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Acclimatization to high altitude in goats with ablated carotid bodies.

In awake goats with ablated carotid bodies, we studied resting pulmonary ventilation, CO2 production, composition of arterial blood and cerebrospinal fluid (CSF), and ventilatory responsiveness to hyperoxic CO2 rebreathing at sea level (SL) and after 3 days at simulated high altitude (HA) (PB 446 +/- 5 Torr, equivalent to 4,300 m). At HA, resting pulmonary ventilation was increased, resulting in marked hypocapnia with appropriate base deficit in blood plasma; CSF became more alkaline; CO2-response curves were shifted to lower PCO2 levels, and their slopes were steeper than at SL. Although these changes in regulation of respiration were not demonstrably different from those seen after normal acclimatization to HA with carotid bodies intact, the mechanisms of their initiation and development are probably different.

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Hypoxic insomnia: effects of carbon monoxide and acclimatization.

Hypoxia causes severe disruption of both rapid-eye-movement (REM) and non-REM (NREM) sleep. Experiments were performed on rats to determine if hypoxic insomnia is mediated by peripheral chemoreceptors and if normal sleep is restored during acclimatization to low O2. Novel methods were devised to measure distribution of amplitudes of cortical slow waves during NREM sleep and to detect REM sleep from the ratio of amplitudes of theta-to delta-frequency bands in the hippocampal electroencephalogram (EEG). Acute exposure of rats to 10.5% O2 (5,030 m altitude equivalent) during daylight hours virtually abolished REM sleep and shifted the distribution of amplitudes of slow-wave sleep EEG toward awake values. Similar disruption of sleep occurred during inhalation of 0.05% CO with steady-state carboxyhemoglobin of approximately 35%. Respiratory rate and alveolar ventilation were greatly increased by 10.5% O2 but were unaffected by CO. Therefore, hypoxic disruption of sleep was not mediated by peripheral chemoreceptors regulating breathing. Partial recovery of sleep occurred after 1-2 wk of hypoxia, but both REM and NREM were still subnormal after 1 mo. Decreased intensity of NREM sleep during hypoxia, measured by amplitude of cortical slow waves, may explain the disparity between subjective complaints of insomnia at altitude and evaluations of sleep by direct observation or by conventional EEG. Loss of appetite, loss of weight, irritability, and other symptoms of altitude sickness may be related to hypoxic insomnia.

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Increased dependence on blood glucose after acclimatization to 4,300 m.

To evaluate the hypothesis that altitude exposure and acclimatization result in increased dependency on blood glucose as a fuel, seven healthy males (23 +/- 2 yr, 72.2 +/- 1.6 kg, mean +/- SE) on a controlled diet were studied in the postabsorptive condition at sea level (SL), on acute altitude exposure to 4,300 m (AA), and after 3 wk of chronic altitude exposure to 4,300 m (CA). Subjects received a primed continuous infusion of [6,6-2D]glucose and rested for a minimum of 90 min, followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the SL maximal O2 consumption (VO2 max; 65 +/- 2% of altitude VO2 max). At SL, resting arterial glucose concentration was 82.4 +/- 3.2 mg/dl and rose significantly to 91.2 +/- 3.2 mg/dl during exercise. Resting glucose appearance rate (Ra) was 1.79 +/- 0.02 mg.kg-1.min-1; this increased significantly during exercise at SL to 3.71 +/- 0.08 mg.kg-1.min-1. On AA, resting arterial glucose concentration (85.8 +/- 4.1 mg/dl) was not different from sea level, but Ra (2.11 +/- 0.14 mg.kg-1.min-1) rose significantly. During exercise on AA, glucose concentration rose to levels seen at SL (91.4 +/- 3.0 mg/dl), but Ra increased more than at SL (to 4.85 +/- 0.15 mg.kg-1.min-1; P less than 0.05). Resting arterial glucose was significantly depressed with CA (70.8 +/- 3.8 mg/dl), but resting Ra increased to 3.59 +/- 0.08 mg.kg-1.min-1, significantly exceeding SL and AA values.(ABSTRACT TRUNCATED AT 250 WORDS)

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Altitude acclimatization and energy metabolic adaptations in skeletal muscle during exercise.

