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PubMed2000

The 'lactate paradox', evidence for a transient change in the course of acclimatization to severe hypoxia in lowlanders.

The metabolic response to exercise at high altitude is different from that at sea level, depending on the altitude, the rate of ascent and duration of acclimatization. One apparent metabolic difference that was described in the 1930s is the phenomenon referred to as the 'lactate paradox'. Acute exposure to hypoxia results in higher blood lactate accumulation at submaximal workloads compared with sea level, but peak blood lactate remain the same. Following continued exposure to hypoxia or altitude, blood lactate accumulation at submaximal work and peak blood lactate levels are paradoxically reduced compared with those at sea level. It has recently been shown, however, that, if the exposure to altitude is sufficiently long, blood lactate responses return to those seen at sea level or during acute hypoxia. Thus, to evaluate the 'lactate paradox' phenomenon in relation to time spent at altitude, five Danish lowland climbers were studied at sea level, during acute exposure to hypoxia (10% O2 in N2) and 1, 4 and 6 weeks after arrival in the basecamp of Mt Everest (approximately 5400 m, Nepal). Basecamp was reached after 10 days of gradual ascent from 2800 m. Peak blood lactate levels were similar at sea level (11.0 +/- 0.7 mmol L-1) and during acute hypoxia (9.9 +/- 0.3 mmol L-1), but fell significantly after 1 week of acclimatization to 5400 m (5.6 +/- 0.5 mmol L-1) as predicted by the 'lactate paradox'. After 4 weeks of acclimatization, peak lactate accumulation (7.8 +/- 1.0 mmol L-1) was still lower compared with acute hypoxia but higher than that seen after 1 week of acclimatization. After 6 weeks of acclimatization, 2 days after return to basecamp after reaching the summit or south summit of Mt Everest, peak lactate levels (10.4 +/- 1.1 mmol L-1) were similar to those seen during acute hypoxia. Therefore, these results suggest that the 'lactate paradox' is a transient metabolic phenomenon that is reversed during a prolonged period of exposure to severe hypoxia of more than 6 weeks.

Acclimatization↗
PubMed1992

Use of a hypobaric chamber for pre-acclimatization before climbing Mount Everest.

Climbing Mount Everest needs an acclimatization period of 3 to 4 weeks between 3000 and 6000 m. In order to reduce this period of time spent in dangerous conditions, an experience of pre-acclimatization was performed with 5 elite alpinists (4 male, 1 female), aged 30 +/- 4 yrs (mean +/- SD), before their attempt to climb Mount Everest. Subjects first remained one week on Mont-Blanc (between 4350 and 4807 m), then spent a total of 38 hours in a hypobaric chamber (in 4 consecutive days) from 5000 to 8500 m standard altitude. Then, they flew to Kathmandu and reached 7800 m five days only after leaving the base camp. The pre-acclimatization period showed a 12% increase in hemoglobin concentration, and no change in ventilatory response to hypoxia. Arterial oxygen saturation at submaximal exercise in hypoxia (FIO2 = 0.115) increased from 75 +/- 4 to 82 +/- 3%, probably because of an efficient ventilatory acclimatization. On Mount Everest, the speed of ascent was very high (5600 m of altitude gain in 6 days), knowing that in conventional expeditions, 12 to 32 days are generally necessary to reach, safe, the same altitude. In conclusion, pre-acclimatization seems to have triggered efficient mechanisms which allowed climbers to save 1 to 3 weeks of time in mountain conditions.

Acclimatization↗
PubMed2000

Acclimatizing the world: a history of the paradigmatic colonial science.

This paper examines the institutions, personages, and the theories that informed acclimatization activities in nineteenth-century France, England, and the two colonies of Algeria and Australia. Treating acclimatization as a scientific concept and activity the essay begins with the conditions of its emergence in Enlightenment France. Subsequent sections trace the growth of the acclimatization movement and its translation to the British context, and consider reasons for its decline in the last third of the nineteenth century. Efforts are made to show why many perceived acclimatization to be the paradigmatic colonial science with applications as diverse as agriculture, settlement schemes, field sports, and human health. Emphasis falls on the French and British cultural spheres, as these were the dual epicenters of both modern colonialism and organized acclimatization activity.

