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Composition of cerebral fluids in goats adapted to high altitude.

We explored the ionic composition of cerebral interstitial fluid (cISF) in six unanesthetized goats at sea level (SL) and again after 5 days at a simulated high altitude (HA) of 4,300 m. By measuring net transependymal fluxes of HCO3-, Cl-, and lactate during ventriculocisternal perfusions with lactate-free artificial cerebrospinal fluid (CSF) with various [HCO3-] and [Cl-], we determined [HCO3-] and [Cl-] in the inflowing perfusate that produced zero flux, which are estimates of the concentrations of these ions in cISF. Ventilatory acclimatization to HA was established in the goats with alkaline shift in cisternal CSF pH. At SL zero flux of HCO3- and of Cl- occurred when [HCO3-] and [Cl-] in the perfusate were equal to those in CSF. At HA Cl- flux again was zero when [Cl-] in perfusate and in the goat's own CSF were equal; however, for HCO3-, zero flux occurred at HA when [HCO3-] in perfusate was significantly lower than in CSF. Mean transependymal washout of lactate was 16 times larger at HA than at SL. We conclude that at SL [HCO3-] and [Cl-] in CSF were the same as in cISF. In goats adapted to HA [Cl-] in cISF and in CSF were again equal, whereas [HCO3-] in cISF was lower and [lactate] presumably higher than in CSF. The fluid surrounding the central chemoreceptors appears to be more acidic in goats acclimatized to HA than at SL despite the alkalosis in cisternal CSF. This may contribute to ventilatory acclimatization to HA.

Acclimatization↗

Ventilation in newborn rats after gestation at simulated high altitude.

Pregnant rats were kept at a simulated altitude of 4,500 m (PO2 91 Torr) for the whole of gestation and returned to sea level 1 day after giving birth. During pregnancy, body weight gain and food intake were approximately 30% less than in controls at sea level. Measurements were made on the 1-day-old (HYPO) pups after a few hours at sea level. In normoxia, ventilation (VE) measured by flow plethysmography was more (+17%) and O2 consumption (VO2) measured by a manometric method was less (-19%) than in control (CONT) pups; in HYPO pups VE/VO2 was 44% greater than in CONT pups. In acute hyperoxia, VE/VO2 of HYPO and CONT pups decreased by a similar amount (15-20%), indicating some limitation in O2 availability for both groups of pups in normoxia. However, VE/VO2 of HYPO pups, even in hyperoxia, remained above (+34%) that of CONT pups. HYPO pups weighed slightly less than CONT pups, their lungs were hypoplastic, and their hearts were a larger fraction of body weight. An additional group of female rats was acclimatized (8 days) to high altitude before insemination. During pregnancy, body weight gain and food intake of these females were similar to those of pregnant rats at sea level. Measurements on the 1-day-old pups of this group were similar to those of HYPO pups. We conclude that newborn rats born after hypoxic gestation present metabolic adaptation (low VO2) and acclimatization (high VE/VO2), possibly because of hypoxemia. Maternal acclimatization before insemination substantially alters maternal growth in hypoxia but does not affect neonatal outcome.

Acclimatization↗

Changes in respiratory control during and after 48 h of isocapnic and poikilocapnic hypoxia in humans.

Ventilatory acclimatization to hypoxia is associated with an increase in ventilation under conditions of acute hyperoxia (VEhyperoxia) and an increase in acute hypoxic ventilatory response (AHVR). This study compares 48-h exposures to isocapnic hypoxia (protocol I) with 48-h exposures to poikilocapnic hypoxia (protocol P) in 10 subjects to assess the importance of hypocapnic alkalosis in generating the changes observed in ventilatory acclimatization to hypoxia. During both hypoxic exposures, end-tidal PO2 was maintained at 60 Torr, with end-tidal PCO2 held at the subject's prehypoxic level (protocol I) or uncontrolled (protocol P). VEhyperoxia and AHVR were assessed regularly throughout the exposures. VEhyperoxia (P < 0.001, ANOVA) and AHVR (P < 0.001) increased during the hypoxic exposures, with no significant differences between protocols I and P. The increase in VEhyperoxia was associated with an increase in slope of the ventilation-end-tidal PCO2 response (P < 0.001) with no significant change in intercept. These results suggest that changes in respiratory control early in ventilatory acclimatization to hypoxia result from the effects of hypoxia per se and not the alkalosis normally accompanying hypoxia.

