Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACCLIMATIZATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed2005

The maximum expiratory flow-volume loop in natives of Ladakh and acclimatized lowlanders.

Differences in static and dynamic volumes may exist between high altitude residents of Indian Himalayas and their South American counterparts, as well as with acclimatized lowlander sojourners. Maximum expiratory flow-volume loops were recorded in healthy native highlanders of Ladakh (NH, N = 75) and in healthy acclimatized lowlanders (AL, N = 32) at an altitude of 3450 m in the western Indian Himalayas. The forced vital capacity (FVC) and forced expiratory volume in the first second (FEV1), both corrected for a height of 168 cm, were significantly higher in NH [FVC: 5.02 (0.51) vs. 3.89 (0.45) L, p < 0.0001; FEV1: 4.27 (0.47) vs. 3.44 (0.37) L, p < 0.0001]. The flow rates at larger lung volumes (PEFR, FEF25, and FEF50) were similar in the two groups. The NH showed significantly higher flow rates at low lung volumes, that is, FEF75 and FEF75-85% [FEF75: 2.03 (0.69) vs. 1.70 (0.52) L/s, p = 0.0092; FEF75-85%: 1.42 (0.54) vs. 1.06 (0.35) L/s, p = 0.0001]. The exact mechanisms allowing the higher flow rates at low lung volumes remain to be elucidated, but it is possible that these findings may indicate an inherited adaptive response in the Ladakhi highlander.

Acclimatization↗
PubMed2006

The role of dehydroepiandrosterone levels on physiologic acclimatization to chronic mountaineering activity.

Previous studies have reported that glucose tolerance can be improved by short-term altitude living and activity. However, not all literature agrees that insulin sensitivity is increased at altitude. The present study investigated the effect of a 25-day mountaineering activity on glucose tolerance and its relation to serum levels of dehydroepiandrosterone-sulfate (DHEA-S) and tumor necrosis factor-alpha (TNF-alpha) in 12 male subjects. On day 3 at altitude, we found that serum DHEAS was reduced in the subjects with initially greater DHEA-S value, whereas the subjects with initially lower DHEA-S remained unchanged. To further elucidate the role of DHEA-S in acclimatization to mountaineering activity, all subjects were then divided into lower and upper halves according to their sea-level DHEA-S concentrations: low DHEA-S (n = 6) and high DHEA-S groups (n = 6). Glucose tolerance, insulin level, and the normal physiologic responses to altitude exposure, including hematocrit, hemoglobin, erythropoietin (EPO), and cortisol were measured. We found that glucose and insulin concentrations on an oral glucose tolerance test were significantly lowered by the mountaineering activity only in the high DHEA-S group. Similarly, hematocrit and hemoglobin concentration in altitude were increased only in the high DHEA-S group. In contrast, the low DHEA-S subjects exhibited an EPO value at sea level and altitude greater than the high DHEA-S group, suggesting an EPO resistance. The findings of the study imply that DHEA-S is essential for physiologic acclimatization to mountaineering challenge.

Acclimatization↗
PubMed2006

Establishing an appropriate period of acclimatization following transportation of laboratory animals.

Stress associated with transportation has widespread effects on physiological systems in laboratory animals, including changes in the cardiovascular, endocrine, immune, central nervous, and reproductive systems. Although short-lived, these changes can confound research if animals are utilized before homeostasis is restored and physiological measures return to normal. Therefore, some period of acclimatization following transportation is generally suggested to restore homeostasis. The following two questions should be considered to establish an adequate period for acclimatization: (1) Will anticipated physiological changes confound the research to be conducted? (2) What is the length of time necessary for confounding physiological changes to normalize? Finding answers to those questions in the literature can be a challenge. Most literature on the physiological impact of transportation involves agricultural animals, although the limited literature in common laboratory animal species generally parallels changes documented in agricultural animals. The literature documents elevated heart rate and weight loss, as well as elevated concentrations of adrenaline, noradrenaline, glucose, cortisol, free fatty acids, and beta-hydroxybutyrate. Carbohydrate, protein, and lipid metabolism (both lipolysis and lipogenesis) are altered, and plasma osmolality, albumen, protein, and pack-cell volume increase. Neutrophilia and lymphopenia are also evident. These measures generally return to baseline within 1 to 7 days of transportation, although animals that are young, severely stressed, and have stress-sensitive genotypes may show altered physiological measures for several weeks. Other measures such as circadian rhythm and reproductive performance may take several weeks to months to normalize.