Acclimatization↗
PubMed2001

The re-establishment of the normal blood lactate response to exercise in humans after prolonged acclimatization to altitude.

1. One to five weeks of chronic exposure to hypoxia has been shown to reduce peak blood lactate concentration compared to acute exposure to hypoxia during exercise, the high altitude 'lactate paradox'. However, we hypothesize that a sufficiently long exposure to hypoxia would result in a blood lactate and net lactate release from the active leg to an extent similar to that observed in acute hypoxia, independent of work intensity. 2. Six Danish lowlanders (25-26 years) were studied during graded incremental bicycle exercise under four conditions: at sea level breathing either ambient air (0 m normoxia) or a low-oxygen gas mixture (10 % O(2) in N(2), 0 m acute hypoxia) and after 9 weeks of acclimatization to 5260 m breathing either ambient air (5260 m chronic hypoxia) or a normoxic gas mixture (47 % O(2) in N(2), 5260 m acute normoxia). In addition, one-leg knee-extensor exercise was performed during 5260 m chronic hypoxia and 5260 m acute normoxia. 3. During incremental bicycle exercise, the arterial lactate concentrations were similar at sub-maximal work at 0 m acute hypoxia and 5260 m chronic hypoxia but higher compared to both 0 m normoxia and 5260 m acute normoxia. However, peak lactate concentration was similar under all conditions (10.0 +/- 1.3, 10.7 +/- 2.0, 10.9 +/- 2.3 and 11.0 +/- 1.0 mmol l(-1)) at 0 m normoxia, 0 m acute hypoxia, 5260 m chronic hypoxia and 5260 m acute normoxia, respectively. Despite a similar lactate concentration at sub-maximal and maximal workload, the net lactate release from the leg was lower during 0 m acute hypoxia (peak 8.4 +/- 1.6 mmol min(-1)) than at 5260 m chronic hypoxia (peak 12.8 +/- 2.2 mmol min(-1)). The same was observed for 0 m normoxia (peak 8.9 +/- 2.0 mmol min(-1)) compared to 5260 m acute normoxia (peak 12.6 +/- 3.6 mmol min(-1)). Exercise after acclimatization with a small muscle mass (one-leg knee-extensor) elicited similar lactate concentrations (peak 4.4 +/- 0.2 vs. 3.9 +/- 0.3 mmol l(-1)) and net lactate release (peak 16.4 +/- 1.8 vs. 14.3 mmol l(-1)) from the active leg at 5260 m chronic hypoxia and 5260 m acute normoxia. 4. In conclusion, in lowlanders acclimatized for 9 weeks to an altitude of 5260 m, the arterial lactate concentration was similar at 0 m acute hypoxia and 5260 m chronic hypoxia. The net lactate release from the active leg was higher at 5260 m chronic hypoxia compared to 0 m acute hypoxia, implying an enhanced lactate utilization with prolonged acclimatization to altitude. The present study clearly shows the absence of a lactate paradox in lowlanders sufficiently acclimatized to altitude.

Acclimatization↗
PubMed1966

Regulation of amino acid transport across intestines of goldfish acclimatized to different environmental temperatures.

1. Serosal transfers of valine and threonine were measured using everted sacs of anterior intestine taken from goldfish acclimatized to different temperatures.2. Both valine and threonine were actively transported at incubation temperatures equal to or greater than the previous environmental temperature of the fish. There was also a positive serosal transfer of valine, but not threonine, at incubation temperatures below the previous environmental temperature of the fish.3. The mean stable transmural potentials and amino-acid-evoked potentials depended both on the temperature to which the fish had been acclimatized and on the temperature at which the sacs were incubated.4. There was a linear relation between the transmural potential and the serosal transfer of amino acid, one additional mumole of valine or threonine being transferred/2 hr incubation period for each 3 mV rise in potential. There was a less obvious correlation between the amino-acid-evoked potential and on serosal transfer of amino acid.5. Acclimatization of the goldfish intestine from 8 to 25 degrees C, assessed by changes occurring in the transmural potential and serosal transfer of amino acids, tended to stabilize both parameters, but the compensation in each case was only partial.6. It is possible that the imbalance in transfer of valine-like and threonine-like amino acids, seen at incubation temperatures below the previous acclimatization temperature of the fish, has a special function in initiating the process of acclimatization to the new environmental temperature.

