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Molecular control of membrane properties during temperature acclimation. Fatty acid desaturase regulation of membrane fluidity in acclimating Tetrahymena cells.

This is a study of the molecular mechanisms employed by Tetrahymena pyriformis to change the lipid composition and thereby the fluidity of its various membranes during temperature acclimation. By quantitatively measuring the intramembrane particle aggregation using freeze-fracture electron microscopy, membrane physical properties in 39.5 degrees C grown cells shifted to 15 degrees C were found to be correlated with the degree of phospholipid fatty acid desaturation. Alteration of the phospholipid polar head group distribution from that of 39.5 degrees C-grown cells to the significantly different pattern of 15 degrees C grown cells appeared not to be of critical importance in the acclimation process. Changes in fatty acid desaturation during acclimation from high to low temperatures and vice versa were analyzed using normal cells and cells fed large amounts of polyunsaturated fatty acids. Fatty acid desaturase activity corresponded to the degree of membrane fluidity but not to the cell temperature. All evidence was compatible with the hypothesis that membrane fluidity is self-regulating, with the action of fatty acid desaturases being modulated by the physical state of their membrane environment.

Acetates↗

Epinephrine stimulates prostaglandin synthesis by bullfrog lung from warm-acclimated, but not cold-acclimated, animals.

Exogenous prostaglandins (PGs) have been shown to have differing effects on frog lung contractility. In this study, prostaglandin synthesis was measured in lung tissues from warm-acclimated (WA, 22 degrees C) and cold-acclimated (CA, 5 degrees C) American bullfrogs, Rana catesbeiana, incubated for 30 min at 5 degrees or 22 degrees C. Media were assayed by radioimmunoassay for PGE2, PGF2 alpha, 6-keto PGF 1 alpha (the metabolite of PGI2), and thromboxane (TX)B2 (the metabolite of TXA2). PGE2 was produced in greatest quantity by tissues from WA and CA animals, at both incubation temperatures. Epinephrine stimulated PGE2, PGF2 alpha, and TXB2 synthesis at 22 degrees C but only stimulated PGE2 production at 5 degrees C. In tissues from CA frogs, epinephrine did not stimulate prostaglandin synthesis at either incubation temperature. Ibuprofen (10(-5) M) inhibited basal and epinephrine-stimulated prostaglandin synthesis in tissues from WA frogs incubated at 22 degrees C. The beta receptor antagonist propranolol (10(-6) M) blocked the epinephrine-stimulated synthesis of PGE2, PGF2 alpha and TXB2, suggesting epinephrine stimulates prostaglandin synthesis through beta receptor activation. The absence of stimulation by epinephrine in lung from CA animals, but not in 5 degrees C incubations of tissues from WA animals, suggests that a modification of beta receptors occurs during prolonged cold exposure.

Acclimatization↗

The beneficial acclimation hypothesis versus acclimation of specific traits: physiological change in water-stressed Manduca sexta caterpillars.

Do organisms make beneficial physiological adjustments in response to environmental change? We examined this question by measuring the effects of short-term (12-36 h) and long-term (larval lifetime) hydric stress on the tobacco hornworm, Manduca sexta. Larvae were reared from the first instar on low-water (69%) or high-water (80%) artificial diets and then transferred early in the fifth instar to the same or opposite diet (2x2 design). Within the subsequent 36 h, we measured 24-h growth rates and three primary determinants of the water budget: water gain via consumption and water loss via evaporation and defecation. Larvae preexposed to low-water diet grew less rapidly on low-water diet than those switched acutely to low-water diet from high-water diet, showing that larvae preexposed to a particular environment do not necessarily acclimate beneficially to that environment. Our data on water fluxes to and from larvae, however, strongly suggest that water-stressed larvae did make beneficial physiological adjustments. Larvae responded to short-term hydric stress by minimizing rates of water excretion, primarily by increasing rates of rectal water absorption. Larvae responded to chronic water stress by significantly reducing rates of evaporative water loss; they also showed additional reductions in fecal water excretion, but these decreases were due to lowered consumption and not to further increases in rate of rectal water absorption. This mismatch between maladaptive acclimation of organismal performance and beneficial adjustment of suborganismal traits can be reconciled by recognizing that organismal physiology is hierarchical: fitness-related performance traits represent the aggregate outcome of numerous, more mechanistic physiological traits. Although chronic exposure to an environment may depress the aggregate effect of these mechanistic traits on performance, organisms are not precluded from making beneficial adjustments to individual traits contributing to performance.

