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Rate of ventilatory acclimatization to extreme altitude.

One of the most important factors in the acclimatization of lowlanders to high altitude is hyperventilation which helps to defend the alveolar PO2. However, how rapidly this occurs at very high altitude is poorly understood. Information can be obtained by comparing the alveolar gas values reported from the extended low pressure chamber studies, Operation Everest I and II, and the American medical research expedition to Everest (AMREE) of 1981. Rahn and Otis (1949) reported the alveolar PO2 and PCO2 values for non-acclimatized and well-acclimatized man on an O2-CO2 diagram, and pointed out that the Operation Everest I data fell approximately halfway between the two curves. The AMREE data agree well with the fully-acclimatized curve, and the Operation Everest II values are intermediate. The differences can be partly, though not wholly, attributed to the different periods of acclimatization. The conclusion is that 31 and 36 days are inadequate periods of acclimatization for altitudes over 8000 m, but that 77 days is sufficient. However, other factors are also involved.

Acclimatization↗

The threshold induction temperature of the 90-kDa heat shock protein is subject to acclimatization in eurythermal goby fishes (genus Gillichthys).

Two extremely eurythermal goby fishes, Gillichthys mirabilis and Gillichthys seta, which encounter habitat temperature variations of approximately 30 degrees C, showed seasonal acclimatization of endogenous levels and of onset temperatures for enhanced synthesis of a 90-kDa-class heat shock protein (HSP90). Summer-acclimatized fishes had higher levels of HSP90 in brain tissue than winter-acclimatized specimens, as shown by Western blot analysis. For winter-acclimatized fishes, increased synthesis of HSP90 was observed when the temperature was raised from a control temperature (18 degrees C) to 28 degrees C. For summer-acclimatized fish, no significantly increased synthesis of HSP90 occurred until the experimental temperature was raised to 32 degrees C. These data suggest that the threshold temperature at which enhanced expression of HSP-encoding genes occurs is not hard-wired genetically but may be subject to acclimatization. A causal relationship between seasonal changes in steady-state levels of HSP90 and the threshold temperature for enhanced HSP90 synthesis is discussed in terms of existing models for the regulation of HSP gene expression.

Acclimatization↗

The influence of acute hypothermia on renal function of anaesthetized euthermic and acclimatized rats.

Acute hypothermia has a major impact on cardiovascular control and renal function, but the extent to which these can be correlated with and influenced by changes in the altered pattern of sympathetic outflow to the kidneys is unclear. Moreover, it is unknown whether these responses to acute hypothermia are altered by chronic cold exposure and this study aimed to examine these factors. Renal function and renal sympathetic nerve activity (RSNA) were measured in male Wistar rats, euthermic (control) or acclimatized (exposed to progressively lower environmental temperature and photoperiod over 8 weeks), anaesthetized with chloralose/urethane. Reduction of core temperature (Tc) to 25 degrees C caused approximately 40% reduction in heart rate (HR), approximately 10% fall in mean arterial blood pressure (MABP), and decreased glomerular filtration rate (GFR) by approximately 50% and approximately 5% in euthermic and acclimatized rats, respectively. At 25 degrees C, urine flow increased some two-fold and absolute and fractional sodium excretions by 4- to 6-fold in the euthermic rats and to a lesser extent in the cold acclimatized rats, while basal levels of fluid excretion were higher in the acclimatized rats. A loss of pulsatility in the RSNA signal with cooling was seen in both groups. One of the factors contributing to modest hypotension during acute hypothermia is a reduction in RSNA. There was a progressive fall in the proportion of RSNA power at HR frequency with cooling of 20% in euthermic and 80% in acclimatized rats. All variables were restored to basal levels on rewarming in both groups of rats. We conclude that natriuresis and diuresis in euthermic rats during hypothermia is a consequence of a reduction in nephron reabsorption, reduced urine osmolality and possibly altered patterning of RSNA. In acclimatized rats, the response was modified by altered renal haemodynamics and/or hormonal influences induced by chronic cold exposure to minimize the hypothermic stress on renal function.

Acclimatization↗

Changes in plasma volume and protein content during exposures of working men to various temperatures before and after acclimatization to heat: separation of the roles of cutaneous and skeletal muscle circulation.