To determine whether the working muscle is able to sustain ATP homeostasis during a hypoxic insult and the mechanisms associated with energy metabolic adaptations during the acclimatization process, seven male subjects [23 +/- 2 (SE) yr, 72.2 +/- 1.6 kg] were given a prolonged exercise challenge (45 min) at sea level (SL), within 4 h after ascent to an altitude of 4,300 m (acute hypoxia, AH), and after 3 wk of sustained residence at 4,300 m (chronic hypoxia, CH). The prolonged cycle test conducted at the same absolute intensity and representing 51 +/- 1% of SL maximal aerobic power (VO2 max) and between 64 +/- 2 (AH) and 66 +/- 1% (CH) at altitude was performed without a reduction in ATP concentration in the working vastus lateralis regardless of condition. Compared with rest, exercise performed during AH resulted in a greater increase (P < 0.05) in muscle lactate concentration (5.11 +/- 0.68 to 22.3 +/- 6.1 mmol/kg dry wt) than exercise performed either at SL (5.88 +/- 0.85 to 11.5 +/- 3.1) or CH (5.99 +/- 0.88 to 12.4 +/- 2.1). These differences in lactate concentration have been shown to reflect differences in arterial lactate concentration and glycolysis (Brooks et al. J. Appl. Physiol. 71: 333-341, 1991). The reduction in glycolysis at least between AH and CH appears to be accompanied by a tighter metabolic control. During CH, free ADP was lower and the ATP-to-free ADP ratio was increased (P < 0.05) compared with AH.(ABSTRACT TRUNCATED AT 250 WORDS)

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Role of vasoconstrictors in the systemic hypertension of rats acclimatized to hypoxia.

Exposure to hypoxia (2-5 wk) results in systemic hypertension in rats and in humans. The possible mechanism(s) was investigated in rats acclimatized for 3 wk to barometric pressure of approximately 370 Torr (A) and in nonacclimatized littermates (NA) by administration of alpha-adrenergic [phentolamine (PHLM)], angiotensin II (ANG II), and arginine vasopressin (AVP V1) receptor antagonists. Both A and NA rats were studied in hypoxia (inspiratory O2 fraction = 0.10). Baseline mean arterial blood pressure (MABP) was higher in A than in NA rats: 126 +/- 4 vs. 101 +/- 2 mmHg (P < 0.05). Neither ANG II nor AVP V1 receptor antagonist influenced baseline MABP; however, both contributed to MABP recovery after PHLM. After simultaneous blockade of ANG II and AVP V1, PHLM lowered MABP by 65 +/- 2 and 45 +/- 3 mmHg in A and NA rats, respectively (P < 0.05). After combined blockade of the three systems, the smooth muscle relaxant sodium nitroprusside did not further modify MABP, which remained higher in A rats. It is concluded that 1) the hypertension in A rats is partly due to a higher alpha-adrenergic tone, 2) neither ANG II nor AVP contributes to the hypertension, but ANG II and AVP participate in MABP control after PHLM, 3) no other vasoconstrictor agents operate in either group, and 4) the higher MABP in A rats after sodium nitroprusside may reflect additional hypertensive mechanisms.

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Pulmonary gas exchange and acid-base state at 5,260 m in high-altitude Bolivians and acclimatized lowlanders.

Pulmonary gas exchange and acid-base state were compared in nine Danish lowlanders (L) acclimatized to 5,260 m for 9 wk and seven native Bolivian residents (N) of La Paz (altitude 3,600-4,100 m) brought acutely to this altitude. We evaluated normalcy of arterial pH and assessed pulmonary gas exchange and acid-base balance at rest and during peak exercise when breathing room air and 55% O2. Despite 9 wk at 5,260 m and considerable renal bicarbonate excretion (arterial plasma HCO3- concentration = 15.1 meq/l), resting arterial pH in L was 7.48 +/- 0.007 (significantly greater than 7.40). On the other hand, arterial pH in N was only 7.43 +/- 0.004 (despite arterial O2 saturation of 77%) after ascent from 3,600-4,100 to 5,260 m in 2 h. Maximal power output was similar in the two groups breathing air, whereas on 55% O2 only L showed a significant increase. During exercise in air, arterial PCO2 was 8 Torr lower in L than in N (P < 0.001), yet PO2 was the same such that, at maximal O2 uptake, alveolar-arterial PO2 difference was lower in N (5.3 +/- 1.3 Torr) than in L (10.5 +/- 0.8 Torr), P = 0.004. Calculated O2 diffusing capacity was 40% higher in N than in L and, if referenced to maximal hyperoxic work, capacity was 73% greater in N. Buffering of lactic acid was greater in N, with 20% less increase in base deficit per millimole per liter rise in lactate. These data show in L persistent alkalosis even after 9 wk at 5,260 m. In N, the data show 1) insignificant reduction in exercise capacity when breathing air at 5,260 m compared with breathing 55% O2; 2) very little ventilatory response to acute hypoxemia (judged by arterial pH and arterial PCO2 responses to hyperoxia); 3) during exercise, greater pulmonary diffusing capacity than in L, allowing maintenance of arterial PO2 despite lower ventilation; and 4) better buffering of lactic acid. These results support and extend similar observations concerning adaptation in lung function in these and other high-altitude native groups previously performed at much lower altitudes.

