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PubMed1993

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↗
PubMed1993

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↗
PubMed1976

Serum glucose, serum free fatty acids and adipose tissue lipids after fatal hypothermia of cold acclimatized, reserpine or propranolol treated guinea-pigs.

Surviving ability in frost (-20 degree C) was studied in cold acclimatized guinea-pigs given either reserpine, propranolol or saline. Survival time, rectal temperature at death, serum glucose, serum FFA and triglycerides in the interscapular adipose tissue were determined. Rectal temperature was highest in the reserpine group, in the same animals that endured the frost the shortest time. The survival time had decreased by about a half of that in the controls. Propranolol treatment decreased the living time only slightly. The fact that serum glucose remained high in the reserpine treated animals was obviously related to the short survival time. In the propranolol group glucose values were somewhat higher than in the control group (saline-animals). Reserpine seemed to have inhibited the release of FFA in the warm-acclimatized animals as interpreted from the low serum values. On the other hand, FFA were rather high in the cold-acclimatized reserpine animals. The blocking effect of reserpine reflected also in the higher contents of triglycerides in the adipose tissue both in cold-acclimatized and warm-acclimatized animals. Propranolol prevented slightly the depletion of the triglycerides. Amount of total lipids in the adipose tissue was lower in the cold-acclimatized animals than in the warm-acclimatized ones because of the change of the type of the adipocytes from unilocular to multilocular. The results corroborated the importance of FFA for longer survival in severe cold. Sensitization to reserpine seems to develop during cold-acclimatization. It calls attention to a possible hazard of reserpine treatment in cold environment.

Acclimatization↗
PubMed1995

Possible role of dopamine in ventilatory acclimatization to high altitude.

Ventilatory acclimatization to high altitude is accompanied by increased hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses which may reflect increased carotid body chemosensitivity. Dopamine is an inhibitory neuromodulator of the carotid body and its activity may be reduced by hypoxic exposure. To determine whether decreased dopaminergic activity could account for the increased chemosensitivity of acclimatization, we examined the response to peripheral dopamine receptor (D2) blockade with domperidone on HVR and HCVR in awake cats before and after exposure to simulated altitude of 14,000 ft for 2 days. During anesthesia, we also examined the effects of domperidone on carotid body responses to hypoxia and hypercapnia in acclimatized and low altitude cats. Two days' exposure to hypobaric hypoxia produced an increase in HVR and HCVR. Before acclimatization, domperidone augmented HVR and HCVR, but there was no effect after acclimatization. In anesthetized low altitude cats, domperidone increased carotid body responses to hypoxia and hypercapnia, but had no effect in acclimatized cats. These results indicate that decreased endogenous dopaminergic activity may contribute to increased ventilatory and chemoreceptor responsiveness to hypoxia and hypercapnia during hypoxic ventilatory acclimatization.

Acclimatization↗
PubMed1996

In vitro responses of VLM neurons to hypoxia after normobaric hypoxic acclimatization.

Hypoxic acclimatization involves an initial rapid ventilatory response followed by a more gradual increase in ventilation over a period of 24 to 48 h in both humans and rats. In addition, the acute ventilatory response to hypoxia is accentuated following hypoxic acclimatization. The purpose of the present investigation was to determine if hypoxic acclimatization augments the acute hypoxic response of neurons in the ventrolateral medulla (VLM). Brain slices (400 microns) containing the ventrolateral medulla were prepared from Sprague-Dawley rats acclimatized to hypoxia (10% O2) for 4-5 days (n = 4) and 9-10 days (n = 4) and from rats maintained in a normoxic environment (n = 4). Extracellular recordings demonstrated that there were no significant differences in the basal pattern or discharge rate of VLM neurons from animals exposed to short (10.8 +/- 0.9 Hz, n = 51), or long (10.1 +/- 1.1 Hz, n = 59) periods of hypoxia compared to control neurons (10.8 +/- 1.1 Hz, n = 52). The proportion of neurons stimulated (approximately 70%), inhibited (approximately 20%) and unaffected (approximately 10%) by an acute bout of hypoxia (10% O2) was also similar among groups. However, acute hypoxia elicited a greater increase in discharge frequency in neurons from rats exposed to the short period of hypoxia compared to the responses from neurons in the control and longer acclimatization groups. Thus, the responsivity of VLM neurons during the early stages of hypoxic acclimatization is altered in a manner consistent with the respiratory responses associated with acclimatization.