Acclimatization↗

Effect of sustained hypobaric hypoxia during maturation and aging on rat myocardium. I. Mechanical activity.

Long-lasting cardioprotection may be attained by chronic hypoxia. The basal parameters of contractile function and their response to hypoxia/reoxygenation were measured under isometric conditions, in papillary muscles isolated from left ventricle of rats that were submitted to 53.8 kPa in a hypobaric chamber from 7 wk of age and for their lifetime and of their siblings kept at 101.3 kPa. During acclimatization, hematocrit increased, body weight gain decreased, and heart weight increased with right ventricle hypertrophy. Papillary muscle cross-sectional area was similar in both control and hypoxic groups up to 45 wk of exposure. Developed tension (DT) was 34-64% higher in rats exposed to hypoxia for 10, 26, and 45 wk than in their age-matched controls, whereas resting tension was unchanged. Maximal rates of contraction and relaxation showed a similar pattern of changes as DT. Recovery of DT and maximal rates of contraction and relaxation after 60-min hypoxia and 30-min reoxygenation was also improved in adult hypoxic rats to values similar to those of young rats. Heart acclimatization was lost after 74 wk of exposure. Results are consistent with the development of cardioprotection during high-altitude acclimatization and provide an experimental model to study the mechanisms involved, which are addressed in the accompanying paper.

Acclimatization↗

Respiratory and circulatory control at high altitudes.

Hyperventilation is one of the most important features of acclimatization to high altitude. Resting ventilation at extreme altitudes increases up to fourfold and exercise ventilation for a given work level increases to the same extent. Hypoxic stimulation of the peripheral chemoreceptors is the chief mechanism for the hyperventilation but there is also evidence that central sensitization of the respiratory centres occurs. Permanent residents of high altitude have a blunted hypoxic ventilatory response compared to acclimatized lowlanders. Cardiac output increases in responses to acute hypoxia but returns to normal in acclimatized lowlanders. Oxygen uptake at extreme altitudes is markedly limited by the diffusion properties of the blood gas barrier. As a consequence the maximal oxygen consumption of a climber near the summit of Mount Everest is near his basal oxygen requirements. Maximal oxygen consumption is so sensitive to barometric pressure that it may be that day-to-day variations will affect the chances of a climber reaching the summit without supplementary oxygen.

Acclimatization↗

Urinary characteristics of the Cape porcupine Hystrix africaeaustralis: effects of photoperiod and temperature.

The Cape porcupine Hystrix africaeaustralis is a large (11-18 kg), nocturnal, burrowing and group-living rodent. It experiences a metabolic response to seasonal acclimatization and is a hind gut fermenter. Changes in the urinary electrolyte and free urinary catecholamine concentrations of Cape porcupines were related to combined changes of ambient temperature and photoperiod regime. Three groups, A) Ta = 25 degrees C, 12L:12D; B) Ta = 32 degrees C, 16L:8D; C) Ta = 10 degrees C, 8L:16D, were studied to assess the influence of seasonal acclimatization on urinary bicarbonate and catecholamine concentrations. Urine volume was significantly (p < 0.001) higher in group C than in the other two groups. In groups B and C urinary pH was above 7 and this was associated with high concentrations of HCO3-. The total amount of catecholamines was higher in groups B and C than in group A. It is apparent that seasonal acclimatization of the Cape porcupine is also reflected by these parameters.

Acclimatization↗

Climate, altitude, and blood pressure.