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Autonomic control of the cardiovascular system during acclimatization to high altitude: effects of sildenafil.

Both acute hypoxia and sildenafil may influence autonomic control through transient cardiovascular effects. In a double-blind study, we investigated whether sildenalfil (Sil) could interfere with cardiovascular effects of hypoxia. Twelve healthy men [placebo (Pla) n = 6; Sil, n = 6] were exposed to an altitude of 4,350 m during 6 days. Treatment was continuously administered from 6 to 8 h after arrival at altitude (3 x 40 mg/day). The autonomic control on the heart was assessed by heart rate variability (HRV) during sleep at sea level (SL) and between day 1-2 and day 5-6 in hypoxia. Arterial pressure (AP) and total peripheral resistances (TPR) were obtained during daytime. There was no statistical difference between groups in HRV, AP, and TPR throughout the study. Hypoxia induced a decrease in R-R interval and an increase in AP in both groups. Low frequency-to-high frequency ratio increased at day 1-2 (Pla, P = 0.04; Sil, P = 0.02) and day 5-6 (Pla and Sil, P = 0.04) vs. SL, whereas normalized high-frequency power decreased only in Pla (P = 0.04, day 1-2 vs. SL). Normalized low-frequency power increased at high altitude (Pla and Sil, P = 0.04, day 5-6 vs. SL). TPR decreased at day 2 in Pla (P = 0.02) and tended to normalize at day 6 (P = 0.07, day 6 vs. day 2). Acute hypoxia induced a decrease in parasympathetic and increase in sympathetic tone, which tended to be reversed with acclimatization. Sil had no deleterious effects on the cardiovascular response to high-altitude exposure and its control by the autonomic nervous system.

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Ventilatory acclimatization in response to very small changes in PO2 in humans.

Ventilatory acclimatization to hypoxia (VAH) consists of a progressive increase in ventilation and decrease in end-tidal Pco(2) (Pet(CO(2))). Underlying VAH, there are also increases in the acute ventilatory sensitivities to hypoxia and hypercapnia. To investigate whether these changes could be induced with very mild alterations in end-tidal Po(2) (Pet(O(2))), two 5-day exposures were compared: 1) mild hypoxia, with Pet(O(2)) held at 10 Torr below the subject's normal value; and 2) mild hyperoxia, with Pet(O(2)) held at 10 Torr above the subject's normal value. During both exposures, Pet(CO(2)) was uncontrolled. For each exposure, the entire protocol required measurements on 13 consecutive mornings: 3 mornings before the hypoxic or hyperoxic exposure, 5 mornings during the exposure, and 5 mornings postexposure. After the subjects breathed room air for at least 30 min, measurements were made of Pet(CO(2)), Pet(O(2)), and the acute ventilatory sensitivities to hypoxia and hypercapnia. Ten subjects completed both protocols. There was a significant increase in the acute ventilatory sensitivity to hypoxia (Gp) after exposure to mild hypoxia, and a significant decrease in Gp after exposure to mild hyperoxia (P < 0.05, repeated-measures ANOVA). No other variables were affected by mild hypoxia or hyperoxia. The results, when combined with those from other studies, suggest that Gp varies linearly with Pet(O(2)), with a sensitivity of 3.5%/Torr (SE 1.0). This sensitivity is sufficient to suggest that Gp is continuously varying in response to normal physiological fluctuations in Pet(O(2)). We conclude that at least some of the mechanisms underlying VAH may have a physiological role at sea level.

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Increased calcium current in carotid body glomus cells following in vivo acclimatization to chronic hypoxia.

