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PubMed1966

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.

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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.

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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.

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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.

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PubMed2004

Pulmonary gas exchange at maximal exercise in Danish lowlanders during 8 wk of acclimatization to 4,100 m and in high-altitude Aymara natives.

We aimed to test effects of altitude acclimatization on pulmonary gas exchange at maximal exercise. Six lowlanders were studied at sea level, in acute hypoxia (AH), and after 2 and 8 wk of acclimatization to 4,100 m (2W and 8W) and compared with Aymara high-altitude natives residing at this altitude. As expected, alveolar Po2 was reduced during AH but increased gradually during acclimatization (61 +/- 0.7, 69 +/- 0.9, and 72 +/- 1.4 mmHg in AH, 2W, and 8W, respectively), reaching values significantly higher than in Aymaras (67 +/- 0.6 mmHg). Arterial Po2 (PaO2) also decreased during exercise in AH but increased significantly with acclimatization (51 +/- 1.1, 58 +/- 1.7, and 62 +/- 1.6 mmHg in AH, 2W, and 8W, respectively). PaO2 in lowlanders reached levels that were not different from those in high-altitude natives (66 +/- 1.2 mmHg). Arterial O2 saturation (SaO2) decreased during maximum exercise compared with rest in AH and after 2W and 8W: 73.3 +/- 1.4, 76.9 +/- 1.7, and 79.3 +/- 1.6%, respectively. After 8W, SaO2 in lowlanders was not significantly different from that in Aymaras (82.7 +/- 1%). An improved pulmonary gas exchange with acclimatization was evidenced by a decreased ventilatory equivalent of O2 after 8W: 59 +/- 4, 58 +/- 4, and 52 +/- 4 l x min x l O2(-1), respectively. The ventilatory equivalent of O2 reached levels not different from that of Aymaras (51 +/- 3 l x min x l O2(-1)). However, increases in exercise alveolar Po2 and PaO2 with acclimatization had no net effect on alveolar-arterial Po2 difference in lowlanders (10 +/- 1.3, 11 +/- 1.5, and 10 +/- 2.1 mmHg in AH, 2W, and 8W, respectively), which remained significantly higher than in Aymaras (1 +/- 1.4 mmHg). In conclusion, lowlanders substantially improve pulmonary gas exchange with acclimatization, but even acclimatization for 8 wk is insufficient to achieve levels reached by high-altitude natives.

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PubMed2005

[Effects of hypoxic acclimatization on myocardial sarcoplasmic reticulum ATPase and 45Ca2+ uptake in rats].

OBJECTIVE: To study the effect of acute hypoxia and hypoxic acclimatization on myocardial function of rats. METHOD: Eighteen male Wistar rats were randomly divided into three groups: normoxic control, acute hypoxia and intermittent hypoxic acclimatization group (n=6). After being exposed to hypoxia (8000 m) for 4 h before and after intermittent hypoxic acclimatization (3000 m and 5000 m, 14 d respectively, 4 h/d), the rats were decapitated and then myocardial sarcoplasmic reticulum (SR) were derived from cardiac muscles. Activities of Na+, K(+)-ATPase, Ca2+, Mg2(+)-ATPase in SR, phosphorylation of phospholamban (PLB) and the ability of 45Ca2+ uptake in SR were observed in all these three groups. RESULT: 1) Hypoxia had no effects on the activity of Na+, K(+)-ATPase in rats myocardial SR of rats. 2) Compared with normoxic control rats, the activity of Ca2+, Mg2(+)-ATPase in myocardial SR of rats after acute hypoxia was reduced significantly (P<0.01). After intermittent hypoxic acclimatization, its activity increased significantly as compared with that of acute hypoxic rats (P<0.01). 3) The phosphorylation of PLB in acute hypoxic rats was reduced significantly compared with normoxic control rats. After intermittent hypoxic acclimatization, its phosphorylation was increased significantly compared with that of acute hypoxic rats. It suggests that hypoxic acclimatization could alleviate the inhibition of calcium pump. 4) The ability of 45Ca2+ uptake of SR in acute hypoxic rats was decreased significantly. After hypoxic acclimatization, its ability was strengthened significantly. CONCLUSION: These results suggest that the increased function of myocardial SR calcium pump, the strengthened phosphorylation of PLB to alleviate the inhibition of calcium pump and the increased function of Ca2+ transport in SR are the mechanisms of hypoxic acclimatization protecting cardiac functions from injury induced by severe hypoxia.

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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.

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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.

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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.

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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.

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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.

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PubMed2006

Relationships between leaf conductance to CO2 diffusion and photosynthesis in micropropagated grapevine plants, before and after ex vitro acclimatization.

In vitro-cultured plants typically show a low photosynthetic activity, which is considered detrimental to subsequent ex vitro acclimatization. Studies conducted so far have approached this problem by analysing the biochemical and photochemical aspects of photosynthesis, while very little attention has been paid to the role of leaf conductance to CO(2) diffusion, which often represents an important constraint to CO(2) assimilation in naturally grown plants. Mesophyll conductance, in particular, has never been determined in in vitro plants, and no information exists as to whether it represents a limitation to carbon assimilation during in vitro growth and subsequent ex vitro acclimatization. In this study, by means of simultaneous gas exchange and chlorophyll fluorescence measurements, the stomatal and mesophyll conductance to CO(2) diffusion were assessed in in vitro-cultured plants of the grapevine rootstock '41B' (Vitis vinifera 'Chasselas'xVitis berlandieri), prior to and after ex vitro acclimatization. Their impact on electron transport rate partitioning and on limitation of potential net assimilation rate was analysed. In vitro plants had a high stomatal conductance, 155 versus 50 mmol m(-2) s(-1) in acclimatized plants, which ensured a higher CO(2) concentration in the chloroplasts, and a 7% higher electron flow to the carbon reduction pathway. The high stomatal conductance was counterbalanced by a low mesophyll conductance, 43 versus 285 mmol m(-2) s(-1), which accounted for a 14.5% estimated relative limitation to photosynthesis against 2.1% estimated in acclimatized plants. It was concluded that mesophyll conductance represents an important limitation for in vitro plant photosynthesis, and that in acclimatization studies the correct comparison of photosynthetic activity between in vitro and acclimatized plants must take into account the contribution of both stomatal and mesophyll conductance.

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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.

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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.

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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.

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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.

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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.

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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.

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