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PubMed2004

Acclimatization to neurological decompression sickness in rabbits.

Diving acclimatization refers to a reduced susceptibility to acute decompression sickness (DCS) in individuals undergoing repeated compression-decompression cycles. We demonstrated in a previous study that the mechanism responsible for this acclimatization is similar to that of stress preconditioning. In this study, we investigated the protective effect of prior DCS preconditioning on the severity of neurological DCS in subsequent exposure to high pressure in rabbits. We exposed the rabbits (n = 10) to a pressure cycle of 6 absolute atmospheres (ATA) for 90 min, which induced signs of neurological DCS in 60% of the animals. Twenty-four hours after the pressure cycle, rabbits with DCS expressed more heat-shock protein 70 (HSP70) in the lungs, liver, and heart than rabbits without signs of disease or those in the control group (n = 6). In another group of rabbits (n = 24), 50% of animals presented signs of neurological DCS after exposure to high pressure, with a neurological score of 46.5 (SD 19.5). A course of hyperbaric oxygen therapy alleviated the signs of neurological DCS and ensured the animals' survival for 24 h. Experiencing another pressure cycle of 6 ATA for 90 min, 50% of 12 rabbits with prior DCS preconditioning developed signs of DCS, with a neurological score of 16.3 (SD 28.3), significantly lower than that before hyperbaric oxygen therapy (P = 0.002). In summary, our results show that the occurrence of DCS in rabbits after rapid decompression is associated with increased expression of a stress protein, indicating that the stress response is induced by DCS. This phenomenon was defined as "DCS preconditioning." DCS preconditioning attenuated the severity of neurological DCS caused by subsequent exposure to high pressure. These results suggest that bubble formation in tissues activates the stress response and stress preconditioning attenuates tissue injury on subsequent DCS stress, which may be the mechanism responsible for diving acclimatization.

Acclimatization↗
PubMed1976

Acclimatization in a hot, humid environment: body fluid adjustments.

Four trained men worked 4 h/day at 40-50% of their maximum aerobic capacity first for 3 days at 25 degrees C db, 18 degrees C wb and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. Between days 1 and 2 of heat exposure mean total circulating protein (TCP) and plasma volume (PV) increased 11.6% and 9%, respectively. Preexposure TCP and PV increased until day 6 of heat exposure. Of the protein fractions beta-globulins underwent the largest relative increase. During work movement of protein into and out of the vascular compartment was similar in control and acclimatizing subjects but the latter generally maintained a greater amount of protein and fluid within the vascular volume. There was no evidence of salt and water retention. The increase in vascualr volume was ascribed to transfer of interstitial protein and water to the vascular volume. Regression coefficients indicated significant correlations for changes in plasma volume versus heart rate, stroke volume, and cardiac output during acclimatization. It was concluded that the most critical event in heat acclimatization is the expansion of the plasma volume.

Acclimatization↗
PubMed1987

Altitude acclimatization attenuates plasma ammonia accumulation during submaximal exercise.

This study examined the effects of acclimatization to 4,300 m altitude on changes in plasma ammonia concentrations with 30 min of submaximal [75% maximal O2 uptake (VO2max)] cycle exercise. Human test subjects were divided into a sedentary (n = 6) and active group (n = 5). Maximal uptake (VO2max) was determined at sea level and at high altitude (HA; 4,300 m) after acute (t less than 24 h) and chronic (t = 13 days) exposure. The VO2max of both groups decreased 32% with acute HA when compared with sea level. In the sedentary group, VO2max decreased an additional 16% after 13 days of continuous residence at 4,300 m, whereas VO2max in the active group showed no further change. In both sedentary and active subjects, plasma ammonia concentrations were increased (P less than 0.05) over resting levels immediately after submaximal exercise at sea level as well as during acute HA exposure. With chronic HA exposure, the active group showed no increase in plasma ammonia immediately after submaximal exercise, whereas the postexercise ammonia in the sedentary group was elevated but to a lesser extent than at sea level or with acute HA exposure. Thus postexercise plasma ammonia concentration was decreased with altitude acclimatization when compared with ammonia concentrations following exercise performed at the same relative intensity at sea level or acute HA. This decrease in ammonia accumulation may contribute to enhanced endurance performance and altered substrate utilization with exercise following acclimatization to altitude.

