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Respiratory, circulatory and neuropsychological responses to acute hypoxia in acclimatized and non-acclimatized subjects.

Respiratory, circulatory and neuropsychological responses to stepwise, acute exposure at rest to simulated altitude (6,000 m) were compared in ten acclimatized recumbent mountaineers 24 days, SD 11 after descending from Himalayan altitudes of at least 4,000 m with those found in ten non-acclimatized recumbent volunteers. The results showed that hypoxic hyperpnoea and O2 consumption at high altitudes were significantly lower in the mountaineers, their alveolar gases being, however, similar to those of the control group. In the acclimatized subjects the activation of the cardiovascular system was less marked, systolic blood pressure, pulse pressure, heart rate and thus (calculated) cardiac output being always lower than in the controls; diastolic blood pressure and peripheral vascular resistance, however, were maintained throughout in contrast to the vasomotor depression induced by central hypoxia which occurred in the non-acclimatized subjects at and above 4,000 m [alveolar partial pressure of O2 less than 55-50 mmHg (7.3-6.6 kPa)]. It was concluded that in the acclimatized subjects at high altitude arterial vasodilatation and neurobehavioural impairment, which in the non-acclimatized subjects reflect hypoxia of the central nervous system, were prevented; that acclimatization to high altitude resulted in a significant improvement of respiratory efficiency and cardiac economy, and that maintaining diastolic blood pressure (arterial resistance) at and above 4,000 m may represent a useful criterion for assessing hypoxia acclimatization.

Acclimatization↗

De-acclimatization process of rats acclimatized to high altitude hypoxia.

The de-acclimatization process in rats acclimatized to high altitude hypoxia was analyzed according to the changes in the activities of hepatic enzymes. The activities of tryptophan 2,3-dioxygenase and tyrosine aminotransferase in the liver of non-acclimatized rats were increased, whereas those of acclimatized rats were decreased after exposure to a simulated altitude of 8,000 m. When the acclimatized rats were kept under normoxic conditions for 8 days and over, the suppression of enzyme induction was nullified, and both enzymes were induced by exposure to the simulated 8,000 m altitude. De-acclimatization of rats acclimatized to hypoxia can be completed in 8-11 days.

Acclimatization↗

Altitude diuresis: endocrine and renal responses to acute hypoxia of acclimatized and non-acclimatized subjects.

As a result of our recently published studies we have thought that altitude diuresis resulting from hypoxic stimulation of the arterial chemoreceptors reduces the cardiac volume overload. To test this hypothesis, cardiovascular, endocrine and renal responses to stepwise acute exposure to simulated altitude (6,000 m) were compared in ten acclimatized recumbent mountaineers a mean of 24 days, SD 11, after descending from Himalayan altitudes of at least 4,000 m, with those found in ten non-acclimatized recumbent volunteers. The results showed that natriuresis and diuresis typified the renal responses to altitude exposure of both the acclimatized as well as non-acclimatized subjects, as long as altitude was well tolerated. It was concluded that the renal effects were mediated by atrial natriuretic peptide release and slight suppression of arginine-vasopressin (AVP) secretion, that the increased urine flow at altitude offset the cardiac (volume) overload resulting from hypoxic stimulation of the arterial chemoreceptors, and that enhanced AVP secretion, as found in the non-acclimatized subjects at and above 4,000 m, coincided with subjective and objective distress, i.e. with inadequate altitude adjustment owing to insufficient chemoreflex effects and central hypoxia.

Acclimatization↗

Effects of exercise training on acclimatization to hypoxia: systemic O2 transport during maximal exercise.