Acclimatization↗
PubMed1975

Relative susceptibility of altitude-acclimatized mice to acute oxygen toxicity.

The influence of hypoxic acclimatization at altitudes of 0, 5,000, or 15,000 ft on the relative susceptibility to acute oxygen poisoning was determined in 288 adult female mice. After acclimatization periods of 1, 2, 4, or 8 wk, the mice were exposed to oxygen at high pressures (OHP) of 4, 6, or 9 ATA and the times to convulsion and death recorded. A factorial analysis of variance indicated that altitude and OHP level had inverse, log-linear effects on both parameters. The duration of acclimatization progressively decreased the time to death. The onset of convulsions and death was independent of body weight. There were significant interactions on the measured parameters between various combinations of altitude, OHP level, and duration of acclimatization. While alterations in the metabolism of gamma-aminobutyric acid and high-energy compounds are common to both hypoxia and hyperoxia, the most plausible explanation of the results relates to the decrease in buffer base induced by hypoxic acclimatization which might have caused CO2 potentiation of OHP symptoms.

Acclimatization↗
PubMed1976

Effect of heat acclimatization on intravascular responses to acute heat stress in man.

The effects of a 185-min exposure to 48 degrees C db/33 degrees C wb, on intravascular volume and osmolarity and on intravascular electrolyte, aldosterone, and cortisol concentrations have been studied in five male subjects before and after acclimatization to heat. Changes in the hematocrit and plasma protein concentration indicated that a hemodilution occurred during the first 35 min of the heat exposures, and that this was followed by a hemoconcentration. Although these changes in intravascular volume were not affected by acclimatization, the plasma volume after heat acclimatization was 6.7% greater than before. This increase in plasma volume was associated with an elevation in the ratio [Na]/[K]. However, since plasma osmolarity decreased the intravascular expansion could not be explained in terms of elevated electrolyte levels. Plasma aldosterone and cortisol levels were not affected by heat acclimatization, although both were elevated following exercise in the heat. It is concluded that the adrenal cortex is not an important factor in maintaining a state of heat acclimatization once a salt balance has been achieved.

Acclimatization↗
PubMed1984

Effects of sleep state on ventilatory acclimatization to hypoxia in humans.

We assessed the influence of sleep state on ventilatory acclimatization to hypoxia. Ventilation, arterial O2 saturation (SaO2), and arterial acid-base status were monitored in healthy adult males during wakefulness, nonrapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep in normoxia [barometric pressure (PB) = 740 Torr] and over 4 continuous days of hypobaric hypoxia (PB = 455 Torr). The relative hypoventilation observed during sleep compared with wakefulness in normoxia was also observed during all stages of hypoxic acclimatization. The characteristic time-dependent changes associated with acclimatization to chronic hypoxia were similar during wakefulness and all sleep states: 1) arterial CO2 partial pressure (PaCO2) decreased 27-31% by night 4 with approximately half of this fall occurring acutely (0.3-3 h hypoxia); 2) minute ventilation increased progressively with duration of hypoxic exposure including increased levels of hyperventilation throughout the initial night of sleep in hypoxia; 3) SaO2 was lowest acutely and gradually increased coincident with the progressive hyperventilation; and 4) pHa increased acutely and remained unchanged despite additional hyperventilation due to a compensatory reduction in [HCO3-]a. In addition, in the acclimatized subject hyperventilation persisted following acute restoration of normoxia, and this continued hyperventilation was similar in magnitude during both wakefulness and NREM sleep. These results indicate that suprapontine influences on ventilatory control associated with the state of wakefulness are not required in the process of ventilatory acclimatization to chronic hypoxia.