Acclimatization↗
PubMed1976

Heat illness. III. Acclimatization.

In this third paper on heat illness, the position of acclimatization in prevention of heat illness is reviewed. Both short and long-term acclimatization are considered, the former in more detail with discussion of present knowledge of the differences arising from artificial and natural acclimatization, the effects of training, water intake and increasing salt intake, and climatic chamber and vapour-barrier suit acclimatization. The possibility of the development of a safe drug to accelerate acclimatization is considered remote. The effects of age and acclimatization in the healthy and unhealthy elderly and the very young are reviewed briefly as is also the possibility that air conditioning may have an adverse effect on acclimatization.

Acclimatization↗
PubMed2002

Cardioventilatory effects of acclimatization to aquatic hypoxia in channel catfish.

The mechanisms responsible for altering cardioventilatory control in vertebrates in response to chronic hypoxia are not well understood but appear to be mediated through the oxygen-sensitive chemoreceptor pathway. Little is known about the effects of chronic hypoxia on cardioventilatory control in vertebrates other than mammals. The purpose of this study was to determine how cardioventilatory control and the pattern of response is altered in channel catfish (Ictalurus punctatus) by 1 week of moderate hypoxia. Fish were acclimatized for 7 days in either normoxia (P(O(2)) approximately 150 Torr) or hypoxia (P(O(2)) approximately 75 Torr). After acclimatization, cardioventilatory, blood-gas and acid/base variables were measured during normoxia (P(O(2)) 148+/-1 Torr) then at two levels of acute (5 min) hypoxia, (P(O(2)) 72.6+/-1 and 50.4+/-0.4 Torr). Ventilation was significantly greater in hypoxic acclimatized fish as was the ventilatory sensitivity to hypoxia (Delta ventilation/Delta P(O(2))). The increase in ventilation and hypoxic sensitivity was due to increases in opercular pressure amplitude, gill ventilation frequency did not change. Heart rate was greater in hypoxic acclimatized fish but decreased in both acclimatization groups in response to acute hypoxia. Heart rate sensitivity to hypoxia (Delta heart rate/Delta P(O(2))) was not affected by hypoxic acclimatization. The ventilatory effects of hypoxic acclimatization can be explained by increased sensitivity to oxygen but the effects on heart rate cannot.

Acclimatization↗
PubMed2003

Improving oxygenation at high altitude: acclimatization and O2 enrichment.

When lowlanders go to high altitude, the resulting oxygen deprivation impairs mental and physical performance, quality of sleep, and general well-being. This paper compares the effects of ventilatory acclimatization and oxygen enrichment of room air on the improvement of oxygenation as judged by the increase in the alveolar P(O2) and the reduction in equivalent altitude. The results show that, on the average, complete ventilatory acclimatization at an altitude of 5000 m increases the alveolar P(O2) by nearly 8 torr, which corresponds to a reduction in equivalent altitude of about 1000 m, although there is considerable individual variability. By comparison, oxygen enrichment to 27% at 5000 m can easily reduce the equivalent altitude to 3200 m, which is generally well tolerated. Because full ventilatory acclimatization at altitudes up to about 3600 m reduces the equivalent altitude to about 3000 m, oxygen enrichment is not justified for well-acclimatized persons. At an altitude of 4200 m, where several telescopes are located on the summit of Mauna Kea, full acclimatization reduces the equivalent altitude to about 3400 m, but the pattern of commuting probably would not allow this. Therefore, at this altitude, oxygen enrichment would be beneficial but is not essential. At higher altitudes such as 5050 m, where other telescopes are located or planned, the gain in oxygenation from acclimatization is insufficient to produce an adequate mental or physical performance for most work, and oxygen enrichment is highly desirable. Full ventilatory acclimatization requires at least a week of continuous exposure, although much of the improvement is seen in the first 2 days.