1. Ten male subjects were trained in stair stepping for 2 weeks. Group A (six subjects) was thereupon sequentially exposed for 45 min to dry bulb temperatures of 20, 40 and 30 degrees C, a vapour pressure of 10-11 mm Hg and a wind speed of 1 m/sec in a climate tunnel. While temperature changes were being effected the subjects rested in an antechamber. Group B (four subjects) was exposed to a sequence of 40, 20 and 30 degrees C. Work rate was the same for all subjects, i.e. 216 kg m/min ( approximately to an oxygen consumption of 0.9 l./min). Duplicate experiments were run on both groups of subjects before and after acclimatization to heat.2. Throughout, periodic samples of venous blood, water and protein movement into or out of the extravascular compartment was assessed during exercise periods wherein blood flow was increased to exercising muscles (Group A, 20 degrees C) or to both exercising muscles and skin (Group B, 40 degrees C; Groups A and B, 30 degrees C.)3. Mild exercise in a cool environment before and after acclimatization to heat was accompanied by expansion of the vascular volume and an increase in the amount of circulating protein.4. Mild exercise in a warm environment for 45 min was accompanied by haemoconcentration and loss of protein from the vascular volume before subjects were heat acclimatized. The results were reversed following heat acclimatization; i.e. exposure of Group B to 40 degrees C and of Groups A and B to 30 degrees C was accompanied by haemodilution and addition to (or maintenance of) plasma protein concentration.5. Effects of heat acclimatization on exposure of Group A to 40 degrees C were also noted.6. The effects of heat acclimatization were ascribed to:(a) a change in permeability of cutaneous capillaries to large molecules,(b) an increased availability of translocatable protein within cutaneous interstitial spaces, and(c) a combination of both a and b.7. Further, the results supported a previous suggestion that addition or loss of water and protein from the vascular volume is dependent on the ratio of cutaneous to muscle blood flow.

Acclimatization↗

Catecholamine-synthesizing enzymes in adrenals of seasonally acclimatized voles.

Tyrosine hydroxylase (TH) and phenylethanolamine-N-methyltransferase (PNMT) activities were assayed in adrenal glands of the following groups of the Alaskan red-backed vole (Clethrionomys rutilus dawsoni): 1) laboratory reared at 20 degrees C and 2) exposed to 5 degrees C for 1, 3, 7, and 28 days; 3) wild, summer acclimatized; 4) wild, fall acclimatized; and 5) wild, winter acclimatized. TH activity in laboratory-acclimated voles exposed to 5 degrees C was increased by 2 times after 3 days and remained elevated after 28 days. PNMT activity in these same voles was increased after 7 days and also remained elevated after 28 days of cold exposure. In wild-acclimatized voles TH activity and PNMT activity in summer were equivalent to levels in 28-day cold-acclimated laboratory voles. In fall, TH activity was increased to 2.5 times the summer value. It decreased by midwinter, but remained elevated above the summer level. In contrast, PNMT activity appeared unchanged from summer through fall and winter. Pregnant summer voles had markedly increased TH activity. Adrenal norepinephrine and epinephrine did not change significantly with cold acclimation or seasonal acclimatization. Thus, acclimatization of wild voles to fall and winter conditions involved aquisition of a greater capacity to synthesize adrenal catecholamines than that produced by exposing laboratory-reared voles to an extended period of cold.

Acclimatization↗

Conditioning versus exercise in heat as methods for acclimatizing 8- to 10-yr-old boys to dry heat.

Two heat-acclimatization protocols were studied in 8- to 10-yr-old boys: exercise in dry heat (WH, n = 9) and exercise in neutral climate (W, n = 9). Five 90-min acclimatization sessions were conducted within a 12-day period. Base-line (BL) and criterion (CT) tests sessions were held at 43 degrees C db and 24 degrees C wb, with three 20-min exercise bouts at approximately 40 Ws. With acclimatization, the WH group showed a significant reduction in heart rate (HR) (11.4 beat x min-1), mean skin temperature (0.64 degrees C), and an increase in the population density of heat-activated sweat glands (HASG) (25.2 glands x cm-2). The W group showed a significant reduction in HR (13.4 beat x min-1) and rectal temperature (0.24 C). Total sweat rate per body surface area did not increase significantly in either group. However, the sweat rate relative to rise in core temperature increased in both groups. No significant differences were found between the two acclimatization procedures in any of the variables studies except for the HASG, which showed a greater increase in the WH group. It is suggested that in 8- to 10-yr-old boys physiological changes compatible with heat acclimatization could be achieved either by exercise in heat or by mere physical conditioning (approximately 65% of VO2max), in neutral climate. It is postulated that age-related factors associated with the thermoregulatory system prevent children from deriving full effectiveness of exercise-in-heat acclimatization protocol as used in this study.