Acclimatization↗
PubMed1989

Effects of altitude acclimatization on pulmonary gas exchange during exercise.

Pulmonary gas exchange was studied in eight normal subjects both before and after 2 wk of altitude acclimatization at 3,800 m (12,470 ft, barometric pressure = 484 Torr). Respiratory and multiple inert gas tensions, ventilation, cardiac output (Q), and hemoglobin concentration were measured at rest and during three levels of constant-load cycle exercise during both normoxia [inspired PO2 (PIO2) = 148 Torr] and normobaric hypoxia (PIO2 = 91 Torr). After acclimatization, the measured alveolar-arterial PO2 difference (A-aPO2) for any given work rate decreased (P less than 0.02). The largest reductions were observed during the highest work rates and were 24.8 +/- 1.4 to 19.7 +/- 0.8 Torr (normoxia) and 22.0 +/- 1.1 to 19.4 +/- 0.7 Torr (hypoxia). This could not be explained by changes in ventilation-perfusion inequality or estimated O2 diffusing capacity, which were unaffected by acclimatization. However, Q for any given work rate was significantly decreased (P less than 0.001) after acclimatization. We suggest that the reduction in A-aPO2 after acclimatization is a result of more nearly complete alveolar/end-capillary diffusion equilibration on the basis of a longer pulmonary capillary transit time.

Acclimatization↗
PubMed1996

Altitude acclimatization and blood volume: effects of exogenous erythrocyte volume expansion.

We studied sea-level residents during 13 days of altitude acclimatization to determine 1) altitude acclimatization effects on erythrocyte volume and plasma volume, 2) if exogenous erythrocyte volume expansion alters subsequent erythrocyte volume and plasma volume adaptations, 3) if an increased blood oxygen content alters erythropoietin responses during altitude acclimatization, and 4) mechanisms responsible for plasma loss at altitude. Sixteen healthy men had a series of hematologic measurements made at sea level, on the first and ninth days of altitude (4,300 m) residence, and after returning to sea level. Twenty-four hours before the ascent to altitude, one group received a 700-ml infusion of autologous erythrocytes (42% hematocrit), whereas the other group received only a saline infusion. Erythrocyte infusion increased erythrocyte volume by approximately 10%, whereas saline infusion had no effect; in addition, initially at altitude, blood oxygen content was 8% higher in erythrocyte-infused than in saline-infused subjects. The new findings regarding altitude acclimatization are summarized as follows: 1) erythrocyte volume does not change during the first 13 days and is not affected by prior exogenous expansion, 2) a modest increase in blood oxygen content does not modify erythropoietin responses, 3) plasma losses are related to vascular protein losses, and 4) exogenous erythrocyte volume expansion coincides with transient increases in plasma loss, vascular protein loss, and mean arterial pressure elevation. These findings better define human blood volume responses during altitude acclimatization.

Acclimatization↗
PubMed2001

Women at altitude: ventilatory acclimatization at 4,300 m.

Women living at low altitudes or acclimatized to high altitudes have greater effective ventilation in the luteal (L) compared with follicular (F) menstrual cycle phase and compared with men. We hypothesized that ventilatory acclimatization to high altitude would occur more quickly and to a greater degree in 1) women in their L compared with women in their F menstrual cycle phase, and 2) in women compared with men. Studies were conducted on 22 eumenorrheic, unacclimatized, sea-level (SL) residents. Indexes of ventilatory acclimatization [resting ventilatory parameters, hypoxic ventilatory response, hypercapnic ventilatory response (HCVR)] were measured in 14 women in the F phase and in 8 other women in the L phase of their menstrual cycle, both at SL and again during a 12-day residence at 4,300 m. At SL only, ventilatory studies were also completed in both menstrual cycle phases in 12 subjects (i.e., within-subject comparison). In these subjects, SL alveolar ventilation (expressed as end-tidal PCO(2)) was greater in the L vs. F phase. Yet the comparison between L- and F-phase groups found similar levels of resting end-tidal PCO(2), hypoxic ventilatory response parameter A, HCVR slope, and HCVR parameter B, both at SL and 4,300 m. Moreover, these indexes of ventilatory acclimatization were not significantly different from those previously measured in men. Thus female lowlanders rapidly ascending to 4,300 m in either the L or F menstrual cycle phase have similar levels of alveolar ventilation and a time course for ventilatory acclimatization that is nearly identical to that reported in male lowlanders.