Acclimatization↗
PubMed1976

Norepinephrine thermogenesis in seasonally acclimatized and cold acclimated red-backed voles in Alaska.

The calorigenic response (millilitres O2 per gram pre hour) to injected norepinephrine (NE) was compared as an index of nonshivering thermogenesis (NST) in the following groups of the Alaska red-backed vole (Clethrionomys rutilus): (1) summer, (2) fall acclimatized, (3) winter acclimatized, (4) 20 degrees C acclimated and (5) 5 degrees C acclimated. The metabolic response was tested at thermoneutrality (25 degrees C) and during cold exposure (5 degrees C). Winter acclimatized voles showed a significantly greater metabolic response to NE than summer voles at both 25 degrees C and 5 degrees C. In summer or winter voles the total metabolic rate after NE (Mne) was similar at 25 degrees C and 5 degrees C but the fraction of the total caused by exogenous NE was lower at 5 degrees C. Thus, thermogenesis during cold exposure and resulting from exogenous NE appear to be based on the same mechanism, and NE has thermoregulatory significance in these voles. The magnitude of the NE response in winter voles was comparable to he highest values reported for bats and exceeded levels reported for other adult small mammal species. Summer acclimatized voles and those acclimatized to 20 degrees C in the laboratory were comparable in their response to NE but winter acclimatized voles were significantly more sensitive to NE than voles acclimated to 5 degrees C. The seasonal winter peak in MNE coincided with peaks previously found for maximum metabolic capacity (MMAX), maximum brown fat, and the period of coldest temperature in December-January. the ratio of MNE to Mmax was similar throughout the year. The results suggest that small arctic-subarctic rodents have a greater capacity for NE stimulated NST than rodents from temperate latitudes probably because they are acclimatized to colder seasonal condtions.

Acclimatization↗
PubMed1981

Blood volume and plasma protein responses to heat acclimatization in humans.

The effects of heat acclimatization on intravascular volume and protein responses to acute heat stress and exercise were studied in six male subjects. Absolute values for hematocrit and hemoglobin concentration were lower after, than before, acclimatization, indicating hemodilution. Also, after acclimatization, the magnitude of the hemoconcentration response to exercise in the heat was significantly increased. There ws no change in the concentration of plasma protein during or after acclimatization compared with before acclimatization, but there was a net increase in the total intravascular protein content. It is suggested that the hemodilution associated with heat acclimatization may be explained in terms of an increase in the intravascular oncotic pressure following an exercise-induced augmentation of protein, occurring at the expense of the interstitial compartment. It is concluded that this hemodilution is unlikely to be primarily responsible for the cardiovascular adjustment accompanying heat acclimatization and that it should be regarded as a secondary feature of adaptation to heat.

Acclimatization↗
PubMed1981

Effect of saline loading during heat acclimatization on adrenocortical hormone levels.

Six male subjects were acclimatized to heat; once they were given sufficient 1% saline to prevent the occurrence of a salt deficit during acclimatization, and another time they were given no saline. Plasma aldosterone (PA), plasma cortisol (PC), plasma renin activity (PRA), and plasma electrolytes were measured before, during, and after and sweat electrolytes before and after the 11-day acclimatization program. PRA and PA were significantly increased by the acute stress of heat and exercise but were unaffected by acclimatization. These increases were attenuated, but not prevented, by drinking saline, whereas sweat [Na] and PC were reduced by acclimatization but were unaffected by saline. Thus adrenocortical activity has been shown not to be increased after heat acclimatization, and mineralocorticoid activity, although potentiated by a Na deficit, appears to be determined primarily by the acute stress of heat and of exercise. Hence, the increased Na conservation with acclimatization is likely to be a normal response to heat and exercise even in the absence of a negative Na balance.

Acclimatization↗
PubMed1987

Increased carotid body hypoxic sensitivity during acclimatization to hypobaric hypoxia.