Acclimatization↗

Acclimatization to dry heat: active men vs. active women.

Physiological responses to exercise in dry heat were compared between six active men [maximum O2 consumption (VO2max), 51.4 +/- 1.2 ml . kg-1 . min-1] and four active women (VO2max, 47.2 +/- 1.3 ml . kg-1 . min-1) before, during, and after heat acclimatization. Subjects cycled a maximum of 2 h at 40% VO2max at 45 degrees C dry-bulb temperature, 23 degrees C wet-bulb temperature for 11 days. Prior to acclimatization there were no sexual differences for performance time, rate of increase of rectal temperature (delta Tre), or sweat rate per degree C increase of rectal temperature (msw/delta Tre). Sweat rate (msw) was greater for the men than for the women. Although there was no difference in the rate of increase of heart rate (delta HR), HR for the women was maintained 15-20 beats . min-1 higher than for the men. Acclimatization occurred for both sexes as indicated by reduced Tre and HR and increased msw and performance time. With acclimatization the women had longer performance times than the men. Even though the men still had greater msw, delta Tre was also greater; therefore msw/delta Tre for the men was less than for the women. Neither HR nor delta HR was different between the sexes. Throughout, resting hematocrit for the women was less than for the men; no changes in hematocrit were observed during exercise or with acclimatization. Plasma protein concentration increased during exercise on all days; no changes in plasma osmolality were observed. It is concluded that active women perform exercise of equal relative intensity in dry heat as well as active men. Moreover active women acclimatized to heat at a faster rate or to a greater extent than did active men.

Acclimatization↗

Muscle accounts for glucose disposal but not blood lactate appearance during exercise after acclimatization to 4,300 m.

We hypothesized that the increased blood glucose disappearance (Rd) observed during exercise and after acclimatization to high altitude (4,300 m) could be attributed to net glucose uptake (G) by the legs and that the increased arterial lactate concentration and rate of appearance (Ra) on arrival at altitude and subsequent decrease with acclimatization were caused by changes in net muscle lactate release (L). To evaluate these hypotheses, seven healthy males [23 +/- 2 (SE) yr, 72.2 +/- 1.6 kg], on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6-D2]glucose (Brooks et al., J. Appl. Physiol. 70: 919-927, 1991) and [3-13C]lactate (Brooks et al., J. Appl. Physiol. 71:333-341, 1991) and rested for a minimum of 90 min, followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the sea level peak O2 uptake (65 +/- 2% of both acute altitude and acclimatization peak O2 uptake). Glucose and lactate arteriovenous differences across the legs and arms and leg blood flow were measured. Leg G increased during exercise compared with rest, at altitude compared with sea level, and after acclimatization. Leg G accounted for 27-36% of Rd at rest and essentially all glucose Rd during exercise. A shunting of the blood glucose flux to active muscle during exercise at altitude is indicated. With acute altitude exposure, at 5 min of exercise L was elevated compared with sea level or after acclimatization, but from 15 to 45 min of exercise the pattern and magnitude of L from the legs varied and followed neither the pattern nor the magnitude of responses in arterial lactate concentration or Ra. Leg L accounted for 6-65% of lactate Ra at rest and 17-63% during exercise, but the percent Ra from L was not affected by altitude. Tracer-measured lactate extraction by legs accounted for 10-25% of lactate Rd at rest and 31-83% during exercise. Arms released lactate under all conditions except during exercise with acute exposure to high altitude, when the arms consumed lactate. Both active and inactive muscle beds demonstrated simultaneous lactate extraction and release. We conclude that active skeletal muscle is the predominant site of glucose disposal during exercise and at high altitude but not the sole source of blood lactate during exercise at sea level or high altitude.

Acclimatization↗

In vitro reactivity of ventral aorta to acetylcholine and noradrenaline in yellow freshwater eel (Anguilla anguilla L.) acclimatized to 10.1 MPa hydrostatic pressure.

We examined in vitro vascular reactivity of eels previously acclimatized to 10.1 MPa hydrostatic pressure (HP) for 21 days. The isometric tension developed by ventral aortic rings was measured at atmospheric pressure. Dose-response curves for either acetylcholine (ACh) or noradrenaline (NA), as well as contractions evoked by 80 mM K+, were compared with time-matched experiments conducted on rings obtained from control eels. Results showed that neither the optimal tension nor the maximal force of the K+-evoked contraction were significantly modified, suggesting that acclimatization to high HP did not change the vascular smooth muscle contractile machinery. The dose-response curve to ACh was not significantly changed. Conversely, although NA always relaxed aortic rings, the response of acclimatized eels was significantly reduced over the entire range of the agonist concentration tested (10(-8) to 10(-3) M), except for the lowest one (10(-9) M). The maximal amplitude of the NA-induced relaxation was significantly reduced in aortic rings from acclimatized eels as compared with non-acclimatized samples (339.3 +/- 86.5 vs. 744.3 +/- 72.1 mg x mg(-1) dry weight, P < 0.005). Our results suggest that acclimatization to high HP could selectively alter the control of vascular tone by catecholamines.