Acclimatization↗

HIF-1alpha-targeted pathways are activated by heat acclimation and contribute to acclimation-ischemic cross-tolerance in the heart.

Hypoxia-inducible factor-1 (HIF-1) is a key regulator of the cellular hypoxic response. We previously showed that HIF-1 activation is essential for heat acclimation (AC) in Caenorhabditis elegans. Metabolic changes in AC rat hearts indicate HIF-1alpha activation in mammals as well. Here we characterize the HIF-1alpha profile and the transcriptional activation of its target genes following AC and following heat stress (HS) in hearts from nonacclimated (C; 24 degrees C) and AC (34 degrees C, 1 mo) rats. We used Western blot and immunohistochemistry to measure HIF-1alpha levels and EMSA and RT-PCR/quantitative RT-PCR to detect expression of the HIF-1alpha-targeted genes, including vascular endothelial growth factor (Vegf), heme oxygenase-1 (HO1), erythropoietin (Epo), and Epo receptor (EpoR). EpoR and Epo mRNA levels were measured to determine systemic effects in the kidneys and cross-tolerance effects in C and AC ischemic hearts (Langendorff, 75% ischemia, 40 min). The results demonstrated that 1) after AC, HIF-1alpha protein levels were increased, 2) HS alone induced transient HIF-1alpha upregulation, and 3) VEGF and HO1 mRNA levels increased after HS, with greater magnitude in the AC hearts. Epo mRNA in AC kidneys and EpoR mRNA in AC hearts were also elevated. In AC hearts, EpoR expression was markedly higher after HS or ischemia. Hearts from AC rats were dramatically protected against infarction after ischemia-perfusion. We conclude that HIF-1 contributes to the acclimation-ischemia cross-tolerance mechanism in the heart by induction of both chronic and inducible adaptive components.

Animals↗

The influence of thermal acclimation on power production during swimming. II. Mechanics of scup red muscle under in vivo conditions.

We have previously shown that the power output of red muscle from warm-acclimated scup is greatly reduced when the fish swim at low temperatures. This reduction occurs primarily because, despite the slowing of muscle relaxation rate at cold temperatures, warm-acclimated scup swim with the same tail-beat frequency and the same stimulation durations, thereby not affording the slower-relaxing muscle any extra time to relax. We hypothesize that power output during swimming could be increased if the stimulus duration were reduced or if the relaxation rate of the red muscle were increased during cold acclimation. Scup were acclimated to 10 degrees C (cold-acclimated) and 20 degrees C (warm-acclimated) for at least 6 weeks. Cold acclimation dramatically increased the ability of scup red muscle to produce power at 10 degrees C. Power output measured from cold-acclimated muscle bundles driven through in vivo conditions measured from cold-acclimated scup swimming at 10 degrees C (i.e. work loops) was generally much greater than that from warm-acclimated muscle driven through its respective in vivo conditions at 10 degrees C. The magnitude of the increase depended both on the anatomical location of the muscle and on swimming speed. Integrated over the length of the fish, the red musculature from cold-acclimated fish generated 2.7, 8.9 and 5.8 times more power than the red musculature from warm-acclimated fish while swimming at 30 cm s(-)(1), 40 cm s(-)(1) and 50 cm s(-)(1), respectively. Our analysis suggests that the cold-acclimated fish should be able to swim in excess of 40 cm s(-)(1) with just their red muscle whereas the warm-acclimated fish must recruit their pink muscle well below this speed. Because the red muscle is more aerobic than the pink muscle, cold acclimation may increase the sustained swimming speed at which scup perform their long seasonal migrations at cool temperatures. We then explored the underlying mechanisms for the increase in muscle power output in cold-acclimated fish. Contrary to our expectations, cold-acclimated muscle did not have a faster relaxation rate; instead, it had an approximately 50 % faster activation rate. Our work-loop studies showed that this faster activation rate, alone, can increase the mechanical power production during cyclical contractions to a surprising extent. By driving cold-acclimated muscle through warm- and cold-acclimated in vivo conditions, we were able to partition the improvement in power production associated with increased activation rate and the approximately 20 % reduction in the duration of electromyographic activity found in the accompanying study. Depending on the position and swimming speed, approximately 60 % of the increase in power output was due to the change in the red muscle's contractile properties (i.e. faster activation); the remainder was due to the shorter stimulus duty cycle of cold-acclimated scup. Thus, by both shortening the in vivo stimulation duration and speeding up the rate of muscle activation as part of cold-acclimation, scup achieve a very large increase in the power output of their red muscle during swimming at low temperature. This increase in power output probably results in an increase in muscle efficiency and, hence, a reduction in the energetic cost of swimming. This increase in power output also reduces reliance on the less aerobic and less fatigue-resistant pink muscle. Both these abilities may increase the swimming speed at which prolonged aerobic muscle activity can occur and thus reduce the travel time for the long seasonal migrations in which scup engage.