Mechanisms of ventilatory acclimatization to chronic hypoxia remain unclear. To determine whether the sensitivity of peripheral chemoreceptors to hypoxia increases during acclimatization, we measured ventilatory and carotid sinus nerve responses to isocapnic hypoxia in seven cats exposed to simulated altitude of 15,000 ft (barometric pressure = 440 Torr) for 48 h. A control group (n = 7) was selected for hypoxic ventilatory responses matched to the preacclimatized measurements of the experimental group. Exposure to 48 h of hypobaric hypoxia produced acclimatization manifested as decrease in end-tidal PCO2 (PETCO2) in normoxia (34.5 +/- 0.9 Torr before, 28.9 +/- 1.2 after the exposure) as well as in hypoxia (28.1 +/- 1.9 Torr before, 21.8 +/- 1.9 after). Acclimatization produced an increase in hypoxic ventilatory response, measured as the shape parameter A (24.9 +/- 2.6 before, 35.2 +/- 5.6 after; P less than 0.05), whereas values in controls remained unchanged (25.7 +/- 3.2 and 23.1 +/- 2.7; NS). Hypoxic exposure was associated with an increase in the carotid body response to hypoxia, similarly measured as the shape parameter A (24.2 +/- 4.7 in control, 44.5 +/- 8.2 in acclimatized cats). We also found an increased dependency of ventilation on carotid body function (PETCO2 increased after unilateral section of carotid sinus nerve in acclimatized but not in control animals). These results suggest that acclimatization is associated with increased hypoxic ventilatory response accompanied by enhanced peripheral chemoreceptor responsiveness, which may contribute to the attendant rise in ventilation.

Acclimatization↗
PubMed1989

Decreased exercise muscle lactate release after high altitude acclimatization.

Blood lactate concentration during exercise decreases after acclimatization to high altitude, but it is not clear whether there is decreased lactate release from the exercising muscle or if other mechanisms are involved. We measured iliac venous and femoral arterial lactate concentrations and iliac venous blood flow during cycle exercise before and after acclimatization to 4,300 m. During hypoxia, at a given O2 consumption the venous and arterial lactate concentrations, the venous and arterial concentration differences, and the net lactate release were lower after acclimatization than during acute altitude exposure. While breathing O2-enriched air after acclimatization at a given O2 consumption the venous and arterial lactate concentrations and the venous and arterial concentration differences were significantly lower, and the net lactate release tended to be lower than while breathing ambient air at sea level before acclimatization. We conclude that the lower lactate concentration in venous and arterial blood during exercise after altitude acclimatization reflected less net release of lactate by the exercising muscles, and that this likely resulted from the acclimatization process itself rather than the hypoxia per se.

Acclimatization↗
PubMed1975

Tolerance of altitude-acclimatized rats to exercise in the cold.

The tolerance of altitude-acclimatized (18,000 ft 4 wk) and unacclimatized rats to exercise at 5 degrees was determined. Fewer unacclimatized than acclimatized rats became fatigued during 9 hr of exercise in the cold. Normal body temperatures were maintained in both groups during 9 hr in the cold at rest, but after exercise unacclimatized rats became mildly hypothermic (body temperature 35 degrees) and acclimatized rats severely hypothermic (body temperature 27.9 degrees). Polycythemia (hematocrit 69) was produced during the altitude acclimatization. Altitude-acclimatized rats developed more severe hypoglycemia and lower liver glycogen and serum lactic acid concentrations after exercise than did controls. No pathological changes were found in resting altitude-acclimatized rats, but after exercise in the cold, a higher percentage of acclimatized than unacclimatized rats developed focal myocardial necrosis within 4 days. Reduced exercise tolerance is attributed to severe hypothermia with associated decreased metabolism, polycythemia, hypoglycemia, and a higher incidence of pathological changes in the cardiac and striated muscles.

Acclimatization↗
PubMed1970

Functional significance of isoenzymes in thermal acclimatization. Acetylcholinesterase from trout brain.