Acclimatization↗

Increased affinity to substrate in sarcolemmal ATPases from hearts acclimatized to high altitude hypoxia.

It has been well documented that acclimatization to chronic high altitude hypoxia involves a complex of adaptation changes which are capable of protecting the myocardium in diverse situations such as in acute hypoxia, coronary occlusion-induced ischaemia or isoprenaline-induced calcium overload. Since many of the former changes concern membrane functions, namely those of the sarcolemma, the activities and kinetic properties of sarcolemmal Mg2+-, Ca2+- and (Na+ + K+)-ATPase were investigated in right heart ventricles of rats acclimatized to intermittent high altitude hypoxia simulated in a barochamber. In the course of the experiment, the ventricles were subjected to a special anoxic test in vitro. The high altitude induced increase in cardiac tolerance to anoxia was not accompanied by any preservation of the sarcolemmal ATPase activities. On the contrary, membrane preparations obtained from the right ventricles of hearts acclimatized to high altitude exhibited significantly lower ATPase activities in comparison to non-acclimatized controls. The significant diminution in Km values of ATPases established in acclimatized hearts points to an increase in the affinity of their active sites to ATP. The latter effect is in agreement with the lowered rate of both the decrease in ATPase activities and the reduction of contractility in acclimatized hearts during the anoxic test, as well as with the considerably improved postanoxic reparability of contractions as compared to the controls. It is being concluded that the sarcolemmal changes at the level of ATPases involved in ionic transport processes represent an integral part of the adaptation complex to chronic high altitude hypoxia.

Acclimatization↗

Reprogramming of nucleolar gene expression during the acclimatization of the carp.

During seasonal acclimatization of eurythermal fish, the nucleolus of the hepatocyte undergoes ultrastructural reprogramming. In winter acclimatized carp, the nucleolar components are segregated, a condition that suggests a decreased transcription of rRNA. The same nucleolar reorganization was observed when pituitary cells from winter- and summer-acclimatized carp were examined. In situ analyses of nucleolar RNA revealed a marked lowering of RNA content in the segregated nucleoli. Accordingly, in vitro synthesis of RNA was shown to be significantly lower in pituitary tissue from cold-acclimatized fish where precursor accumulated. Conversely, in pituitary tissue from summer-adapted fish the rate and extent of synthesis and of rRNA processing was notably higher. The involvement of pre-rRNA processing events during seasonal acclimatization was corroborated by the strong differences of U3 RNA content detected by in situ hybridization in pituitary cells from summer- and winter-fish. When RNA polymerase I activity from both acclimatized states were assayed, no differences were detected. Thus, it appears that in fish RNA polymerase I itself does not play an important role in the control of nucleolar gene expression and the nucleolar gene expression reprogramming that the seasonal rearrangement represents might involve, among the many nucleolar-specific proteins, transcription factors.

Acclimatization↗

The evolution of photosynthetic capacity and the antioxidant enzymatic system during acclimatization of micropropagated Calathea plants.

The effects of an increased PPFD on photosynthesis, the functioning of the photosynthetic apparatus and the response of the antioxidant enzymatic system were studied during the ex vitro establishment of micropropagated Calathea 'Maui Queen' plantlets. Measured chlorophyll and carotenoids contents in ex vitro formed leaves were almost three times higher compared to the in vitro formed ones. At the end of the acclimatization, an inverse relation between PPFD and the chlorophyll (a+b)/carotenoids ratio was observed. During the first days after transplantation Calathea plants are not photosynthetically active, as is illustrated by the photosynthetic light response curves. With the appearance of new leaves, higher photosynthetic capacities were observed and light saturation point increased (days 17 and 25). Also the maximal photosynthetic efficiency enlarged as shown by the increased initial slope of the curves. F(v)/F(m) decreased directly after transplantation of the micropropagated plantlets, afterwards a recovery was observed, but highest F(v)/F(m) values were observed in low light (LL) plants. The photochemical quenching coefficient increased gradually during the first two weeks of the acclimatization. In high light (HL) plants, q(P) decreased directly after transfer, while this was not observed in LL and medium light (ML). During the acclimatization period to increasing light intensities significant changes in the activity of the antioxidant enzymatic system were observed. A decrease in superoxide dismutase (SOD) activity was measured during the first half of the acclimatization period followed by a recovery in ML and HL plants by day 35. Dehydroascorbate reductase (DHAR) activity decreased during acclimatization. At the end of the experimental period the lowest levels were measured in ML plants. Catalase (CAT) activity increased significantly during the first two weeks after transfer, a clear inverse relationship to PPFD was detected. The relation between the adquisition of full photosynthetic capacity and the activation of the enzymatic antioxidant system in the leaves of calathea plants during ex vitro acclimatization is discussed.

