of the subject to continue; (4) the elapse of 120 min. The training regimen increased mean VO2max by 16% and mean plasma volume by 8%. When tested in normal combat clothing, the rates of increase in T(re) and fc were slower after training. However, when wearing NBC protective clothing, the only significant change induced by training was a higher mean skin temperature (Tsk) in the early part of the test. Heat acclimation increased the mean plasma volume of untrained subjects by 8%, but their VO2max remained unchanged. When tested in normal combat clothing, acclimation decreased their mean values of T(re), Tsk, fc, and metabolic rate. When wearing NBC protective clothing, the only significant decrease after acclimation was in overall T(re). In trained subjects, heat acclimation induced no further improvement in any physiological variable when wearing normal combat clothing, but reduced overall T(re) and Tsk when wearing NBC protective clothing. Training- or acclimation-induced increases of sweat secretion (an average increment of 0.14-0.23 kg.h-1) were not accompanied by any statistically significant increase in sweat evaporation when wearing NBC protective clothing. Moreover, tolerance times were unchanged in either normal combat (116-120 min) or NBC protective clothing (47-52 min). We conclude that neither endurance training nor heat acclimation do much to improve exercise tolerance when wearing NBC protective clothing in hot environments, because any added sweat secretion decreases blood volume and increases discomfort without augmenting body cooling.

Acclimatization↗

PubMed1978

Effects of reserpine and propranolol on urinary excretion of histamine and 5-hydroxytryptamine in severe cold exposure in normal and cold-acclimated Guinea-pigs.

The effects of cold-acclimation, reserpine and propranolol were investigated on the survival time, rectal temperature and urinary excretion of histamine and 5-HT in guinea-pigs at -20 degrees C. Both reserpine and propranolol shortened survival time by 3 hours and 1.5 hours respectively, the shortest time being in the cold-acclimated reserpine-treated animals. There was a trend in severe cold exposure to increased excretion of histamine both in the non-acclimated and in cold-acclimated animals. Reserpine did not change the excretion but increased the concentration of histamine from 0.08 to 0.25 microgram/ml. Propranolol proved to be a histamine liberator by increasing the excretion in non-acclimated from 0.10 to 1.40 microgram/h and concentration from 0.10 to 4.52 microgram/ml and in cold-acclimated animals the excretion from 0.20 to 2.85 microgram/h and the concentration from 0.08 to 3.23 microgram/ml. Severe cold increased the excretion of 5-HT in the non-acclimated animals from 0.08 to 0.21 microgram/h and cold acclimation increased this to 0.17 microgram/h. Reserpine diminished the excretion from 0.08 to 0.03 microgram/h in the non-acclimated animals, but propranolol had no effect. The results showed that the excretion of histamine and 5-HT into urine are changed in cold and can be modified with drugs. The application of the findings in proving a cold stress deserves further study.

Acclimatization↗

PubMed2006

Temperature acclimation alters cardiac performance in the lobster Homarus americanus.

The American lobster is a poikilotherm that inhabits a marine environment where temperature varies over a 25 degrees C range and depends on the winds, the tides and the seasons. To determine how cardiac performance depends on the water temperature to which the lobsters are acclimated we measured lobster heart rates in vivo. The upper limit for cardiac function in lobsters acclimated to 20 degrees C is approximately 29 degrees C, 5 degrees C warmer than that measured in lobsters acclimated to 4 degrees C. Warm acclimation also slows the lobster heart rate within the temperature range from 4 to 12 degrees C. Both effects are apparent after relatively short periods of warm acclimation (3-14 days). However, warm acclimation impairs cardiac function at cold temperatures: following several hours exposure to frigid (<5 degrees C) temperatures heart rates become slow and arrhythmic in warm acclimated, but not cold acclimated, lobsters. Thus, acclimation temperature determines the thermal limits for cardiac function at both extremes of the 25 degrees C temperature range lobsters inhabit in the wild. These observations suggest that regulation of cardiac thermal tolerance by the prevailing environmental temperature protects against the possibility of cardiac failure due to thermal stress.