Acclimatization to hypoxia has minimal effect on maximal O2 uptake (Vo2 max). Prolonged hypoxia shows reductions in cardiac output (Q), maximal heart rate (HR-max), myocardial beta-adrenoceptor (beta-AR) density, and chronotropic response to isoproterenol. This study tested the hypothesis that exercise training (ET), which attenuates beta-AR downregulation, would increase HRmax and Q of acclimatization and result in higher Vo2 max. After 3 wk of ET, rats lived at an inspired Po2 of 70 Torr for 10 days (acclimatized trained rats) or remained in normoxia, while both groups continued to train in normoxia. Controls were sedentary acclimatized and nonacclimatized rats. All rats exercised maximally in normoxia and hypoxia (inspired Po2 of 70 Torr). Myocardial beta-AR density and the chronotropic response to isoproterenol were reduced, and myocardial cholinergic receptor density was increased after acclimatization; all of these receptor changes were reversed by ET. Normoxic Vo2 max (in ml.min-1.kg-1) was 95.8 +/- 1.0 in acclimatized trained (n = 6), 87.7 +/- 1.7 in nonacclimatized trained (P < 0.05, n = 6), 74.2 +/- 1.4 in acclimatized sedentary (n = 6, P < 0.05), and 72.5 +/- 1.2 in nonacclimatized sedentary (n = 8; P > 0.05 acclimatized sedentary vs. nonacclimatized sedentary). A similar distribution of Vo2 max values occurred in hypoxic exercise. Q was highest in trained acclimatized and nonacclimatized, intermediate in nonacclimatized sedentary, and lowest in acclimatized sedentary groups. ET preserved Q in acclimatized rats thanks to maintenance of HRmax as well as of maximal stroke volume. Q preservation, coupled with a higher arterial O2 content, resulted in the acclimatized trained rats having the highest convective O2 transport and Vo2 max. These results show that ET attenuates beta-AR downregulation and preserves Q and Vo2 max after acclimatization, and support the idea that beta-AR downregulation partially contributes to the limitation of Vo2 max after acclimatization in rats.

Acclimatization↗

Summer acclimatization in the short-tailed field vole, Microtus agrestis.

We investigated the changes that occurred in basal and noradrenaline-induced metabolic rate, body temperature and body mass in short-tailed field voles, Microtus agrestis, during exposure to naturally increasing photoperiod and ambient temperature. These parameters were first measured in winter-acclimatized voles (n = 8) and then in the same voles which had been allowed to seasonally acclimatize to photoperiod and ambient temperature (6 months later). Noradrenaline induced metabolic rate, basal metabolic rate and non-shivering thermogenesis were significantly higher in winter-acclimatized compared to summer-acclimatized voles. There was a significant positive relationship between basal metabolic rate and noradrenaline-induced metabolic rate. Body mass was significantly higher in summer-acclimatized compared to winter-acclimatized voles. There was a significant positive relationship between body mass and noradrenaline-induced metabolic rate in both winter-acclimatized and summer-acclimatized voles; however, there was no relationship between basal metabolic rate and body mass in either seasonal group of voles. Body temperature after measurements of basal metabolic rate was not significantly different in the seasonal cohorts of voles. However, body temperature was significantly higher in winter-acclimatized compared to summer-acclimatized voles after injection of noradrenaline. Previously we have found that a long photoperiod was not a sufficient stimulus to reduce thermogenic capacity in winter-acclimatized voles during cold exposure, since basal metabolic rate increased to compensate for a reduction in regulatory non-shivering thermogenesis. Here we found that a combination of increased ambient temperature and photoperiod did significantly reduce thermogenic capacity in winter-acclimatized voles. This provided evidence that the two aspects of non-shivering thermogenesis, obligatory and regulatory, are stimulated by different exogenous cues. Summer acclimatization in the short-tailed field vole is manifest as a significant decrease in both basal and noradrenaline-induced metabolic rate, combined with a significant increase in body mass.

Acclimatization↗

Influence of temperature acclimatization on sodium--glucose interactions in the goldfish intestine.