Acclimatization↗
PubMed1992

Brain tissue pH and ventilatory acclimatization to high altitude.

31P nuclear magnetic resonance spectroscopy (31P-NMRS) was performed on brain cross sections of four human subjects before and after 7 days in a hypobaric chamber at 447 Torr to test the hypothesis that brain intracellular acidosis develops during acclimatization to high altitude and accounts for the progressively increasing ventilation that develops (ventilatory acclimatization). Arterial blood gas measurements confirmed increased ventilation. At the end of 1 wk of hypobaria, brain intracellular pH was 7.023 +/- 0.046 (SD), unchanged from preexposure pH of 6.998 +/- 0.029. After return to sea level, however, it decreased to 6.918 +/- 0.032 at 15 min (P less than 0.01) and 6.920 +/- 0.046 at 12 h (P less than 0.01). The ventilatory response to hypoxia increased [from 0.35 +/- 0.11 (l/min)/(-%O2 saturation) before exposure to 0.69 +/- 0.19 after, P = 0.06]. Brain intracellular acidosis is probably not a supplemental stimulus to ventilatory acclimatization to high altitude. However, brain intracellular acidosis develops on return to normoxia from chronic hypoxia, suggesting that brain pH may follow changes in blood and cerebrospinal fluid pH as they are altered by changes in ventilation.

Acclimatization↗
PubMed1993

Sea-level PCO2 relates to ventilatory acclimatization at 4,300 m.

There is considerable variation among individuals in the extent of, and the time required for, ventilatory acclimatization to altitude. Factors related to this variation are unclear. The present study tested whether interindividual variation in preascent ventilation or magnitude of hypoxic ventilatory response related to ventilatory acclimatization to altitude. Measurements in 37 healthy resting male subjects at sea level indicated a wide range (34-48 Torr) of end-tidal PCO2 values. When these subjects were taken to Pikes Peak, CO (4,300 m, barometric pressure 462 mmHg), the end-tidal PCO2 values measured on arrival and repeatedly over 19 days were correlated with the sea-level end-tidal PCO2. At 4,300 m, subjects with high end-tidal PCO2 had low values of arterial oxygen saturation (SaO2). Also, sea-level end-tidal PCO2 related to SaO2 after 19 days at 4,300 m. Twenty-six of the subjects had measurements of isocapnic hypoxic ventilatory response (HVR) at sea level. The end-tidal PCO2 values on arrival and after 19 days residence at 4,300 m were inversely related to the sea-level HVR values. Thus both the PCO2 and the HVR as measured at sea level related to the extent of subsequent ventilatory acclimatization (decrease in end-tidal PCO2) and the level of oxygenation at altitude. The finding in our cohort of subjects that sea-level end-tidal PCO2 was inversely related to HVR raised the possibility that among individuals the magnitude of the hypoxic drive to breathe influenced the amount of ventilation at all altitudes, including sea level.

Acclimatization↗
PubMed1995

Acclimatization at high altitude in gradual and acute induction.

The study assessed physiological responses to induction to high altitude first to 3,500 m and then to 4,200 m and compared the time course of altitude acclimatization in two groups of male volunteers. The acutely inducted group was transported by aircraft (AI) to 3,500 m in 1 h, whereas the gradually inducted group was transported by road (RI) in 4 days. Baseline recordings of basal cardiovascular, respiratory, and blood gas variables were monitored at sea level as well as at 3,500 m on days 1, 3, 5, and 7. Blood gases were measured on day 10 also. After 15 days at 3,500 m, the subjects were inducted to 4,200 m by road, and measurements were repeated on days 1, 3, and 5, except blood gas variables, which were done on day 10 only. Acute mountain sickness symptoms were recorded throughout. The responses of RI were stable by day 3 of induction at 3,500 m, whereas it took 5 days for AI. Four days in transit for RI appear equivalent to 2 days at 3,500 m for AI. Acclimatization schedules of 3 and 5 days, respectively, for RI and AI are essential to avoid malacclimatization and/or high-altitude illness. Both groups took 3 days at 4,200 m to attain stability for achieving acclimatization.