Adaptation, Physiological↗

Ca2+-ATPase activity and Ca2+ uptake by sarcoplasmic reticulum in fish heart: effects of thermal acclimation.

This study was designed to compare the activities of sarcoplasmic (SR) Ca2+-ATPase and Ca2+ uptake in fish and mammalian hearts and to determine whether thermal acclimation has any effect on the function of the cardiac SR in fish. To this end, we measured thapsigargin-sensitive Ca2+-ATPase activity and thapsigargin-inhibitable Ca2+ uptake velocity in crude cardiac homogenates of newborn and adult rats and of two teleost fish (crucian carp and rainbow trout) acclimated to low (4 degrees C) and high (17 degrees C and 24 degrees C for trout and carp, respectively) ambient temperatures. The TG-sensitive Ca2+-ATPase activity was highest in adult rat, and the corresponding activities of cold-acclimated trout, warm-acclimated trout, warm-acclimated carp, cold-acclimated carp and newborn rat were 76, 58, 43, 28 and 23 %, respectively, of that of the adult rat at 25 degrees C. SR Ca2+ uptake velocity, measured using Fura-2 at room temperature (approximately 22 degrees C), was highest in cold-acclimated trout, and the values for adult rat, warm-acclimated trout, newborn rat, warm-acclimated carp and cold-acclimated carp were 93, 56, 24, 21 and 14 % of the uptake velocity of cold-acclimated trout, respectively. When corrected to the body temperature of the animal, the relative rates of SR Ca2+ uptake were 100, 26, 19, 18, 11 and 2 % for adult rat, newborn rat, cold-acclimated trout, warm-acclimated trout, warm-acclimated carp and cold-acclimated carp, respectively. These findings show that SR Ca2+ uptake is slower in fish than in mammalian hearts and that marked species-specific differences exist among teleost fish in this respect. Furthermore, acclimation to cold increases the Ca2+ uptake rate of trout cardiac SR (complete thermal compensation) but decreases the SR Ca2+ uptake rate of crucian carp heart. This difference in acclimation response probably reflects the different activity patterns of the two species in their natural habitat during the cold season.

Adaptation, Physiological↗

Extended alternating-temperature cold acclimation and culture duration improve pear shoot cryopreservation.

Meristems of many pear genotypes can be successfully cryopreserved following 1 week of cold acclimation, but an equal number do not survive the process or have very little regrowth. This study compared commonly used cold acclimation protocols to determine whether the cold acclimation technique used affected the cold hardiness of shoots or the regrowth of cryopreserved meristems. In vitro-grown pear (Pyrus L.) shoots were cold acclimated for up to 16 weeks, then either the shoot tips were tested for cold hardiness or the meristems were cryopreserved by controlled freezing. Cold acclimation consisted of alternating temperatures (22 degrees C with light/-1 degrees C darkness with various photo- and thermoperiods) or a constant temperature (4 degrees C with an 8-h photoperiod or darkness). Compared with nonacclimated controls, both alternating- and constant-temperature acclimation significantly improved postcryopreservation regrowth of P. cordata Desv. and P. pashia Buch. -Ham. ex D. Don meristems. Alternating-temperature acclimation combined with either an 8-h photoperiod or darkness was significantly better than constant-temperature acclimation. Alternating-temperature shoot acclimation for 2 to 5 weeks significantly increased postcryopreservation meristem regrowth, and recovery remained high for up to 15 weeks acclimation. Postcryopreservation meristem regrowth increased with 1 to 5 weeks of constant-temperature acclimation and then declined with longer acclimation. Shoot cold hardiness varied with the acclimation procedure. The LT(50) of shoots acclimated for 10 weeks with alternating temperatures was -25 degrees C; that with constant temperature was -14.7 degrees C; and that of the nonacclimated control was -10 degrees C. Less frequent transfer of cultures also improved acclimation of shoots. Shoots grown without transfer to fresh medium for 6-12 weeks had higher postcryopreservation recovery with shorter periods of acclimation than shoots with a 3-week transfer cycle.