1. The effects of acclimatization temperature on the catalytic properties of acetylcholinesterase from rainbow-trout brain were examined. 2. Trout brain acetylcholinesterase occurs in two distinct forms. A single ;warm' variant of the enzyme is present after acclimatization to 17 degrees C; a single ;cold' variant appears after acclimatization to 2 degrees C. Both forms are present in fish after acclimatization to an intermediate temperature. 3. The K(m) values of the enzyme variants for acetylcholine are temperature-dependent, the lowest values coinciding with the acclimatization temperature at which each enzyme was induced. 4. It is concluded that the K(m)-temperature relationship is adaptive, and that the critical process during thermal acclimatization, in cases where enzymes show sharp changes in K(m) with temperature, is the synthesis of a new enzyme variant that is better suited for catalysis and control of catalysis under the conditions of the acclimatized state.

Acetylcholinesterase↗
PubMed1983

Thermal acclimatization of hepatic polysubstrate monooxygenase and UDP-glucuronosyltransferase of mature rainbow trout (Salmo gairdneri).

The thermal acclimatization of hepatic cytochrome P-450-dependent polysubstrate monooxygenase (PSMO) and UDP-glucuronosyltransferase of mature rainbow trout (Salmo gairdneri) was studied. The results indicate that the PSMO system, 7-ethoxycoumarin and benzo(a)pyrene as substrates, shows almost ideal acclimatization pattern in autumn during water cooling. The enzyme activities were identical if measurements were carried out at acclimatization (=environmental) temperatures which were 20 degrees C in August and 5 degrees C in November. If a constant incubation temperature (18 degrees C) was used, the PSMO activities were significantly higher in cold (5 degrees C)-acclimatized fish. The acclimatization process could be seen both in specific and total activities. The content of cytochrome P-450 remains at constant level from August to November. In early summer during water warming the PSMO activities increased considerably in both sexes in all incubation conditions. The specific and total UDP-glucuronosyltransferase activities were significantly higher in warm-acclimatized fish both in the autumn and in the spring if the activities were measured at environmental temperature. No differences could be detected if the measurements were carried out at constant experimental temperature (18 degrees C).

Acclimatization↗
PubMed1986

Hyperoxic ventilatory responses of high altitude acclimatized cats.

We have examined the effect of steady-state hyperoxia on the ventilation of sea level (SL) cats and cats acclimatized to simulated high altitude (HA) at 5500 m for three weeks. Three groups of cats were studied. In group I, the ventilatory responses to 10%, 21% and 100% O2 were studied at SL, and after acclimatization to HA, the ventilatory responses to 10% and 100% O2 were measured. In group II the ventilatory responses and femoral artery and superior sagittal sinus blood gases were measured in two sets of cats, one at SL and one at HA, during exposure to the gases outlined in group I. In group III, we examined the effect of chronic vagotomy on the ventilatory responses to the gas mixtures outlined in group I. Breathing 100% O2 at SL had no significant effect on ventilation, tidal volume, respiratory frequency, or cerebral blood flow (inferred from the cerebral veno-arterial CO2 difference). Ventilation was constant in the HA acclimatized cats while breathing 10% and 100% O2, but the ventilatory pattern changed dramatically during hyperoxia: respiratory frequency increased and tidal volume fell. Breathing 100% O2 was associated with changes in CBF, and venous PCO2 that might be expected to stimulate ventilation, but the change in ventilatory pattern suggests to us that hyperoxic disinhibition of central respiratory processes (which were modified by HA acclimatization) is the mechanism whereby ventilation is sustained during hyperoxia at HA. After vagotomy at HA, ventilation remained constant while breathing 100% O2, but the changes in respiratory pattern were no longer apparent. Therefore, vagal afferents seems to have a role in determining the pattern, but not necessarily the absolute level, of ventilation during hyperoxia. Cats vagotomized at SL prior to HA exposure did not show any evidence of HA ventilatory acclimatization; thus, the vagi may also play a heretofore unrecognized role in the process of acclimatization.

Acclimatization↗
PubMed1988

Rate of ventilatory acclimatization to extreme altitude.

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

Acclimatization↗