Acclimatization↗
PubMed2002

Unchanged cerebral blood flow and oxidative metabolism after acclimatization to high altitude.

The authors investigated the effect of acclimatization to high altitude on cerebral blood flow and oxidative metabolism at rest and during exercise. Nine healthy, native sea-level residents were studied 3 weeks after arrival at Chacaltaya, Bolivia (5,260 m) and after reacclimatization to sea level. Global cerebral blood flow at rest and during exercise on a bicycle ergometer was measured by the Kety-Schmidt technique. Cerebral metabolic rates of oxygen, glucose, and lactate were calculated by the Fick principle. Cerebral function was assessed by a computer-based measurement of reaction time. At high altitude at rest, arterial carbon dioxide tension, oxygen saturation, and oxygen tension were significantly reduced, and arterial oxygen content was increased because of an increase in hemoglobin concentration. Global cerebral blood flow was similar in the four conditions. Cerebral oxygen delivery and cerebral metabolic rates of oxygen and glucose also remained unchanged, whereas cerebral metabolic rates of lactate increased slightly but nonsignificantly at high altitude during exercise compared with high altitude at rest. Reaction time was unchanged. The data indicate that cerebral blood flow and oxidative metabolism are unaltered after high-altitude acclimatization from sea level, despite marked changes in breathing and other organ functions.

Acclimatization↗
PubMed1995

Cardiovascular response to exercise in humans following acclimatization to extreme altitude.

The purpose of this study was to assess the effects of acclimatization to extreme altitude on the cardiovascular system, using vagal and adrenergic blockade and acute restoration of normoxia during exercise to maximum with one and two legs. Fourteen climbers on an expedition to the Himalayas were studied at a lower base camp (5250 m) following 56-81 days at altitudes between 5250 and 8700 m. After acclimatization, peak heart rate (HRpeak), oxygen uptake (VO2peak) and noradrenaline (NA) were similar during maximal one- and two-legged cycling, whereas peak plasma lactate was higher during the one-legged protocol. HRpeak (range 113-168 beats min-1) was lowest when subjects returned from the higher camps. The degree of partial restoration of HRpeak to more normal values within seconds of 60% O2 inhalation (range 5-35 beats min-1 HRpeak increase) was greatest in subjects with low HRpeak. HR responses to beta-1 blockade increased as a function of HRpeak and the HR responses to atropine were the least in subjects with high HRpeak. These findings suggest that (a) the reduction in HRpeak is linked to the duration and severity of the hypoxaemia, (b) the degree of restoration of HRpeak with acute normoxia is dependent on the level of attenuation or down-regulation of cardiac sympathetic activation (SNA), (c) cardiac vagal drive is masked to a lesser extent in chronic hypoxia because of attenuated SNA and lower HRpeak values, and (d) the lower blood lactate levels at altitude is a function of muscle mass involvement rather than adrenergic activation, as normal peak values were reached during exercise with a small muscle mass.

Acclimatization↗
PubMed1972

Habituation and acclimatization of sheep to cold following exposures of varying length and severity.

1. Male and female Scottish Blackface sheep were shorn and exposed for 2 weeks either to a thermoneutral temperature (+30 degrees C), to chronic cold (+8 degrees C) or to +30 degrees C interrupted by daily short cold shocks (-10 degrees C). During and at the end of these conditioning treatments, the sheep also received two acute cold exposures (-20 degrees C, 4 m.p.h. wind for 2-8 hr) 1 week apart. Some of these sheep and a fourth (control) group, were subsequently re-shorn and slowly cooled to +8 degrees C.2. Resting metabolism and the metabolic response to cooling (both inferred from heart rates) were increased by previous chronic cold treatment. Resistance to body cooling (measured during acute cold exposure) was generally increased by both chronic and acute cold, and non-shivering thermogenesis was probably induced in the female sheep. These effects were defined as acclimatization.3. In contrast, cold shocks reduced the subsequent metabolic response to cold and encouraged facultative body cooling. This pattern of response (defined as habituation) therefore caused greater thermolability.4. Habituation and acclimatization were antagonistic. Habituation was removed by acute cold exposure and, conversely, acclimatization was inhibited by short cold shocks.5. There were sex differences in response but these were confounded by probable differences in insulation and in body condition (males thinner).6. It was concluded that the induction of different forms of adaptation depended on the length, severity and frequency of cold exposures. Habituation to whole body cold exposure apparently involved central nervous system centres normally receiving peripheral cold stimuli.