Acclimatization↗
PubMedDate not supplied

The growth of brown adipose tissue in cold-acclimatized rats after depletion of mast cell histamine by compound 48/80.

Cold acclimatization (4-5 degree C) is accompanied by 2-3 fold increase of brown adipose tissue (BAT). This rapid growth of interscapular BAT was studied after histamine depletion. In control rats maintained at room temperature (28 +/- 2 degree C) the BAT histamine content was 23.4 +/- 5.9 (mean +/- SD) microgram/g of tissue and cold acclimatization (5 +/- 1 degree C) produced a significant increase of BAT weight, but reduced the histamine content to 8.4 +/- 1.9 microgram/g. The total weight of BAT after 20 days of acclimatization was unaffected by depletion of histamine due to compound 48/80. The low level of histamine in BAT of cold acclimatized rats could be due to a fast rate of amine utilization; alternatively an altered synthesis or storage process may occur during acclimatization.

Acclimatization↗
PubMedDate not supplied

The effect of local acclimatization to cold on the intensity of vasomotor reaction caused by locally applied vibration.

In two groups of men, acclimatized or non-acclimatized locally to cold, hand skin temperature and the arterial blood pressure were measured during exposure to locally applied vibration of strictly defined parameters. It was found that in acclimatized subjects the intensity of vasomotor response was smaller than in non-acclimatized ones. The results obtained indicate that local acclimatization to cold may be a factor alleviating the action of locally applied vibration on the peripheral vascular system.

Acclimatization↗
PubMed1986

Transport ATPases in the erythrocytes of rats acclimatized to intermittent altitude hypoxia.

The activity of Na+/K+- and Ca2+-ATPase and some allosteric properties of Na+/K+-ATPase were studied in whole erythrocytes and their membrane preparations (ghosts) from rats exposed to intermittent altitude hypoxia (10 and 24 exposures, 8 h/day in an altitude chamber, stepwise up to an altitude of 7,000 m). Ca2+-ATPase activity was increased both in whole erythrocytes and ghosts after the first phase of acclimatization (10 exposures). In a standard incubation medium (containing 3 mmol.l-1 MgCl2 ), Na+/K+-ATPase activity in the ghosts was also increased after the initial phase of acclimatization whereas in whole erythrocytes Na+/K+-ATPase was only decreased in the regression phase. At high MgCl2 concentrations (12 mmol.l-1) changes of Na+/K+-ATPase activity both in whole erythrocytes and in the ghosts followed similar time course with a pronounced increase in the first phase of acclimatization (10 exposures) followed by an abrupt drop (24 exposures) and then by a gradual normalization in the regression phase. Sensitivity of the enzyme to mounting MgCl2 concentrations was increased in the ghosts at the end of acclimatization and was decreased in whole erythrocytes during acclimatization and especially in the regression phase. It has been suggested that chronic altitude hypoxia leads to the alteration of cooperative interaction of the Na+/K+-ATPase subunits in the erythrocyte membrane and accumulation of some factor in the cells inhibiting this enzyme.

Acclimatization↗
PubMed1985

Physiological acclimatization to heat after a spell of cold conditioning in tropical subjects.