Acclimatization↗
PubMed1996

Peak blood lactate and blood lactate vs. workload during acclimatization to 5,050 m and in deacclimatization.

Peak blood lactate ([Labl]peak) and blood lactate concentration ([Labl]) vs. workload (W) relationships during acclimatization to altitude and in the deacclimatization were evaluated in 10 Caucasian lowlanders at sea level (SL0); after approximately 1 wk (Alt1wk), 3 wk (Alt3wk), and 5 wk (Alt5wk) at 5,050 m; and weekly during the first 5 wk after return to sea level (SL1wk-SL5wk). Incremental bicycle ergometer exercises (30 W added every 4 min up to exhaustion) were performed. At Alt1wk and at Alt5wk, the experiments were repeated in hypobaric normoxia (Alt1wk-O2 and Alt5wk-O2). [Labl] was determined at rest and during the last approximately 30 s of each W. [Labl]peak was taken as the highest [Labl] during recovery. Acid-base status (pH and concentration of HCO-3 in arterialized capillary blood) was determined at rest. Mean [Labl]peak values were 11.5 (SL0), 8.0 (Alt1wk), 6.4 (Alt3wk), 6.3 (Alt5wk), 8.0 (SL1wk), 9.4 (SL2wk), 10.8 (SL3wk), 11.3 (SL4wk), and 11.6 (SL5wk) mM. At Alt1wk-O2 and Alt5wk-O2, peak W increased, compared with Alt1wk and Alt5wk, whereas no changes were observed for [Labl]peak. [Labl] vs. W was shifted to the left (i.e., higher [Labl] values were found for the same W) at Alt1wk compared with SL0 and partially shifted back to the right (i.e., lower [Labl] values were found for the same W) at Alt3wk and Alt5wk. At Alt1wk-O2 and Alt5wk-O2, [Labl] vs. W values were superimposed on that at SL0. At SL1wk-SL5wk, [Labl] vs. W values were shifted to the right compared with that at SL0. At Alt1wk, a condition of respiratory alkalosis was found, which was only partially compensated for during acclimatization. At SL1wk, the acid-base status was back to normal. We conclude that 1) the reduced [Labl]peak at altitude is still present for 2-3 wk after return from altitude; is not attributable to reduced peak W nor to hypoxia per se, nor to a reduced buffer capacity; alternatively, it could be related to some central determinants of fatigue. 2) The [Labl] vs. W leftward shift at altitude was due to hypoxia per se. 3) The factor(s) responsible for the [Labl] vs. W partial rightward shift during acclimatization could still be effective during the first weeks after return to sea level.

Acclimatization↗
PubMed2002

Heat stress attenuates air bubble-induced acute lung injury: a novel mechanism of diving acclimatization.

Diving acclimatization refers to a reduced susceptibility to acute decompression sickness (DCS) in individuals undergoing repeated compression-decompression cycles. We postulated that mechanisms responsible for the acclimatization are similar to that of a stress preconditioning. In this study, we investigated the protective effect of prior heat shock treatment on air embolism-induced lung injury and on the incidence of DCS in rats. We exposed rats (n = 31) to a pressure cycle that induced signs of severe DCS in 48% of the rats, greater wet-to-dry ratio (W/D) of lung weight compared with the control group (5.48 +/- 0.69 vs. 4.70 +/- 0.17), and higher protein concentration in bronchoalveolar lavage (BAL) fluid (362 +/- 184 vs. 209 +/- 78 mg/l) compared with the control group. Rats with DCS expressed more heat shock protein 70 (HSP70) in the lungs than those without signs of disease. Prior heat shock (n = 12) increased the expression of HSP70 in the lung and attenuated the elevation of W/D of lung weight (5.03 +/- 0.17) after the identical decompression protocol. Prior heat shock reduced the incidence of severe DCS by 23%, but this failed to reach statistical significant (chi(2) = 1.94, P = 0.163). Venous air infusion (1.0 ml/40 min) caused profound hypoxemia (54.5 +/- 3.8 vs. 83.8 +/- 3.2 Torr at baseline; n = 6), greater W/D of lung weight (5.98 +/- 0.45), and high protein concentration in BAL fluid (595 +/- 129 mg/l). Prior heat shock (n = 6) did not alter the level of hypoxemia caused by air embolism, but it accelerated the recovery to normoxemia after air infusion was stopped. Prior heat shock also attenuated the elevation of W/D of lung weight (5.19 +/- 0.40) and the increase in BAL protein (371 +/- 69 mg/l) in air embolism group. Our results showed that the occurrence of DCS after rapid decompression is associated with increased expression of a stress protein (HSP70) and that prior heat shock exposure attenuates the air bubble-induced lung injury. These results suggest that bubble formation in tissues activates a stress response and that stress preconditioning attenuates lung injury on subsequent stress, which may be the mechanism responsible for diving acclimatization.