The effects of climate and altitude on casual blood pressure are examined from the perspectives of initial exposure, acclimatization, long-term residence, and birthplace. Hot arid and hot humid climates seem to have little effect on blood pressure, although a slight reduction may be found in some naturally acclimatized groups. Exposure of the total body to mild cold likewise has little apparent effect. Local exposure of the extremities to severe cold occasions significant increases in blood pressure during exposure but not at other times. Acclimatization reduces but does not eliminate that response. The effects of altitude on blood pressure are variable. There is initial hypertension, followed by gradual normalization. After years of residence at high altitude blood pressure may actually be lower than that observed among residents at sea level.

Acclimatization↗

[Respiratory adaptation to altitude and risk factors due to respiratory illnesses].

Adaptation to altitude is a complex ability of the organism which involves primarily the cardiovascular and respiratory system in order to increase the oxygen supply for body tissues. Cardiovascular adaptations to rapid altitude challenge are regulated sympathetically and manifest themselves first of all as variations of cardiac output, systolic blood pressure and heart rate at rest. However, respiration plays an important role in compensating hypobaric hypoxia at altitude. The hypoxic ventilatory response (HVR) to alveolar hypoxia expressed as alveolar hyperventilation happens within a very short period of exposure to hypoxic conditions. This immediate adaptation response is followed by the acclimatization period, which encompasses longer lasting compensation processes such as the increase of blood hemoglobin concentration improving the arterial oxygen content. This final stage of adaptation is reached within days or weeks of persisting exposure and will vary somewhat depending on the degree of altitude. For healthy, acclimatized individuals the oxygen supply to the organism does not limit the exercise performance at moderate altitudes and higher. However, above 5000 meters (15,000 ft) long term adaptation cannot occur because oxygen-diffusion becomes a limiting factor to physical exercise capacity. Altitude-related disorders are contributing significantly to the morbidity and mortality of non-acclimatized individuals. Subjects already suffering from symptomatic underlying respiratory disease and hypoxemia at rest have a higher risk and incidence of altitude adaptation disorders even at lower altitudes. Therefore, several diseases with impaired respiratory function are contraindicated for any stay at altitude.

Acclimatization↗

Energy intake deficit and physical performance at altitude.

BACKGROUND: Physical performance of sea-level (SL) residents acutely exposed to altitude (ALT) is diminished and may improve somewhat with ALT acclimatization. HYPOTHESIS: A large reduction in lean body mass (LBM), due to severe energy intake deficit during the first 21 d of ALT (4300 m) acclimatization, will adversely affect performance. METHODS: At ALT, 10 men received a deficit (DEF) of 1500 kcal x d(-1) below body weight (BW) maintenance requirements and 7 men received adequate (ADQ) kcal x d(-1) to maintain BW. Performance was assessed by: 1) maximal oxygen uptake (VO2max); 2) time to complete 50 cycles of a lift and carry task (L+C); 3) number of one-arm elbow flexions (10% BW at 22 flexions x min(-1); and 4) adductor pollicis (AP) muscle strength and endurance time (repeated 5-s static contractions at 50% of maximal force followed by 5-s rest, to exhaustion). Performance and body composition (using BW and circumference measures) were determined at SL and at ALT on days 2 through 21. RESULTS: At SL, there were no between-group differences (p > 0.05) for any of the performance measures. From SL to day 21 at ALT, BW and LBM declined by 6.6 +/- 3 kg and 4.6 kg, respectively, for the DEF group (both p < 0.01), but did not change (both p > 0.05) for the ADQ group. Performance changes from day 2 or 3 to day 20 or 21 at ALT were as follows (values are means +/- SD): VO2max (ml x min(-1)): DEF = +97 +/- 237, ADQ = +159 +/- 156; L + C (s): DEF = -62 +/- 35*, ADQ = -35 +/- 20* (*p < 0.05; improved from day 3); arm flex (reps): DEF = -2 +/- 7, ADQ = +2 +/- 8; AP endurance (min): DEF = +1.4 +/- 2, ADQ = + 1.9 +/- 2; AP strength (kg): DEF = -0.7 +/- 4, ADQ = -1.2 +/- 2. There were no differences in performance between groups. CONCLUSIONS: A significant BW and LBM loss due to underfeeding during the first 21 d of ALT acclimatization does not impair physical performance at ALT.