The effects of brief spells of cold conditioning on heat acclimatized tropical subjects on the decay and reacclimatization status to heat were evaluated on 12 Indian male infantry soldiers in the cooler months at Delhi. After 8 d of heat acclimatization in a climatic chamber maintained at 45 degrees C dry bulb (Tdb) and 30% relative humidity (rh), the subjects were conditioned to cold for 21 d by exposing them to a temperature of 10 degrees C daily for 4 h. During the cold conditioning phase the subjects had no access to either heat exposure or strenuous work. The cold conditioning was followed by reacclimatization to heat. Significant loss in heat acclimatization status was observed, both in terms of exercise oral temperature and heart rate. The loss in status after 1 d reinduction to heat acclimatization was in the range of 45-56%. However, within 3 d all of the subjects once again regained the full acclimatization status. The cold conditioning did not alter the sweat output during the reinduction to heat phase.

Acclimatization↗
PubMed1978

Heat acclimatization by a method utilizing microclimate cooling.

A new approach to heat acclimatization has been shown to be feasible during laboratory experimentation. Wearing microclimate suits containing dry ice as the coolant, three groups of men were subjected to a moderate work rate in three different environments for 4 h/d for 8 d. Physiological responses on a subsequent heat tolerance test indicate that the group subjected to an environment of 32.0 degrees C W. B. and 33.5 degrees C D.B. were fully heat acclimatized. The 33/35 degrees C group were also well-acclimatized but developed dangerously high body temperatures during the first 2 d. Only partial acclimatization was achieved by the 31/33 degrees C group. The reason why the men acquire heat acclimatization while wearing the microclimate suits in a hot environment is probably that microclimate cooling does not prevent body temperature from rising--it only prevents it from rising excessively. It should be remembered that only one-third of the body is cooled while the rest shows the normal sweating response.

Acclimatization↗
PubMed1995

The effect of altitude pre-acclimatization on acute mountain sickness during reexposure.

BACKGROUND: Acclimatization to high altitude appears to prevent acute mountain sickness (AMS), as evidenced by a decline in AMS symptoms as acclimatization progresses. HYPOTHESIS: We hypothesized that partial retention of acclimatization would attenuate the incidence and/or severity of AMS upon reinduction to altitude. METHODS: To test this hypothesis 6 male lowlanders returned to sea level after the acclimatizing of the 16 d at 4300 m (HA). After 8 d at sea level (PA), they were reexposed to 4300 m in a hypobaric chamber for 30 h (RA). AMS symptom severity was determined by the AMS-cerebral (AMS-C) scores calculated from the daily administration of the Environmental Symptoms Questionnaire during HA and RA. RESULTS: The mean AMS-C scores were reduced from 0.6 on HA day 1 (HA1) to 0.1 during RA (p < 0.05). Four subjects were "sick" (AMS-C > 0.7) during HA1, while only one was "sick" during RA. The % oxyhemoglobin, hemoglobin concentration and hematocrit were higher during RA compared to HA1. CONCLUSIONS: These results suggest that the retention of acclimatization after 8 d at low altitude is sufficient to attenuate AMS upon reinduction to high altitude.

Acclimatization↗
PubMed1977

Effect of heat acclimatization on testicular enzymes involved in androgen biosynthesis via the 5-ene pathway.

The metabolism of 3beta-hydroxy-5-ene steroids by testicular homogenates of heat-acclimatized and control mice was investigated in vitro. Acclimatization was achieved by keeping the animals in a hot room (33-35 degrees C, 25-40% R.H.) for 5 weeks. The control animals were kept in a temperate environment (20-22 degrees C, 30-50% R.H.). Some of the heat-acclimatized animals were supplied with additional water in a trough placed inside each cage (HAII mice). This source of water was used by the mice mainly for body cooling. A pronounced decrease in body weight and testis weight, and a smaller decrease in the weight of seminal vesicles which was associated with atrophy of the seminiferous tubules and hyperplasia of the Leydig cells was characteristic of heat-acclimatized mice with only drinking water available (HAI), but not of HAII mice. Although body cooling abolished the adverse physiological response described, it did not prevent specific changes in enzyme activity associated with androgen production. There was increased activity of 3beta-hydroxysteroid dehydrogenase and isomerase, and of 5-ene-17beta-hydroxysteroid dehydrogenase. These data offer partial explanation for the lower peripheral blood testosterone level observed in some species of heat-acclimatized mammals.

17-alpha-Hydroxypregnenolone↗