1. Rat pups were gestated and born in normoxia (inspired O2 pressure 149 mmHg) or chronic hypoxia (insured O2 pressure 80 mmHg) to test whether chronic hypoxia alters carotid body glomus cell calcium currents. Carotid bodies were removed from 5- to 8-day-old-pups under halothane anesthesia, at which time blood hematocrits averaged 52 +/- 1% (mean +/- SE) in the chronically hypoxic pups and 36 +/- 1% in the normoxic pups (P < 0.05). Glomus cells were then enzymatically isolated from the carotid bodies, and calcium currents were recorded with whole cell patch clamp. 2. Compared with normoxic glomus cells (n = 29), chronically hypoxic glomus cells (n = 32) superfused with 10 mM CaCl2 had larger peak calcium current (146 +/- 16 pA vs. 49 +/- 7 pA, P < 0.05), larger peak calcium current density (12.0 +/- 1.1 pA/pF vs. 7.3 +/- 1.0 pA/pF, P < 0.05), and larger membrane capacitance (12.1 +/- 0.9 pF vs. 7.5 +/- 0.6 pF, P < 0.05). 3. Threshold for calcium current activation was approximately -40 mV. Currents showed little inactivation during 45-ms test pulses and were half-inactivated by a steady holding voltage of -11 +/- 2 mV (n = 15). Currents were reduced 43 +/- 13% by 50 microM nifedipine (n = 6, P < 0.05), and were augmented with barium as the charge carrier. These properties suggest that glomus cell calcium current is carried in part through L-type channels, and that is is relatively resistant to steady-state inactivation. 4. Augmented calcium influx through voltage-gated channels in glomus cells from chronically hypoxic neonatal rats may increase carotid body excitability through increased stimulus-secretion coupling. Overall, acclimatization to chronic hypoxia is known to depress acute hypoxic ventilatory reflex responses in neonates. The observations reported here suggest that inhibition of ventilatory reflexes by chronic hypoxia in neonates occurs centrally rather than peripherally.

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Ventilatory acclimatization to high altitude is prevented by CO2 breathing.

The hypoxia of high altitude stimulates ventilation. If the resultant respiratory alkalosis inhibits the initial increase in ventilation, then with prevention of alkalosis, ventilation should rise immediately to a stable plateau. 4 subjects inspired CO2 (3.77%) from ambient air in a hypobaric chamber (PB = 440-455 Torr) during 100 h at high altitude. Ventilation (for given oxygen uptakes at rest and during exercise) increased promptly and remained stable. 4 control subjects exposed to high altitude without CO2 supplementation showed the expected progressive increases in ventilation with time. The hyperoxic CO2 ventilatory response curve shifted progressively to the left with time in the control subjects, but not in those given supplemental CO2. The latter group also failed to increase the ventilatory response to isocapnic hypoxia. Thus, CO2 supplementation at high altitude prevented the so-called "ventilatory acclimatization' from occurring. Prevention of respiratory alkalosis at high altitude probably permitted maintenance of [H+] at some central nervous system locus, thus allowing an uninhibited hypoxic stimulation of ventilation.

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Acclimatization to 4100 m does not change capillary density or mRNA expression of potential angiogenesis regulatory factors in human skeletal muscle.

Increased skeletal muscle capillary density would be a logical adaptive mechanism to chronic hypoxic exposure. However, animal studies have yielded conflicting results, and human studies are sparse. Neoformation of capillaries is dependent on endothelial growth factors such as vascular endothelial growth factor (VEGF), a known target gene for hypoxia inducible factor 1 (HIF-1). We hypothesised that prolonged exposure to high altitude increases muscle capillary density and that this can be explained by an enhanced HIF-1alpha expression inducing an increase in VEGF expression. We measured mRNA levels and capillary density in muscle biopsies from vastus lateralis obtained in sea level residents (SLR; N=8) before and after 2 and 8 weeks of exposure to 4100 m altitude and in Bolivian Aymara high-altitude natives exposed to approximately 4100 m altitude (HAN; N=7). The expression of HIF-1alpha or VEGF mRNA was not changed with prolonged hypoxic exposure in SLR, and both genes were similarly expressed in SLR and HAN. In SLR, whole body mass, mean muscle fibre area and capillary to muscle fibre ratio remained unchanged during acclimatization. The capillary to fibre ratio was lower in HAN than in SLR (2.4+/-0.1 vs 3.6+/-0.2; P<0.05). In conclusion, human muscle VEGF mRNA expression and capillary density are not significantly increased by 8 weeks of exposure to high altitude and are not increased in Aymara high-altitude natives compared with sea level residents.