Acclimatization↗
PubMed2001

Acclimatization and response of minipigs toward humans.

As a first step toward making an efficient acclimatization methodology for minipigs, the reaction of Göttingen minipigs, 3-24 months of age, toward humans was investigated. All minipigs were kept in an individual cage, and the reaction toward humans (acclimatization index) was evaluated by simple observations. The acclimatization index was evaluated as the total number of points scored (0-30 points) based on the following criteria: (1) the position of the minipig when the cage door was opened; (2) the reaction of the minipig when the observer approached; and (31 the reaction of the minipig when the observer touched it. Subsequently, each animal was ranked by total points scored: 30 points = AA, 20 points < or = A < 30 points, 10 points < or = B < 20 points, 0 points < or = C < 10 points. Based on this evaluation, the reactions of minipigs under three conditions were investigated. The following findings were confirmed: first, minipig reaction to humans was influenced by monthly age; second, taming was possible under ordinary conditions of care, but we had to wait until 10 months of age on average for this to occur; third, if simple contact was made during care time, minipigs became tame within less than 4 weeks after the commencement of contact. We therefore consider it possible to artificially control the reaction of minipigs toward humans, and to make minipigs more available for experiments by adding control of the hereditary factors that influence this reaction.

Acclimatization↗
PubMed2000

Acclimatization near home? Early respiratory changes after short-term intermittent exposure to simulated altitude.

OBJECTIVE: With the ultimate goal of finding a straightforward protocol for acclimatization at simulated altitude, we evaluated the early effects of repeated short-term exposure to hypobaric hypoxia on the respiratory response to exercise in hypoxia. METHODS: Nine subjects were exposed to a simulated altitude of 5000 m for 2 hours a day for 14 days. Arterial oxygen saturation (SaO2), expired volume per minute (VE), respiratory rate, tidal volume (VT), and heart rate were measured during rest and during exercise (cycloergometer, at 30% of maximum oxygen consumption at sea level), both in normoxia and at 5000 m of simulated altitude on the first and 15th days. On the same days, blood samples were obtained for hematological tests. RESULTS: During exercise in hypoxia, SaO2 rose from 65 to 71% (P = .02), and VE rose from 55.5 to 67.6 L.min-1 (P = .02) due to an increase in VT from 2 to 2.6 L (P = .003). No significant differences were found in any of the variables studied at rest either in normoxia or in hypoxia or in exercise in normoxia after the exposure program. In the second week, changes in packed cell volume and blood hemoglobin concentration were nonsignificant. CONCLUSIONS: After short-term intermittent exposure to hypobaric hypoxia, subjects increased their ventilatory response and SaO2 during exercise at simulated altitude. These changes may be interpreted as acclimatization to altitude. The monitoring of ventilatory response and SaO2 during moderate exercise in hypobaric hypoxia may be used to detect the first stages of acclimatization to altitude.

Acclimatization↗
PubMed1984

Activity of LH receptor, LH-stimulated cyclic AMP and testosterone production in the Leydig cell of heat-acclimatized rats.

Key reactions associated with the capacity of the isolated Leydig cell to synthesize testosterone were studied in male rats acclimatized to a hot environment (33-35 degrees C, 25-40% relative humidity) and controls (20-22 degrees C, 30-50% relative humidity). The results demonstrate that acclimatization to heat coincides with: (1) a lower number of human chorionic gonadotrophin (hCG) receptors (P less than 0.01) in the Leydig cell, (2) higher affinity of the Leydig cell for hCG (P less than 0.05), (3) lower hCG-stimulated cyclic AMP production (P less than 0.05) by the Leydig cell and (4) lower capacity of the Leydig cell to synthesize testosterone (P less than 0.01) after hCG challenge. It is suggested that the major cellular alteration responsible for the decreased testosterone secretion by the Leydig cell lies distal to the step involving the binding of the trophic hormone to its receptor and that heat-acclimatization induces changes in the integrity of the various cellular membranes leading to the impeded function of adenylate cyclase and 17 beta-hydroxysteroid oxidoreductase.