Acclimatization↗
PubMed1973

Thermoregulatory changes induced during heat acclimatization by controlled hypothermia in man.

1. Heat acclimatization has been carried out by a controlled hyperthermia procedure, and induced thermoregulatory changes have been investigated for nine fit young men.2. During the experiments two types of thermal responses became apparent. The subjects tolerating the rise in the central temperature during hyperthermia displayed a marked improvement of their sweating capacity and their sweating performances, and a parallel shift towards lower body temperatures of the curves relating sweat rate to tympanic, rectal and mean skin temperatures.3. This shift occurred without any change in the slope, that is without any change in the gain of the central control system. It was accompanied by a concomitant shift of the threshold of sweating onset, so that for a given central temperature there was a higher sweat rate following treatment.4. The sweat decline appeared late in tolerant subjects. This decline was early in the intolerant subjects and appeared as early as the first day of heat treatment. Moreover, these subjects displayed no increase of sweat output with repeated sessions of heat treatment.5. The core-periphery temperature gradient measured during the cooling stage did not change in the tolerant subjects when acclimatization had developed. This gradient increased in the intolerant subjects because deep temperature decreased slowly whilst skin temperature decreased rapidly. The core of intolerant subjects retained the stored heat and dissipated it slowly. The tolerant subjects seemed on the contrary to display in the same conditions increased tissue conductance enabling rapid dissipation of the stored heat.

Acclimatization↗
PubMed2002

Effect of fourteen days of acclimatization on athletic performance in tropical climate.

In order to study the acclimatization process over 14 days of exposure to tropical climate, 9 triathletes performed 4 outdoor indirect continuous multistage tests in both thermoneutral and tropical conditions. The thermoneutral test (TN, 14 degree C, 45% rh) was performed before traveling to the tropical area (Martinique, FWI). The tropical tests were performed 2, 8, and 14 days after arrival (32.9 degree C, 78% rh). During each trial, we measured tympanic temperature, sweat rate, body mass loss, heart rate (HR), and performance. The results showed that 1). the mean tympanic temperature was greater in T2 (P <.001), T8 (P <.01) and T14 (P <.01) than in TN and significantly lower in T14 than in T2 (P <.05); 2). the mean sweat rate was significantly greater (P <.001) in T2, T8 and T14 than in TN and significantly greater (P <.05) in T8 and T14 than in T2; 3). the body mass loss after trials was significantly greater (P <.001) in T2, T8 and T14 than in TN and significantly greater (P <.05) in T8 and T14 than in T2; 4). the mean HR and HR at rest were significantly higher (P <.005) in T2 than in TN, T8, T14 and the mean HR was significantly lower (P <.05) in T14 than in the other trials; and 5). the performance time was significantly lower in T2 (P < 0.02), T8 (P < 0.03) and T14 (P < 0.05) than in TN. We concluded that 14 days of exposure to tropical climate led to changes in physiological parameters but were still insufficient to ensure complete acclimatization in well-trained athletes. The hot/wet climate induced impairment of physiological responses and performance that were still evident on the 14th day.

Acclimatization↗
PubMed2002

Similar carbohydrate but enhanced lactate utilization during exercise after 9 wk of acclimatization to 5,620 m.

We hypothesized that reliance on lactate as a means of energy distribution is higher after a prolonged period of acclimatization (9 wk) than it is at sea level due to a higher lactate Ra and disposal from active skeletal muscle. To evaluate this hypothesis, six Danish lowlanders (25 +/- 2 yr) were studied at rest and during 20 min of bicycle exercise at 146 W at sea level (SL) and after 9 wk of acclimatization to 5,260 m (Alt). Whole body glucose Ra was similar at SL and Alt at rest and during exercise. Lactate Ra was also similar for the two conditions at rest; however, during exercise, lactate Ra was substantially lower at SL (65 micro mol. min(-1). kg body wt(-1)) than it was at Alt (150 micro mol. min(-1). kg body wt(-1)) at the same exercise intensity. During exercise, net lactate release was approximately 6-fold at Alt compared with SL, and related to this, tracer-calculated leg lactate uptake and release were both 3- or 4-fold higher at Alt compared with SL. The contribution of the two legs to glucose disposal was similar at SL and Alt; however, the contribution of the two legs to lactate Ra was significantly lower at rest and during exercise at SL (27 and 81%) than it was at Alt (45 and 123%). In conclusion, at rest and during exercise at the same absolute workload, CHO and blood glucose utilization were similar at SL and at Alt. Leg net lactate release was severalfold higher, and the contribution of leg lactate release to whole body lactate Ra was higher at Alt compared with SL. During exercise, the relative contribution of lactate oxidation to whole body CHO oxidation was substantially higher at Alt compared with SL as a result of increased uptake and subsequent oxidation of lactate by the active skeletal muscles.