Journal Article↗

Effects of acclimatization and deprivation on non-speech auditory abilities.

This article reviews the evidence for acclimatization and deprivation with respect to non-speech auditory abilities. Although this subject has not been studied extensively, clear evidence exists for acclimatization and/or deprivation effects on intensity discrimination, binaural masking level difference, and auditory localization and lateralization. There is also some argument for such effects with regard to changes in tolerance for intense sounds or preferred levels of amplification. However, the main evidence for these effects, changes in loudness discomfort levels with repeated testing, may reasonably be explained as procedural or task-related effects rather than changes in auditory abilities. On the other hand, the successful use of tinnitus maskers to treat hyperacusis suggests that particularly low tolerance levels may be improved by exposure to certain types of auditory stimulation. Overall, this retrospective review of changes in non-speech auditory abilities, associated with the presence or absence of listening experience, indicates that acclimatization or deprivation effects may have influenced the results of some of the experiments reviewed. This suggests that experiments designed to study acclimatization or deprivation are timely and useful. In addition, acclimatization and deprivation are potential variables that should be considered, and preferably controlled, within experiments on auditory abilities. Clinically, the review adds weight to the argument for considering acclimatization and/or deprivation in hearing aid fitting and evaluation.

Functional Laterality↗

Decreased reliance on lactate during exercise after acclimatization to 4,300 m.

We hypothesized that the increased exercise arterial lactate concentration on arrival at high altitude and the subsequent decrease with acclimatization were caused by changes in blood lactate flux. Seven healthy men [age 23 +/- 2 (SE) yr, wt 72.2 +/- 1.6 kg] on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6-2D]glucose (Brooks et al. J. Appl. Physiol. 70:919-927, 1991) and [3-13C]lactate and rested for a minimum of 90 min followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the sea level peak O2 consumption (VO2peak; 65 +/- 2% of both acute altitude and acclimatization). During rest at sea level, lactate appearance rate (Ra) was 0.52 +/- 0.03 mg.kg-1.min-1; this increased sixfold during exercise to 3.24 +/- 0.19 mg.kg-1.min-1. On acute exposure, resting lactate Ra rose from sea level values to 2.2 +/- 0.2 mg.kg-1.min-1. During exercise on acute exposure, lactate Ra rose to 18.6 +/- 2.9 mg.kg-1.min-1. Resting lactate Ra after acclimatization (1.77 +/- 0.25 mg.kg-1.min-1) was intermediate between sea level and acute exposure values. During exercise after acclimatization, lactate Ra (9.2 +/- 0.7 mg.kg-1.min-1) rose from resting values but was intermediate between sea level and acute exposure values. The increased exercise arterial lactate concentration response on arrival at high altitude and subsequent decrease with acclimatization are due to changes in blood lactate appearance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

The effects of altitude training are mediated primarily by acclimatization, rather than by hypoxic exercise.