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Changes in gut and Malpighian tubule transport during seasonal acclimatization and freezing in the gall fly Eurosta solidaginis.

Since few studies have examined cold tolerance at the organ level in insects, our primary objective was to characterize the functional responses of the gut and Malpighian tubules (MT) to seasonal acclimatization, chilling and freezing in larvae of the goldenrod gall fly Eurosta solidaginis Fitch (Diptera, Tephritidae). From September to December, hemolymph osmolality (455-926 mOsmol kg l(-1)) and freezing tolerance increased markedly in field-collected larvae. Chlorophenol Red was readily transported into the lumen of the foregut, the posterior portion of the midgut, the ureter, the proximal region of the anterior pair of MT, and entire posterior pair of MT. Ouabain and KCN inhibited transport of Chlorophenol Red in the gut and MT. Transport was readily detected at 0 degrees C and the rate of transport was directly related to temperature. The rate of fluid transport by the MT decreased steadily from a monthly high in September (10.7+/-0.8 nl min(-1) for the anterior pair; 12.7+/-1.0 nl min(-1) for the posterior pair) until secretion was no longer detectable in December; this decrease parallels entry into diapause for this species. Even in larvae that died following freezing for 40 days at -20 degrees C, individual organ function was retained to a limited extent. Through the autumn, cholesterol concentrations in the hemolymph increased nearly fourfold. In contrast, the ratio of cholesterol to protein content (nmol mg l(-1)) in the MT membrane remained relatively constant (22 approximately 24 nmol mg l(-1) protein) during this period. Freezing of larvae for 20 days at -20 degrees C caused a significant decrease in cholesterol levels in the hemolymph and the MT membranes compared to unfrozen controls. These results suggest that cholesterol plays a role in seasonal cold hardening and freeze tolerance in insects.

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Ion transport and morphological changes of mitochondria in brown adipocytes of warm- and cold-acclimatized obese Zucker rats.

Brown adipose tissue plays the dominant role in response to cold acclimatization through its capacity to produce heat. To demonstrate the cellular function for thermogenesis induced by cold acclimation in the brown adipose tissue of obese Zucker rats, we examined the changes for the area as well as the Na, K, Cl, and Ca concentrations in the mitochondria of brown adipocytes after the warm (25 degrees C, WG) and the cold acclimations (10 degrees C, CG). Moreover, the respiratory quotients (RQs) of these rats were measured. After the acclimations, the RQ in the CG was decreased and the oxygen consumption increased. A morphometric analysis of electron micrographs of brown adipocytes from the two groups of rats showed a marked increase in the area of the mitochondria in the CG. An electron probe X-ray microanalysis showed an increase in the Ca concentration and decreases in the Na and K concentrations in the matrix of the mitochondria of the cells in the CG. These results suggest that the reduction in the RQ of obese Zucker rats acclimated to cold is the consequence of the metabolism of a large quantity of lipid in the brown adipocytes. Our data also indicate that the observed change in the mitochondrial area and the increase for Ca in the mitochondria were associated with the cold-induced thermogenesis in brown adipocytes of obese Zucker rats.

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Seasonal acclimatization of antioxidants and photosynthesis in Chondrus crispus and Mastocarpus stellatus, two co-occurring red algae with differing stress tolerances.

Mastocarpus stellatus and Chondrus crispus are red macroalgae that co-dominate the lower rocky intertidal zones of the northern Atlantic coast. M. stellatus is more tolerant than C. crispus of environmental stresses, particularly those experienced during winter. This difference in tolerance has been attributed, in part, to greater contents or activities of certain antioxidants in M. stellatus. We compared the photosynthetic capacities and activities of three antioxidant enzymes--superoxide dismutase (SOD), ascorbate peroxidase (APX), and glutathione reductase (GR)--as well as the contents of ascorbate from fronds of M. stellatus and C. crispus collected over a year. Photosynthetic capacity increased in winter, but did not differ between species in any season. The activities of the three antioxidant enzymes and the contents of ascorbate were significantly greater in tissues collected during months with mean air and water temperatures below 7.5 degrees C ("cold" months; December, February, March, April) than in months with mean air temperatures above 11 degrees C ("warm" months; June, July, August, October). Overall, C. crispus had significantly greater SOD and APX activities, while M. stellatus had higher ascorbate contents. Species-specific differences in GR activity depended upon mean monthly temperatures at the time of tissue collection; C. crispus had higher activities during cold months, whereas M. stellatus had higher activities during warm months. Taken together, these data indicate that increased ROS scavenging capacity is a part of winter acclimatization; however, only trends in ascorbate content support the hypothesis that greater levels of antioxidants underlie the relatively greater winter tolerance of M. stellatus in comparison to C. crispus.