Acclimatization↗
PubMed2001

Women at altitude: forearm hemodynamics during acclimatization to 4,300 m with alpha(1)-adrenergic blockade.

We hypothesized that blockade of alpha(1)-adrenergic receptors would prevent the rise in peripheral vascular resistance that normally occurs during acclimatization. Sixteen eumenorrheic women were studied at sea level (SL) and at 4,300 m (days 3 and 10). Volunteers were randomly assigned to take the selective alpha(1)-blocker prazosin or placebo. Venous compliance, forearm vascular resistance, and blood flow were measured using plethysmography. Venous compliance fell by day 3 in all subjects (1.39 +/- 0.30 vs. 1.62 +/- 0.43 ml. Delta 30 mmHg(-1) x 100 ml tissue(-1) x min(-1) at SL, means +/- SD). Altitude interacted with prazosin treatment (P < 0.0001) such that compliance returned to SL values by day 10 in the prazosin-treated group (1.68 +/- 0.19) but not in the placebo-treated group (1.20 +/- 0.10, P < 0.05). By day 3 at 4,300 m, all women had significant falls in resistance (35.2 +/- 13.2 vs. 54.5 +/- 16.1 mmHg x ml(-1) x min(-1) at SL) and rises in blood flow (2.5 +/- 1.0 vs. 1.6 +/- 0.5 ml. 100 ml tissue(-1) x min(-1) at SL). By day 10, resistance and flow returned toward SL, but this return was less in the prazosin-treated group (resistance: 39.8 +/- 4.6 mmHg x ml(-1) x min(-1) with prazosin vs. 58.5 +/- 9.8 mmHg x ml(-1) x min(-1) with placebo; flow: 1.9 +/- 0.7 ml. 100 ml tissue(-1) x min(-1) with prazosin vs. 2.3 +/- 0.3 ml x 100 ml tissue(-1) x min(-1) with placebo, P < 0.05). Lower resistance related to higher circulating epinephrine in both groups (r = -0.50, P < 0.0001). Higher circulating norepinephrine related to lower venous compliance in the placebo-treated group (r = -0.42, P < 0.05). We conclude that alpha(1)-adrenergic stimulation modulates peripheral vascular changes during acclimatization.

Acclimatization↗
PubMed2002

Why is VO2 max after altitude acclimatization still reduced despite normalization of arterial O2 content?

Acute hypoxia (AH) reduces maximal O2 consumption (VO2 max), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O2 saturation that can normalize arterial O2 concentration ([O2]), VO2 max remains low. To determine why, seven lowlanders were studied at VO2 max (cycle ergometry) at sea level (SL), after 9-10 wk at 5,260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (FiO2 = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of O2 transport were measured in each condition. Both cardiac output and leg blood flow were reduced by approximately 15% in both AH and CH (P < 0.05). At maximal exercise, arterial [O2] in AH was 31% lower than at SL (P < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O2 extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76% of the cardiac output perfused the legs, in CH the legs received only 67%. Pulmonary VO2 max (4.1 +/- 0.3 l/min at SL) fell to 2.2 +/- 0.1 l/min in AH (P < 0.05) and was only 2.4 +/- 0.2 l/min in CH (P < 0.05). These data suggest that the failure to recover VO2 max after acclimatization despite normalization of arterial [O2] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH.

Acclimatization↗
PubMed1982

Substrate metabolism in seasonally acclimatized American goldfinches.