Acclimatization↗

Thermal acclimation of locomotor performance in tadpoles and adults of the aquatic frog Xenopus laevis.

Among amphibians, the ability to compensate for the effects of temperature on the locomotor system by thermal acclimation has only been reported in larvae of a single species of anuran. All other analyses have examined predominantly terrestrial adult life stages of amphibians and found no evidence of thermal acclimatory capacity. We examined the ability of both tadpoles and adults of the fully aquatic amphibian Xenopus laevis to acclimate their locomotor system to different temperatures. Tadpoles were acclimated to either 12 degrees C or 30 degrees C for 4 weeks and their burst swimming performance was assessed at four temperatures between 5 degrees C and 30 degrees C. Adult X. laevis were acclimated to either 10 degrees C or 25 degrees C for 6 weeks and their burst swimming performance and isolated muscle performance was determined at six temperatures between 5 degrees C and 30 degrees C. Maximum swimming performance of cold-acclimated X. laevis tadpoles was greater at cool temperatures and lower at the highest temperature in comparison with the warm-acclimated animals. At the test temperature of 12 degrees C, maximum swimming velocity of tadpoles acclimated to 12 degrees C was 38% higher than the 30 degrees C-acclimation group, while at 30 degrees C, maximum swimming velocity of the 30 degrees C-acclimation group was 41% faster than the 12 degrees C-acclimation group. Maximum swimming performance of adult X. laevis acclimated to 10 degrees C was also higher at the lower temperatures than the 25 degrees C acclimated animals, but there was no difference between the treatment groups at higher temperatures. When tested at 10 degrees C, maximum swimming velocity of the 10 degrees C-acclimation group was 67% faster than the 25 degrees C group. Isolated gastrocnemius muscle fibres from adult X. laevis acclimated to 10 degrees C produced higher relative tetanic tensions and decreased relaxation times at 10 degrees C in comparison with animals acclimated to 25 degrees C. This is only the second species of amphibian, and the first adult life stage, reported to have the capacity to thermally acclimate locomotor performance.

Acclimatization↗

Acclimation of entomopathogenic nematodes to novel temperatures: trehalose accumulation and the acquisition of thermotolerance.

The effect of thermal acclimation on trehalose accumulation and the acquisition of thermotolerance was studied in three species of entomopathogenic nematodes adapted to either cold or warm temperatures. All three Steinernema species accumulated trehalose when acclimated at either 5 or 35 degrees C, but the amount of trehalose accumulation differed by species and temperature. The trehalose content of the cold adapted Steinernema feltiae increased by 350 and 182%, of intermediate Steinernema carpocapsae by 146 and 122% and of warm adapted Steinernema riobrave by 30 and 87% over the initial level (18.25, 27.24 and 23.97 microg trehalose/mg dry weight, respectively) during acclimation at 5 and 35 degrees C, respectively. Warm and cold acclimation enhanced heat (40 degrees C for 8h) and freezing (-20 degrees C for 4h) tolerance of S. carpocapsae and the enhanced tolerance was positively correlated with the increased trehalose levels. Warm and cold acclimation also enhanced heat but not freezing tolerance of S. feltiae and the enhanced heat tolerance was positively correlated with the increased trehalose levels. In contrast, warm and cold acclimation enhanced the freezing but not heat tolerance of S. riobrave, and increased freezing tolerance of only warm acclimated S. riobrave was positively correlated with the increased trehalose levels. The effect of acclimation on maintenance of original virulence by either heat or freeze stressed nematodes against the wax moth Galleria mellonella larvae was temperature dependent and differed among species. During freezing stress, both cold and warm acclimated S. carpocapsae (84%) and during heat stress, only warm acclimated S. carpocapsae (95%) maintained significantly higher original virulence than the non-acclimated (36 and 47%, respectively) nematodes. Both cold and warm acclimated S. feltiae maintained significantly higher original virulence (69%) than the non-acclimated S. feltiae (0%) during heat but not freezing stress. In contrast, both warm and cold acclimated S. riobrave maintained significantly higher virulence (41%) than the non-acclimated (14%) nematodes during freezing, but not during heat stress. Our data indicate that trehalose accumulation is not only a cold associated phenomenon but is a general response of nematodes to thermal stress. However, the extent of enhanced thermal stress tolerance conferred by the accumulated trehalose differs with nematode species.