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Variations of rat brown adipose tissue composition during cold acclimatization.

The modifications in weight and composition (lipids, proteins, water) of rat interscapular brown adipose tissue (BAT) were studied along the six first weeks of cold exposure and acclimatization. The variations of noreponephrine content was also investigated. During the first day of cold exposure, the major part of tissue lipids was released. During the following two days there was a fall in lipid and norepinehprine contents and uptake of water. Then, until the end of the first week a rapid repletion occurred. At that moment the relative pass of the tissue and the amounts of its principal components reached values which are not changed during the following weeks. We can conclude that the adaptative changes in the levels of BAT essential components are carried out at the end of the first week of cold exposure, long time before the non shivering thermogenesis is entirely effective.

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In situ hybridization of somatolactin transcripts in the pituitary glands from acclimatized carp (Cyprinus carpio).

We isolated and cloned a carp somatolactin SL DNA fragment, of which 78% of the nucleotides were identical to the corresponding salmon SL sequence. The results obtained upon Northern blot hybridization of carp pituitary RNA allowed the identification of two transcripts as described for other fish. When the content of SL transcripts in pituitary sections from summer- and winter-acclimatized carp was quantified by in situ hybridization assays, we found no significant differences between the two seasons. In salmonids, plasma SL reaches higher levels in summer than in winter in synchrony with the water temperature cycle; in the eurythermal carp, however, the complex adaptive responses imposed by seasonal environmental changes do not seem to include the regulation of the somatolactin detected with the probe used at the transcriptional level in pituitary glands.

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[Altitude adaptation. Part III. Altitude acclimatization as a problem of human biology (II. Morphology, physiology, biochemistry)].

The physiological mechanisms of adaptation will be reported. In a primary step of adaptation, the body reacts with immediate response, which already leads to a first classification: whether or not altitude will be tolerated by an individual. More steady biological processes follow with the same intention of balancing oxygen deficiency. They may be successful and acclimatization is possible, or they do not achieve the necessary level, i.e. that consequently developing pathological conditions of different severity lead to a next assortation of individuals with insufficient adaptability. The first state of lability can be compensated, or the intolerance will make a further stay in high altitudes impossible. No parameters exist which could allow a prognosis as to what kind of individuals will tolerate altitude or not. A different pattern of biological reaction is seen in permanent inhabitants of high altitudes who have been residing there for generations and haven't experienced conditions other than those of their special altitude in their individual lives. While ascending to higher altitudes, permanent residents also have to undergo new adaptation, as well as when descending to lower altitudes. Returning to their native environment requires reacclimatization. The mechanisms of adaptation on the organ level will be reviewed, as well as on the fluid and cellular level. All those functional and morphological mechanisms of adaptation to oxygen deficiency in high altitudes tend to maintain optimal equilibrium. Maladaptation may result. Expected genetically determined physiological alterations of adaptational value in permanent residents, which could have manifested themselves by way of "soft" selection and change of gene frequency in those high altitude populations, will be discussed. Genetical determination in such physiological parameters does not seem probable, although some pecularities such as the "blunted response" ventilation, the higher Bohr-Effect in Quenchua etc. might be interpreted in this direction.

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Body temperature and basal metabolic changes during acclimatization to altitude (3,500 m) in man.

Oral temperature (Tor), mean weighted skin temperature (Ts), mean body temperature (Tb) and basal oxygen consumption were studied on twelve young men at sea level. Then they were flown to an altitude of 3,500 m and the readings were continued after 24 hours of their arrival and thereafter at four day intervals for a period of 25 days. Thereafter the subjects were flown back and retested at sea level. Oxygen consumption was recorded at weekly intervals only. The changes in body temperature were compared with those of their basal oxygen consumption. The results indicate that there is a slight rise in the Tor on arrival at altitude and thereafter a gradual fall. A steady and continuous fall was recorded in Ts and Tb throughout the stay at altitude. The basal oxygen consumption showed an initial rise which has come back to normal by the third week of their stay at altitude. On retest, the valves of body temperature and oxygen consumption reached their own initial sea-level pattern. The observation suggests that central mechanisms are involved in bringing about a fall in body temperature during altitude acclimatization.

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