Concentration of ([Glc]) and turnover (Ro) of plasma glucose, concentration of free fatty acids in plasma ([FFA]), and concentration of glycogen in muscle and liver were measured in freshly captured summer- and winter-acclimatized American goldfinches (Carduelis tristis). These birds were acutely exposed to one of three thermal regimes: 1) "thermoneutral," 30 degrees C in air, 2) "cold," -15 degrees C in air, and 3) "severe cold," 0 degrees C in 79% He and 21% O2. Additionally, the activities of citrate synthase (CS), phosphofructokinase (PFK), and beta-hydroxyacyl-CoA dehydrogenase (HOAD) were measured in pectoralis and leg muscles of winter and summer birds. Ro for goldfinches at 30 degrees C is unchanged between winter and summer, whereas it is 25% lower at -15 degrees C in winter than in summer birds, even though rates of heat production are similar. Additionally, winter animals depleted muscle glycogen at slower rates than summer individuals when exposed to "cold" or "severe cold." [Glc] and [FFA] for each test regime did not vary between seasons. The activity of the beta-oxidative enzyme HOAD is the pectoralis muscle (the main thermogenic tissue) increases by 50% from summer to winter, but the activities of PFK and CS remain essentially constant. We conclude that the ability to restrict carbohydrate use under cold stress is a component of the winter acclimatization process in the American goldfinch. One mechanism which might foster this ability in the increase in beta-oxidative capacity of the flight muscles, permitting a greater reliance on fatty acids by winter animals during cold-induced thermogenesis.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1976

Effect of ascorbic acid on rate of heat acclimatization.

There is some indication in the literature that ascorbic acid (vitamin C) may reduce the physiological responses to heat stress. Consequently, the effect of ascorbic acid ingestion on heat-strain indicators has been studied on a group of 60 mining recruits undergoing climatic room acclimatization. Of the 60 men, 19 received a daily dose of 250 mg ascorbic acid; 21 a daily dose of 500 mg ascorbic acid; and 20 received a placebo daily. Measurements of rectal temperature, heart rate, and hourly sweat rate were made on all subjects during the 4 h of heat exposure per day for 10 days. The wet bulb temperature was 32.2 degrees C, the dry bulb 33.9 degrees C, the air movement 0.4 m/s, and the work rate 35 W. The results indicate that the rate and degree of acclimatization, as assessed by 4th-h rectal temperature, is enhanced by ascorbic acid supplementation and that no differences in response could be shown between daily dosages of 250 and 500 mg of vitamin C.

Acclimatization↗
PubMed1981

Effect of acclimatization to heat on the regulation of sweating during moderate and severe exercise.

Sweat regulation in two male subjects, one an athlete in training, was examined over a range of exercise intensities and environmental temperatures. The results after artificial heat acclimatization in the nonathlete showed that sweating rate over 1 h of maximal exercise increased to the same level as the athlete, but his evaporative sweat loss remained significantly (15%) lower. Rectal temperature (Tre) was reduced for a given oxygen intake (VO2) and relative work load (%VO2 max), but the difference in Tre/%VO2 max between the subjects was not significant. At different mean skin temperatures (Tsk), relative sweat rate (%msw, max), for a given Tre was unaffected and the relationship of %mSW, max with Tre was the same in both subjects. Lowering the relative work load (and thus Tre) displaced the Tre/%msw, max relationship to the right, and regression lines for different %VO2 max were parallel. The multiple regression equation %msw, max = -1,531 +/- 36.67 Tre (degrees C) + 6.08 Tsk (degrees C) (r = +0.92), related the parameters and was independent of the subject's fitness and state of acclimatization providing %msw, max was expressed in terms of the appropriate msw, max at the time of measurement.

Acclimatization↗
PubMed1986

Ventilatory acclimatization to hypoxia is not dependent on cerebral hypocapnic alkalosis.