Acclimatization↗

Differential Gene Expression in Chilling-Acclimated Maize Seedlings and Evidence for the Involvement of Abscisic Acid in Chilling Tolerance.

An acclimation phenomenon was characterized in seedlings of chilling-sensitive maize (Zea mays L.) inbred G50 (Pioneer). Seedlings were germinated at 27[deg]C for 3 d and then exposed to chilling treatments of 4, 5, or 6[deg]C for 2, 4, 7, or 10 d in darkness. Damage symptoms in the more severe treatments included a waterlogged appearance and a discoloration of the tissue. The symptoms were most obvious in the mesocotyl. After a 10-d grow-out period in the greenhouse, moderately damaged seedlings exhibited chlorotic areas, an occasional disruption in leaf expansion, and a constriction of the mesocotyl. Growth and survival were improved by first exposing seedlings to a 14[deg]C acclimation treatment for 3 d before applying the chilling treatment. After chilling at 5[deg]C for 7 d, 79% of the acclimated seedlings survived, whereas only 22% of the nonacclimated seedlings survived. Differences in gene expression between acclimated and control seedlings were investigated using subtraction and differential screening techniques. Transcripts corresponding to three genes, car333, car30, and car757 (chilling acclimation responsive), were present in higher levels in seedlings after acclimation. Sequence analysis identified car333 as cat3, which encodes maize mitochondrial catalase isozyme 3. Characterization of these three clones revealed that all corresponding transcripts were elevated in acclimated seedlings in a manner that depended on the organ, i.e. coleoptile, mesocotyl, or root. Although transcripts were elevated in all three organs in response to acclimation, car30 was most abundant in the coleoptile and root, whereas cat3 and car757 were most abundant in the coleoptile and mesocotyl. Catalase activity followed the same general trend as cat3 transcript levels. Exogenous treatment with abscisic acid (ABA) resulted in an improvement in growth and survival of nonacclimated, chilled seedlings. Inhibition of ABA biosynthesis with fluridone abolished acclimation-induced chilling tolerance, and exogenous application of ABA to fluridone-treated seedlings restored chilling tolerance. Exogenous ABA treatment also resulted in increases in cat3, car30, and car757 transcript levels and catalase activity in the same organ-specific manner as in acclimated seedlings. These results indicate that ABA synthesis is essential for chilling tolerance. However, measurement of ABA levels in mesocotyls during acclimation and chilling revealed only a marginal increase during acclimation and a dramatic increase during chilling, regardless of whether or not seedlings were acclimated. Thus, although ABA may be required for chilling tolerance, we have no conclusive evidence that the acclimation process is mediated by ABA.

Journal Article↗

Cold-acclimation in Peromyscus: temporal effects and individual variation in maximum metabolism and ventilatory traits.

Thermal acclimation in small endotherms provides an excellent model for the study of physiological plasticity, as energy requirements can be easily manipulated and the results are relevant for natural conditions. Nevertheless, how physiology changes throughout acclimation, and how individuals vary in their response to acclimation, remain poorly understood. Here we describe a high temporal-resolution study of cold acclimation in the deer mouse Peromyscus maniculatus. The experimental design was based on repeated measures at short intervals throughout cold acclimation, with controls (maintained at constant temperature) for measurement artifacts. We monitored body mass, maximum metabolic rate in cold exposure and ventilatory traits (respiratory frequency, tidal and minute volume and oxygen extraction) for 3 weeks at 23 degrees C. Then, half of the individuals were held for 7 weeks at 5 degrees C. Body mass was differently affected by cold acclimation depending on sex. Maximal metabolism ((O(2)max)) increased significantly during the first week of cold acclimation, "overshot" after 5 weeks and dropped to a plateau about 34% above control values at week 7. Similarly, ventilatory traits increased during cold acclimation, though responses were different in their kinetics and magnitude. Body mass, maximum metabolism, and most ventilatory traits were repeatable after 7 weeks in control and cold-acclimated animals. However, repeatability tended to be lower in the cold-acclimated group, especially while animals were still acclimating. Our results show that acclimation effects may be under- and/or overestimated, depending on when trials are performed, and that different traits respond differently, and at different rates, to acclimation. Hence, future studies should be designed to ensure that animals have attained steady-state values in acclimation experiments.