Acclimatization↗
PubMed1999

[Effects of acute hypoxia and hypoxic acclimatization on cardiac functions of rats].

OBJECTIVE: To study the effects of acute hypoxia and intermittent hypoxic acclimatization on cardiac systolic and diastolic functions in rats. METHOD: Cardiac functions were investigated after intermittent hypoxic acclimatizated (3000 m and 5000 m, 2 wk respectively, 4 h/d) and normoxic rats were exposed to hypoxia (8000 m) for 4 h. RESULT: The systolic functional parameters such as LVSP, +dp/dtmax, Vpm, Vmax and the diastolic functional parameter -dp/dtmax of acute hypoxic rats were reduced significantly as compared with normoxic control rats. After hypoxic acclimatization, the left ventricular functions of rats were increased significantly as compared with those of acute hypoxic rats. But they were still lower than those of normoxic control rats. CONCLUSION: Acute hypoxia can affect cardiac functions and hypoxic acclimatization can alleviate the hypoxic effects on cardiac functions.

Acclimatization↗
PubMed1985

Hemodilution during standardized hemorrhage in high-altitude acclimatized rats.

Ten control rats and sixteen high-altitude acclimatized rats were bled at sea level into a reservoir which maintained arterial pressure at 35 mm Hg. As soon as the animals had spontaneously taken back 30% of the maximum bleeding volume, all the shed blood remaining in the reservoir was reinfused. Hemodilution was studied during the first half phase of hypotension starting from the point of initial blood withdrawal and ending at the point of maximum blood loss. Changes in hematocrit, hemoglobin content, total plasma protein, and arterial plasma osmolality were measured. The initial and the maximum blood withdrawal, the oligemic time, and the survival time of the altitude-acclimatized rats were all greater than those for non-acclimatized rats. The higher tolerance to standardized hemorrhagic shock in altitude-exposed rats seemed to be due in part to their more marked hemodilution which allowed more efficient homeostatic regulation of vascular volume. The difference in rate of hemodilution between the two animal groups could not be attributed to arterial hyperosmolality.

Acclimatization↗
PubMed1978

Changes in EEG pattern during acclimatization to high altitude (3500 m) in man.

This study was conducted on 30 healthy soldiers to observe EEG changes during acclimatization to high altitude. Of these subjects, 10 were lowlanders (LL), 10 were acclimatized low landers (AL), and 10 10 were high-altitude natives (HAN). The EEG was recorded by the 10-20 international system of electrode placement in LL at sea level (SL) during rest and hyperventilation (HV). Then they were air-lifted to an altitude of 3500 m where periodic recordings of EEG were made for 4 weeks. For comparison, the altitude recordings were also made in AL and HAN. The quantitative analysis of EEG (occipital) was done to determine alpha index (AI) and average amplitude. The mean AI was 25.5% at SL in LL, which changed to 45.7%, 15.8%, 28.0%, 30.3%, and 33.2% on days 2, 7, 14, 21, and 28, respectively. The average amplitude was 17.3 microV at SL, which changed to 23.3 microV, 11.8 microV, 16.2 microV, 17.3 microV, and 19.8 microV on days 2, 7, 14, 21, and 28, respectively. In two subjects, spiking was seen along with the desynchronized pattern of EEG on days 7 and 14. The AI and average amplitude of AL and HAN were significantly more than those of LL. The magnitude of buildup during HV was greater at altitude. These results indicate that there is cerebral cortical depression in the initial phase of induction which changes to cortical desyncronization in the latter part of the first week of induction. During acclimatization, there is gradual buildup of EEG waves, as observed in AL and HAN.

Acclimatization↗
PubMed2003

Nickel sorption by acclimatized activated sludge culture.