Acclimatization↗

Oxygen and carbon dioxide in the regulation of respiration.

When a sea-level resident ascends to a high altitude, his breathing immediately increases because of hypoxic stimulation of the peripheral chemoreceptors. In many species the aortic bodies are relatively unimportant in this response compared to the carotid bodies. When the subject stays at that altitude, his breathing increases progressively in the next few hours and days in a process termed ventilatory acclimatization and does not immediately return to control levels when hypoxia is terminated. Evidence is summarized indicating that this chronic process does not depend on the peripheral chemoreceptors or an initial respiratory alkalosis. Historical review indicates that the process of ventilatory acclimatization was initially attributed to renal excretion of plasma bicarbonate with development of a metabolic acidosis; but subsequent measurements indicated this process did not lower the arterial pH sufficiently to account for the ventilatory stimulation. More recently, ventilatory acclimatization has been attributed to accelerated removal of bicarbonate from the cerebrospinal fluid (CSF), producing a metabolic acidosis in the region of the medullary chemoreceptors; but still more recent observations indicate that this process, contrary to earlier observations, does not lower the CSF pH sufficiently to account for the ventilatory stimulation, either. Some other mechanism should be sought.

Acclimatization↗

Effects of physical training and cardiorespiratory physical fitness on exercise-heat tolerance: recent observations.

Most authors agree that physical training in a cool environment improves tolerance to exercise in the heat and the rate of heat acclimatization, but the extent or degree of improvement remains controversial. The best improvement in heat tolerance for men is associated with intensive interval or continuous training at a training intensity greater than 50% of maximal oxygen uptake (Vo2max) for 8-12 weeks; the Vo2max should be increased 15-20%. Far less is known about the appropriate type, intensity and duration of endurance training associated with improved exercise-heat tolerance in women. The major benefits of physical training appear to apply to both short term (less than 2 hrs) or long term (greater than 2 hrs) exercise-heat exposures for men. Generally, individuals with high Vo2max values (previously trained and endurance athletes) are at an advantage in the heat. Utilization of proper physical training appears to produce about 50% of the total adjustment resulting from heat acclimatization, while increased fitness is associated with greater retention of acclimatization in cool environments. Female athletes appear somewhat better able to tolerate exercise in hot environments than nonathletic females while differences between highly trained females and males do not appear as dramatic as once thought.

Acclimatization↗

Physiological responses of women to thermal stress: a review.

The recent increase in women's participation in physically challenging activities prompted this review of female responses to heat and cold (68 references). Relevant sex differences include hormone levels, anthropometric factors, and body composition. Many studies show that women are less heat tolerant than men, particularly when physical work is required. Much of the difference is related to women's relatively low level of physical fitness and lack of heat acclimatization, which are in turn a result of their traditionally sedentary lifestyle. When work load is adjusted relative to individual capacity, females respond to heat stress much as males do. Acclimatization mechanisms are the same. Women generally have lower sweat rates, an appropriate adjustment to lesser cooling needs. The menstrual cycle has no meaningful effect on heat tolerance. Cold response reflects individual subcutaneous fat thickness, and women have an advantage there, but in extreme cold exposure they may be handicapped by their small muscle mass. Sex per se is but a small factor in determining human thermal responses; individual body size, physical fitness, and state of acclimatization play for more important roles.

Acclimatization↗

Some fundamental studies on clinical measurement conditions in acoustic rhinometry.