Acclimatization↗

Capillarisation, oxygen diffusion distances and mitochondrial content of carp muscles following acclimation to summer and winter temperatures.

Many species of fish show a partial or complete thermal compensation of metabolic rate on acclimation from summer to winter temperatures. In the present study Crucian carp (Carassius carassius L.) were acclimated for two months to either 2 degrees C or 28 degrees C and the effects of temperature acclimation on mitochondrial content and capillary supply to myotomal muscles determined. Mitochondria occupy 31.4% and 14.7% of slow fibre volume in 2 degrees C- and 28 degrees C-acclimated fish, respectively. Fast muscles of cold- but not warm-acclimated fish show a marked heterogeneity in mitochondrial volume. For example, only 5% of fast fibres in 28 degrees C-acclimated fish contain 5% mitochondria compared to 34% in 2 degrees C-acclimated fish. The mean mitochondrial volume in fast fibres is 6.1% and 1.6% for cold- and warm-acclimated fish, respectively. Increases in the mitochondrial compartment with cold acclimation were accompanied by an increase in the capillary supply to both fast (1.4 to 2.9 capillaries/fibre) and slow (2.2 to 4.8 capillaries/fibre) muscles. The percentage of slow fibre surface vascularised is 13.6 in 28 degrees C-acclimated fish and 32.1 in 2 degrees C-acclimated fish. Corresponding values for fast muscle are 2.3 and 6.6% for warm- and cold-acclimated fish, respectively. Maximum hypothetical diffusion distances are reduced by approximately 23-30% in the muscles of 2 degrees C-compared to 28 degrees C-acclimated fish. However, the capillary surface supplying 1 micron 3 of mitochondria is similar at both temperatures. Factors regulating thermal compensation of aerobic metabolism and the plasticity of fish muscle to environmental change are briefly discussed.

Adaptation, Physiological↗

Thermal acclimation of locomotor performance in tadpoles of the frog Limnodynastes peronii.

Previous analyses of thermal acclimation of locomotor performance in amphibians have only examined the adult life history stage and indicate that the locomotor system is unable to undergo acclimatory changes to temperature. In this study, we examined the ability of tadpoles of the striped marsh frog (Limnodynastes peronii) to acclimate their locomotor system by exposing them to either 10 degrees C or 24 degrees C for 6 weeks and testing their burst swimming performance at 10, 24, and 34 degrees C. At the test temperature of 10 degrees C, maximum velocity (Umax) of the 10 degrees C-acclimated tadpoles was 47% greater and maximum acceleration (Amax) 53% greater than the 24 degrees C-acclimated animals. At 24 degrees C, Umax was 16% greater in the 10 degrees C-acclimation group, while there was no significant difference in Amax or the time taken to reach Umax (T-Umax). At 34 degrees C, there was no difference between the acclimation groups in either Umax or Amax, however T-Umax was 36% faster in the 24 degrees C-acclimation group. This is the first study to report an amphibian (larva or adult) possessing the capacity to compensate for cool temperatures by thermal acclimation of locomotor performance. To determine whether acclimation period affected the magnitude of the acclimatory response, we also acclimated tadpoles of L. peronii to 10 degrees C for 8 months and compared their swimming performance with tadpoles acclimated to 10 degrees C for 6 weeks. At the test temperatures of 24 degrees C and 34 degrees C, Umax and Amax were significantly slower in the tadpoles acclimated to 10 degrees C for 8 months. At 10 degrees C, T-Umax was 40% faster in the 8-month group, while there were no differences in either Umax or Amax. Although locomotor performance was enhanced at 10 degrees C by a longer acclimation period, this was at the expense of performance at higher temperatures.

Acclimatization↗

Cold hardiness in summer and winter diapause and post-diapause pupae of the cabbage armyworm, Mamestra brassicae L. under temperature acclimation.