Acclimatization↗

PubMed2004

Freshwater to seawater acclimation of juvenile bull sharks (Carcharhinus leucas): plasma osmolytes and Na+/K+-ATPase activity in gill, rectal gland, kidney and intestine.

This study examined the osmoregulatory status of the euryhaline elasmobranch Carcharhinus leucas acclimated to freshwater (FW) and seawater (SW). Juvenile C. leucas captured in FW (3 mOsm l(-1) kg(-1)) were acclimated to SW (980-1,000 mOsm l(-1) kg(-1)) over 16 days. A FW group was maintained in captivity over a similar time period. In FW, bull sharks were hyper-osmotic regulators, having a plasma osmolarity of 595 mOsm l(-1) kg(-1). In SW, bull sharks had significantly higher plasma osmolarities (940 mOsm l(-1) kg(-1)) than FW-acclimated animals and were slightly hypo-osmotic to the environment. Plasma Na(+), Cl(-), K(+), Mg(2+), Ca(2+), urea and trimethylamine oxide (TMAO) concentrations were all significantly higher in bull sharks acclimated to SW, with urea and TMAO showing the greatest increase. Gill, rectal gland, kidney and intestinal tissue were taken from animals acclimated to FW and SW and analysed for maximal Na(+)/K(+)-ATPase activity. Na(+)/K(+)-ATPase activity in the gills and intestine was less than 1 mmol Pi mg(-1) protein h(-1) and there was no difference in activity between FW- and SW-acclimated animals. In contrast Na(+)/K(+)-ATPase activity in the rectal gland and kidney were significantly higher than gill and intestine and showed significant differences between the FW- and SW-acclimated groups. In FW and SW, rectal gland Na(+)/K(+)-ATPase activity was 5.6+/-0.8 and 9.2+/-0.6 mmol Pi mg(-1) protein h(-1), respectively. Na(+)/K(+)-ATPase activity in the kidney of FW and SW acclimated animals was 8.4+/-1.1 and 3.3+/-1.1 Pi mg(-1) protein h(-1), respectively. Thus juvenile bull sharks have the osmoregulatory plasticity to acclimate to SW; their preference for the upper reaches of rivers where salinity is low is therefore likely to be for predator avoidance and/or increased food abundance rather than because of a physiological constraint.

Adaptation, Physiological↗

PubMed2001

Family origin and the response of threespine stickleback, Gasterosteus aculeatus, to thermal acclimation.

To establish whether family origin affects the response of the threespine stickleback (Gasterosteus aculeatus) to thermal acclimation, we examined the rates of feeding, growth, and food conversion, relative tissue and organ masses and activities of a mitochondrial and a glycolytic enzyme in pectoral and axial muscle of individually housed fish from six families during acclimation to 8 degrees C and 23 degrees C. Feeding rates differed among families but were consistently higher in warm-acclimated than cold-acclimated fish. Growth rates differed among families. In four families growth was greater at 8 degrees C; these families generally had higher conversion efficiencies at 8 degrees C than 23 degrees C. For two families, growth was greater at 23 degrees C than 8 degrees C and conversion efficiencies did not differ between 8 degrees C and 23 degrees C. Relative tissue and organ masses (percent axial muscle, hepatosomatic, gut and kidney indices) differed with gender and among families (hepatosomatic, gut and kidney indices) but little with acclimation status. In all families and in both muscles, activities of the mitochondrial enzyme, citrate synthase (CS), were increased by cold acclimation. Axial muscle levels of the glycolytic enzyme, lactate dehydrogenase (LDH), were not affected by thermal acclimation or family origin, but were strongly correlated with the hepatosomatic index and axial muscle protein content. Pectoral muscle levels of LDH were affected by family origin which also influenced the response to thermal acclimation. Similar patterns were observed for specific activities and total muscle contents of these enzymes. Stickleback family origin influenced rates of feeding and growth and the thermal sensitivity of growth rates but not the compensatory increase in muscle CS levels with cold acclimation. The differing thermal sensitivities of growth could reflect distinct strategies for the timing of juvenile growth.

Acclimatization↗