The sorption of Ni(2+) by acclimatized activated sludge treating Ni(2+) bearing wastewater was investigated using a once-through completely mixed tank reactor. The culture developed from sewage was acclimatized to 85.2 microM/l Ni(2+) influent concentration by stepwise increases, at a low dilution rate 0.11/h. Acclimation was found to enhance the sorptive capacity of the activated sludge. In fact, at all of the intermediate concentrations, percentage Ni(2+) adsorbed by the biomass and also the sorptive capacity of the activated sludge drastically increased with an increase in the influent Ni(2+) concentration. All influent Ni(2+) concentrations were found to significantly stimulate the observed biomass yield of the culture over that observed in the base line. Experimental findings obtained at two other dilution rates; namely, 0.25/h and 0.45/h revealed that dilution rate is a significant operational parameter affecting the Ni(2+) sorption characteristics of acclimatized activated sludge microorganisms. Considerable complexation of nickel and organic and inorganic ligands in the wastewater appeared to be responsible for a relatively lower Ni(2+) sorption capacity.

Adsorption↗
PubMed1996

Physiological plasticity in the auditory system and its possible relevance to hearing aid use, deprivation effects, and acclimatization.

Alterations in the physiological and/or the anatomical properties of the central auditory system (neural plasticity) can be induced by unilateral or bilateral sensorineural hearing loss, auditory stimulation, and conditioning in which sounds are used as conditioned stimuli. These types of neural plasticity have implications for hearing aid use, acclimatization, and deprivation effects. The occurrence of hearing-loss-induced plasticity suggests that the organization of the central auditory system may be altered by the time a hearing aid is fitted. The success of hearing aids may depend, therefore, on how the auditory system responds to the reintroduction of certain sounds by amplification. For example, enhanced auditory stimulation provided by hearing aids may induce "secondary" plasticity in the auditory system, which might contribute to acclimatization and/or deprivation effects. Such functional changes might be further modulated by reinforcing responses to reintroduced sounds using conditioning techniques. This article reviews relevant literature on auditory system plasticity--drawn largely from animal research--with the goal of providing insight into possible mechanisms of acclimatization and deprivation effects.

Brain↗
PubMed2002

Selected contribution: High-altitude natives living at sea level acclimatize to high altitude like sea-level natives.

Sea-level (SL) natives acclimatizing to high altitude (HA) increase their acute ventilatory response to hypoxia (AHVR), but HA natives have values for AHVR below those for SL natives at SL (blunting). HA natives who live at SL retain some blunting of AHVR and have more marked blunting to sustained (20-min) hypoxia. This study addressed the question of what happens when HA natives resident at SL return to HA: do they acclimatize like SL natives or revert to the characteristics of HA natives? Fifteen HA natives resident at SL were studied, together with 15 SL natives as controls. Air-breathing end-tidal Pco(2) and AHVR were determined at SL. Subjects were then transported to 4,300 m, where these measurements were repeated on each of the following 5 days. There were no significant differences in the magnitude or time course of the changes in end-tidal Pco(2) and AHVR between the two groups. We conclude that HA natives normally resident at SL undergo ventilatory acclimatization to HA in the same manner as SL natives.

Adaptation, Physiological↗
PubMedDate not supplied

Acclimatization in wide dynamic range multichannel compression and linear amplification hearing aids.

Acclimatization was studied in hearing-impaired patients with no previous hearing aid (HA) experience who were fit bilaterally with either wide dynamic range multichannel compression (WDRMCC) or linear amplification (LA) HAs. Throughout 40 weeks of normal HA use, we monitored changes in nonsense syllable perception in speech-spectrum noise. Syllable recognition for WDRMCC users improved by 4.6% over the first 8 weeks, but the 2.2% improvement for LA users was complete in 2 to 4 weeks. Consonant confusion analyses indicated that WDRMCC experience facilitated consonant identification, while LA users primarily changed their response biases. Furthermore, WDRMCC users showed greater improvement for aided than unaided stimuli, while LA users did not. These results demonstrate acclimatization in new users of WDRMCC HAs but not in new users of LA HAs. A switch in amplification type after 32 weeks produced minimal performance change. Thus, acclimatization depended on the type of amplification and the previous amplification experience.

Adaptation, Physiological↗