Cold hardiness and biochemical changes were investigated in winter and summer pupae of the cabbage armyworm Mamestra brassicae at the diapause and post-diapause stages under temperature acclimation. Diapause pupae were successively acclimated to 25, 20 and then 10 degrees C (warm-acclimated group). Pupae at the diapause and post-diapause stages were successively acclimated to 5, 0, -5 and then -10 degrees C (cold-acclimated groups). Supercooling point values in winter and summer pupae remained constant regardless of the diapause stages and acclimated temperatures. Warm-acclimated pupae at the diapause stage did not survive the subzero temperature exposure, whereas, cold-acclimated pupae achieved cold hardiness to various degrees. Winter pupae were more cold hardy than summer pupae, and pupae at the post-diapause stage were more cold hardy than those at the diapause stage. Trehalose contents in winter pupae rose under cold acclimation. Summer pupae accumulated far lower trehalose contents than winter pupae, with the maximal level occurring in winter pupae at the post-diapause stage. Glycogen content remained at a high level in diapause pupae after warm acclimation, whereas it decreased after cold acclimation. Alanine, the main free amino acid in haemolymph after cold acclimation, increased at lower temperatures in both diapause and post-diapause pupae, but the increase was greater in the diapause pupae. These results suggest that cold hardiness is more fully developed in winter pupae than in summer pupae, and cold acclimation provides higher cold hardiness in winter pupae at the post-diapause stage than at the diapause stage.

Journal Article↗

Effects of endurance training and heat acclimation on psychological strain in exercising men wearing protective clothing.

Two experiments examined the influences of endurance training and heat acclimation on ratings of perceived exertion (RPE) and thermal discomfort (RTD) during exercise in the heat while wearing two types of clothing. In experiment 1, young men underwent 8 weeks of physical training [60-80% of maximal aerobic power (VO2max) for 30-45 min day-1, 3-4 days week-1 at 20-22 degrees C dry bulb (db) temperature] followed by 6 days of heat acclimation [45-55% VO2max for 60 min day-1 at 40 degrees C db, 30% relative humidity (rh)] (n = 7) or corresponding periods of control observation followed by heat acclimation (n = 9). In experiment 2, young men were heat-acclimated for 6 or 12 days (n = 8 each). Before and after each treatment, subjects completed bouts of treadmill exercise (1.34 m s-1, 2% grade in experiment 1 and 0% grade in experiment 2) in a climatic chamber (40 degrees C db, 30% rh), wearing in turn normal light clothing (continuous exercise at 37-45% VO2max for a tolerated exposure of 116-120 min in experiment 1 and at 31-34% VO2max for 146-150 min in experiment 2) or clothing protective against nuclear, biological, and chemical agents (continuous exercise at 42-51% VO2max for a tolerated exposure of 47-52 min in experiment 1 and intermittent exercise at 23% VO2max for 97-120 min in experiment 2). In experiment 1, when wearing normal clothing, endurance training and/or heat acclimation significantly decreased RPE and/or RTD at a fixed power output. There were concomitant reductions in relative work intensity (% VO2max) [an unchanged oxygen consumption (VO2) but an increased VO2max, or a reduced VO2 with no change of VO2max], rectal temperature (Tre), mean skin temperature (Tsk), and/or heart rate (HR). When wearing protective clothing, in contrast, there were no significant changes in RPE or RTD. Although training and/or acclimation reduced %VO2max or Tre, any added sweat that was secreted did not evaporate through the protective clothing, thus increasing discomfort after training or acclimation. Tolerance times were unchanged in either normal or protective clothing. In experiment 2, when wearing normal clothing, heat acclimation significantly decreased RPE and RTD at a fixed power output, with concomitant reductions in Tre, Tsk, and HR; the response was greater after 12 than after 6 days of acclimation, significantly so for RPE and HR. When wearing protective clothing, the subjects exercised at a lower intensity for a longer duration than in the moderate exercise trial. Given this tactic, either 6 or 12 days of heat acclimation induces significant reductions RPE and/or RTD, accompanied by reductions in Tre, Tsk, and/or HR. Tolerance times in protective clothing were also increased by 11-15% after acclimation, despite some increase of sweat accumulation in the protective clothing. The results suggest that (1) neither endurance training nor heat acclimation reduce psychological strain when protective clothing is worn during vigorous exercise, because increased sweat accumulation adds to discomfort, and (2) in contrast to the experience during more vigorous exercise, heat acclimation is beneficial to the subject wearing protective clothing if the intensity of effort is kept to a level that allows permeation of sweat through the clothing. This condition is likely to be met in most modern industrial applications.

Acclimatization↗