Acoustic rhinometry is a new method to measure the patency of the nasal airway. In this study the clinical measuring conditions were systematically evaluated. The test-retest validity was analysed by repeated measurements in ordinary, not specially trained patients and was found to be at the level of approximately 15%. The need for acclimatization before measurements was tested by making a series of measurements on two separate occasions: one after a rest period following the patient's arrival at the nose laboratory, and a second in another session where no rest was allowed for. Statistically, no significant differences between the repeated measurements in the two occasions were found. However, there was a tendency towards smaller nasal volumes in the measures of the repeated recordings made without an acclimatization period. Therefore, it seems to be advisable to have an acclimatization period before acoustic rhinometry measurements.

Acclimatization↗

Relation of sympathetic activation to ventilation in man at 4300 m altitude.

BACKGROUND: The sympathetic nervous activity increases at high altitude but is not maximal initially when hypoxemia is most severe. HYPOTHESIS: The sympathetic activation would correlate better to the ventilatory response to chronic hypoxia than to the severity of hypoxia per se. METHODS: Eleven healthy male volunteers (27 +/- 1 yr) had measurements from the abdominal aorta of pressure, catecholamines, and blood gases at sea level, on arrival at 4300 m, and after 21 d of residence. Additionally, we measured 24-h urinary catecholamine excretion at sea level and each day at altitude, and made serial measurements of resting ventilatory parameters. RESULTS: Arterial norepinephrine (NE) concentrations on arrival at 4300 m were little changed from sea level, but were increased following acclimatization at 21 d. Arterial oxygenation was decreased on arrival, but improved with acclimatization. Arterial epinephrine (E) concentrations were increased on arrival, and returned to an intermediate level by 21 d. The urinary NE excretion was increased along with the increase in VE (p < 0.01) and the fall in end-tidal PCO2 (p < 0.001), but not with the decrease in end-tidal PO2 during the sojourn at 4300 m. Excretion of E did not relate to any ventilatory parameters. Propranolol (240 mg.d-1), which was given to 6 of 11 subjects, did not affect any relationships. CONCLUSION: The sympathetic activation was related to the ventilatory response but not to measures of hypoxemia at 4300 m. We conclude that factors related to ventilatory acclimatization, possibly increased chemoreceptor activity, contribute to the development of sympathetic activation at high-altitude.

Acclimatization↗

Applying physiological principles and assessment techniques to swimming the English Channel. A case study.

BACKGROUND: This study presents the use of physiological principles and assessment techniques in addressing four objectives that can enhance a swimmer's likelihood of successfully swimming the English Channel. The four objective were: (1) to prescribe training intensities and determine ideal swimming pace; (2) to determine the amount of insulation needed, relative to heat produced, to diminish the likelihood of the swimmer suffering from hypothermia; (3) to calculate the caloric expenditure for the swim and the necessary glucose replacement required to prevent glycogen depletion; and (4) to determine the rate of acclimatization to cold water (15.56 C/60 F). METHODS: The subject participated in several pool swimming data collection sessions including a tethered swim incremental protocol to determine peak oxygen consumption and onset of lactate accumulation and several steady state swims to determine ideal swimming pace at 4.0 mM/L of lactate. Additionally, these swims provided information on oxygen consumption, which in combination with ultrasound assessment of subcutaneous fat was used to assess heat production and insulation capabilities. Finally, the subject participated in 18 cold water immersions to document acclimatization rate. RESULTS: The data demonstrated the high fitness level of this subject and indicated that at a stroke rate of 63 stokes/min, HR was 130 heats/min and lactate was 4 mM/L. At this swimming pace the swimmer would need to consume 470 kcal of glucose/hr. In addition, the energy produced at this swim pace was 13.25 kcal/min while the energy lost at the present subcutaneous fat quantity was 13.40 kcal/min, requiring a fat weight gain of 6,363.03 g (13.88 lbs) to resist heat loss. CONCLUSIONS: Finally, the data from the cold water immersions suggested that acclimatization occurred following two weeks of immersions. There results were provided to the swimmer and utilized in making decisions in preparation for the swim.