For training at altitude to be effective, it must provide some advantage above and beyond similar training at sea level. This advantage could be provided by: 1) acclimatization to altitude which improves oxygen transport and/or utilization; 2) hypoxic exercise which "intensifies" the training stimulus; or 3) some combination of both. Controlled studies of "typical" altitude training, involving both altitude acclimatization and hypoxic exercise have never been shown to improve sea level performance. This failure has been attributed to reduced training loads at altitude. One approach developed by Levine and Stray-Gundersen, called "living high-training low" has been shown to improve sea level performance over events lasting 8-20 minutes. This strategy combines altitude acclimatization (2,500 m) with low altitude training to get the optimal effect. The opposite strategy, "living low-training high" is proposed by Dr. Hoppeler in this debate. In defense of the primacy of the altitude acclimatization effect, data will be presented to support the following: 1). Living high-training low clearly improves performance in athletes of all abilities; 2). The mechanism of this improvement is primarily an increase in erythropoietin leading to increased red cell mass, VO2max, and running performance; 3). Rather than intensifying the training stimulus, training at altitude leads to the opposite effect--reduced speeds, reduced power output, reduced oxygen flux--and, following the principal of symmorphosis, is not likely to provide any advantage for a well trained athlete; 4). At the moderate altitudes used by most athletes, resting oxygen delivery to skeletal muscle is well preserved, arguing against any detrimental effect on "protein synthesis"; 5). It is possible however, that at significantly higher altitudes, acclimatization leads to appetite suppression, inhibition of protein synthesis, muscle wasting, excessive ventilatory work, and metabolic compensation that is NOT advantageous for a competitive athlete.

Acclimatization↗

Long photophase is not a sufficient stimulus to reduce thermogenic capacity in winter-acclimatized short-tailed field voles (Microtus agrestis) during long-term cold acclimation.

The thermogenic capacity of brown adipose tissue in winter- and summer-acclimatized short-tailed field voles (Microtus agrestis) was investigated by examining changes in mass of brown adipose tissue, the ratio of white adipose tissue to brown adipose tissue, the concentration of the uncoupling protein (thermogenin) in whole depots (micrograms) and in mitochondrial mass (micrograms.mg-1) and the activity of cytochrome c oxidase in the depots (mmol.min-1). The concentration of thermogenin in winter-acclimatized voles (n = 8), per brown adipose tissue depot and per mitochondrial mass, was significantly higher than in summer-acclimatized voles (n = 6). There was no significant difference in the level of cytochrome c oxidase activity between these two groups. Four groups of winter-acclimatized voles (n = 6 in each group) were exposed to 5 degrees C for 10, 20, 50 and 100 days in a 14L:10D photoperiod. Body mass, brown adipose tissue mass, white adipose tissue mass and basal metabolic rate were significantly positively related to the length of time cold exposed up to 100 days. There was a significant inverse relationship between the ratio of white to brown adipose tissue mass and the duration of cold exposure. There was no significant relationship between thermogenin concentration, either per depot or in mitochondrial mass of brown adipose tissue, with the length of time cold exposed. The level of cytochrome c oxidase activity increased significantly from control levels to a maximum after 10 days in the cold but decreased from 10 days onwards. In winter-acclimatized M. agrestis, a 14L:10D photoperiod is not a sufficient stimulus to reduce thermogenic capacity during cold acclimation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

Shift of anaerobic to aerobic metabolism in the rats acclimatized to hypoxia.

1. Metabolic acclimatization by repeated exposure to a simulated altitude of 4000, 5000 and 6000 m for 2 hr per day throughout 2 to 11 days was evaluated by the increased formation of ketone bodies as a marker of fatty acid oxidation and the decreased production of lactate and uric acid, the indicators of anaerobic metabolism in rats exposed to an altitude of 8000 m. 2. Pre-exposure of rats to an altitude of 5000 m and over caused an acclimatization to hypoxia. The rise of the altitude to which rats were pre-exposed reduced the period until the acquisition of metabolic acclimatization. 3. Acclimatized rats showed an increased activity of mitochondrial glutamate dehydrogenase without changes in glycolytic enzyme activity in skeletal muscle, heart and liver. 4. Acclimatization to high altitude hypoxia is concluded to involve a shift of the anaerobic glycolysis to aerobic metabolism by the increase in the oxidative enzymes.

Acclimatization↗

Acclimatization to hypoxia modulates the tryptophan 2,3-dioxygenase activity in rats exposed to simulated high altitude.

1. Exposure of rats to an 8000 m altitude increased the hepatic tryptophan 2,3-dioxygenase (EC 1.13.1.12) activity. 2. Acclimatization to hypoxia by a repeated exposure to an altitude of 5000 m induced a marked decrease in liver tryptophan dioxygenase activity after the rats were subjected to an 8000 m altitude, but a pre-exposure to 4000 m altitude showed no effect on the enzyme activity. 3. Plasma tryptophan was rapidly decreased by exposure to 8000 m altitude to the same extent in the acclimatized and non-acclimatized rats. 4. Plasma tryptophan may be utilized as the substrate for tryptophan dioxygenase in liver of the non-acclimatized rats under highly hypoxic conditions; however, acclimatized rats can reserve tryptophan as the substrate for the alternative metabolism other than the degradation pathway in liver.

Acclimatization↗