1. Transmural potentials across goldfish intestines in vitro were found to depend on the acclimatization temperature of the fish. At any incubation temperature potentials were lower in fish kept previously at a high temperature, and if the transmural potentials were recorded at incubation temperatures equal to the previous acclimatization temperatures the values remained constant from 8 to 30 degrees C. The glucose-evoked potential was also reduced by previous acclimatization of the fish to a high temperature.2. As the sodium concentration was reduced the steady transmural potential increased and later fell in proportion to the low external sodium concentration, but the glucose-evoked potential fell as soon as the sodium concentration was reduced below 140 mM. Similar changes were seen with intestines taken from fish acclimatized to a high temperature but both the steady-state potential and the transitory glucose-evoked potential were more dependent on the external sodium concentration.3. The maximum glucose-evoked potential depended on the concentration of glucose used and temperature acclimatization had no significant effect on this relation. The steady potential was lower in the presence of glucose at low incubation temperatures but higher at higher incubation temperatures, and the temperature at which glucose ceased to inhibit depended on the previous acclimatization temperature. Glucose also lowered the steady potential, whatever the previous acclimatization temperature, when the external sodium concentration was low.4. The inhibitory effect of glucose on the steady potential of an intestine taken from a 30 degrees -acclimatized fish could be abolished by lowering the external concentration of glucose from 27 to 16 mM.5. Intestines taken from fish acclimatized to 3 degrees C gave variable results.6. It is concluded that sodium moves across the luminal membrane of the goldfish mucosa attached to a carrier which can exist in one of two forms. It is changes in this postulated carrier which serve to stabilize sodium transport at different acclimatization temperatures. Changes in the concentration of this postulated carrier may also occur and function in the regulation of sodium transport, particularly at acclimatization temperatures below 15 degrees C, where the switching of the carrier does not operate.

Animals↗

Cardiovascular and metabolic responses to noradrenaline in men acclimatized to cold baths.

The purpose of this study was to see whether artificial acclimatization to cold would reduce the pressor response to noradrenaline (NA) as natural acclimatization has been shown to do, and whether it would induce nonshivering thermogenesis. Three white men were infused with NA at four dosage levels between 0.038 and 0.300 microgram.kg-1.min-1 (2-23 micrograms.min-1), before and after artificial acclimatization to cold and again 4 months later when acclimatization had decayed. Acclimatization was induced by ten daily cold (15 degrees C) baths of 30-60 min followed by rapid rewarming in hot (38-42 degrees C) water, and was confirmed by tests of the subjects' responses to whole-body cooling in air. Three control subjects also underwent the first and third tests. Acclimatization substantially reduced the pressor response to NA at 0.150 and 0.300 micrograms.kg-1.min-1, confirming earlier findings by the same technique in naturally acclimatized men, and its decay increased this response to beyond its initial levels (P < 0.05 for both changes). Acclimatization did not change the response to NA of heart rate, subjective impressions, skin temperature of finger and toe, pulmonary ventilation, or plasma free fatty acids and ketone bodies. At no time did NA increase oxygen consumption, or increase skin temperature or heat flow over reported sites of brown fat. These findings would seem to show that acclimatization to cold reduces sensitivity to the pressor effect of NA but does not induce nonshivering thermogenesis, and that the reduced sensitivity is replaced by a hypersensitivity to NA when acclimatization decays.

Acclimatization↗

Effects of acclimatization to cold baths on men's responses to whole-body cooling in air.

The purpose of this study was to investigate the thermoregulatory mechanisms underlying artificial acclimatization to cold and to compare them with those of naturally acclimatized men. Six white men were cooled, nude, in air at 10 degrees C for 2 h before and after they had been acclimatized by ten daily cold (15 degrees C) baths of 30-60 min followed by rapid rewarming in hot (38-42 degrees C) water, and again 4 months later after acclimatization had decayed. Six control subjects also underwent the same tests, providing an opportunity to discriminate between changes caused by the immersions and those caused by extraneous influences. Acclimatization significantly reduced heat production and heat loss (P < 0.05) but did not change heat debt. The reduced heat production was accompanied by reductions in shivering (P < 0.10) and in cold-induced muscle tenseness; no evidence of nonshivering thermogenesis or active brown fat was found. These findings are attributed to increased tissue insulation, mediated by an enhanced vascular response to cold that did not involve the cutaneous circulation and was probably located in skeletal muscle. Thermal sensation and discomfort did not change, although perceived strain tended to increase (P = 0.08). Acclimatization was accompanied by, but was unrelated to, slower cooling of the finger and toe. The main conclusions, and many specific findings, agree with those of two previous studies made by the same techniques in naturally acclimatized men wintering in Antarctica. Other significant findings included changes--in particular reduced thermoneutral rectal temperature and a delayed onset of shivering--that are commonly regarded as evidence of acclimatization but were in fact unrelated to it as they also occurred in the control group. They are attributed to extraneous influences, in particular the relaxation of heightened arousal ('first-time effects') found in the baseline tests.

Acclimatization↗