Acclimatization↗

Maximal sweating rate in humans.

We reviewed the literature concerning the maximal sweating rate (SRmax) during heat acclimatization, walking in desert heat and marathon running, and analyzed it from the viewpoint of sex, age, level of maximal oxygen uptake, and experimental conditions, i.e., ambient temperature, relative humidity, work intensity, work type, working duration, seasonal factors and the techniques of heat acclimatization. Exercise simulation, walking, running or bicycling, to induce the SRmax was conducted in a hot climatic chamber or in the desert. The SRmaxs due to marathon running were 1,000 to 1,200 g.h-1 in the cold season and 1,500 to 2,000 g.h-1 in the hot season. After several days of heat acclimatization, sweating capacity in the exercise simulation reached a maximum rate, over 2,000 g.h-1. There was a sexual difference in the SRmax, and the sweating capacity in the female was less than that in the male. Thus, the maximal sweating capacity in human was observed by prolonged moderate muscular exercise under thermal stress and internal and/or external heat loads.

Acclimatization↗

Arterial oxygen saturation for prediction of acute mountain sickness.

BACKGROUND: Acute mountain sickness (AMS) is a usually self-limiting syndrome encompassing headache, nausea and dizziness. AMS is seen in those that go from low to high altitudes too quickly, without allowing sufficient time to acclimatize. At present, susceptibility to AMS cannot be predicted. One feature of AMS noted in some studies is impaired gas exchange. If impaired gas exchange presages AMS then those individuals with exaggerated hypoxemia at high altitude may be more likely to develop AMS. If true, then monitoring of arterial oxygen saturation (SaO2%) may differentiate AMS-resistant individuals from those with impending AMS. METHODS: To test this hypothesis, we measured SaO2% and AMS symptom scores in 102 healthy asymptomatic climbers at 4200 m on Denali (Mt. McKinley) prior to their further ascent toward the summit at 6194 m, and on their return from higher altitudes to 4200 m. RESULTS: The results show that exaggerated hypoxemia in asymptomatic climbers prior to further ascent correlates with subsequent AMS (r = -0.48, p < 0.001). Criteria are presented for identification of 80-100% of those climbers who later become ill with AMS. CONCLUSION: We conclude that resting arterial hypoxemia is related to later development of clinical AMS, and can exclude the occurrence and caution those at risk for development of subsequent AMS. Likely mechanisms are hypoventilation relative to normally acclimatizing individuals and/or abnormalities of gas exchange. Thus, non-invasive oximetry provides a simple, specific indicator of inadequate acclimatization to high altitudes and impending AMS.

Acclimatization↗

Gene structure and seasonal expression of carp fish prolactin short receptor isoforms.

The complex adaptive mechanisms that eurythermal fish have evolved in response to the seasonal changes of the environment include the transduction of the physical parameter variations into neuroendocrine signals. Studies in carp (Cyprinus carpio) have indicated that prolactin (PRL) and growth hormone (GH) expression is associated with acclimatization, suggesting that the pituitary gland is a relevant physiological node in this adaptive process. Also, the distinctive pattern of expression that carp prolactin receptor (PRLr) protein depicts upon seasonal acclimatization supports the hypothesis that PRL and its receptor clearly are involved in the new homeostatic stage that the eurythermal fish needs to survive during the cyclical changes of its habitat. Here, we characterize the first prolactin receptor gene in a teleost and show that its expression is not associated with alternative promoters, unlike in humans and rodents. Using the regulatory region to direct the transcription of green fluorescent protein (GFP) in zebrafish embryos, we mapped the appearance of this hormone receptor during fish development. This is the first report identifying a fish prolactin receptor gene expressing transcript isoforms encoding for short forms of the protein (45 kDa). These have been found in osmoregulatory tissues of the carp and are regulated in connection with the seasonal acclimatization of the fish.

Amino Acid Sequence↗