We previously demonstrated that, in awake goats, 6 h of hypoxic carotid body perfusion during systemic normoxia produced time-dependent hyperventilation that is typical of ventilatory acclimatization to hypoxia (VAH). The hypocapnic alkalosis that occurred could have produced VAH by inducing cerebral vasoconstriction and brain lactic acidosis even though systemic arterial normoxia was maintained. In the present study we tested the hypothesis that hypocapnic alkalosis is a necessary component of VAH. Goats were prepared so that one carotid body could be perfused, from an extracorporeal circuit, with blood in which gas tensions could be controlled independently from the blood perfusing the systemic arterial system, including the brain. Using this preparation we carried out 4 h of hypoxic carotid body perfusion while maintaining systemic arterial (and brain) normoxia in awake goats. Expired minute ventilation (VE) was measured while CO2 was added to inspired air to maintain normocapnia. Carotid body PCO2 and PO2 were maintained near 40 Torr during the 4-h carotid body perfusion. Control mean VE was 8.65 +/- 0.48 l/min (mean +/- SE). With acute carotid body hypoxia (30 min) VE increased to 21.73 +/- 2.02 l/min (P less than 0.05); over the ensuing 3.5 h of carotid body hypoxia, VE progressively increased to 39.14 +/- 4.14 l/min (P less than 0.05). These data indicate that neither cerebral hypoxia nor hypocapnic alkalosis are required to produce VAH. After termination of the 4-h carotid body stimulation, hyperventilation was not maintained in these studies, i.e., there was no deacclimatization. This suggests that acclimatization and deacclimatization are produced by different mechanisms.

Acclimatization↗
PubMed1989

Increased exercise SaO2 independent of ventilatory acclimatization at 4,300 m.

Arterial O2 saturation (Sao2) decreases in hypoxia in the transition from rest to moderate exercise, but it is unknown whether other several weeks at high altitude SaO2 in submaximal exercise follows the same time course and pattern as that of ventilatory acclimatization in resting subjects. Ventilatory acclimatization is essentially complete after approximately 1 wk at 4,300 m, such that improvement in submaximal exercise SaO2 would then require other mechanisms. On days 2, 8, and 22 on Pikes Peak (4,300 m), 6 male subjects performed prolonged steady-state cycle exercise at 79% maximal O2 uptake (VO2 max). Resting SaO2 rose from day 1 (78.4 +/- 1.6%) to day 8 (87.5 +/- 1.4%) and then did not increase further by day 20 (86.4 +/- 0.6%). During exercise, SaO2 values (mean of 5-, 15-, and 30-min measurements) were 72.7% (day 2), 78.6% (day 8), and 82.3% (day 22), meaning that all of the increase in resting SaO2 occurred from day 1 to day 8, but exercise SaO2 increased from day 2 to day 8 (5.9%) and then increased further from day 8 to day 22 (3.7%). On day 22, the exercise SaO2 was higher than on day 8 despite an unchanged ventilation and O2 consumption. The increased exercise SaO2 was accompanied by decreased CO2 production. The mechanisms responsible for the increased exercise SaO2 require further investigation.

Acclimatization↗
PubMed1993

Effects of altitude acclimatization on fluid regulatory hormone response to submaximal exercise.

To determine the effect of altitude acclimatization on plasma levels of atrial natriuretic peptide (ANP) during submaximal exercise and its relationship with renin and aldosterone, seven male volunteers aged 17-23 yr exercised to exhaustion on a cycle ergometer at 80-85% of their maximum O2 uptake at sea level (SL; 50 m), during 1 h in a hypobaric chamber [acute altitude (AA); 4,300 m], and after 14 or 16 days of residence on the summit of Pikes Peak, CO [chronic altitude (CA); 4,300 m]. Plasma samples taken before exercise, 10 min after the start of exercise, and 5 min postexercise were analyzed for ANP, plasma renin activity (PRA), and aldosterone (ALDO). ANP showed a progressive increase from rest to postexercise [7.49 +/- 1.63 to 11.32 +/- 1.80 (SE) pmol/ml and 6.05 +/- 2.55 to 10.38 +/- 7.20 pmol/ml; P = 0.049, exercise] at SL and AA, respectively, but not at CA (P = 0.039, altitude). Similarly, PRA and ALDO rose from rest to postexercise (P < 0.001, exercise), but the rise in ALDO with exercise was less during AA than during SL and CA (P = 0.002, phase). The decreased ANP levels during exercise after altitude acclimatization, with no change in PRA and ALDO, suggest that ANP has little effect on PRA and ALDO under these conditions.

Acclimatization↗
PubMed1997

"Living high-training low": effect of moderate-altitude acclimatization with low-altitude training on performance.

The principal objective of this study was to test the hypothesis that acclimatization to moderate altitude (2,500 m) plus training at low altitude (1,250 m), "living high-training low," improves sea-level performance in well-trained runners more than an equivalent sea-level or altitude control. Thirty-nine competitive runners (27 men, 12 women) completed 1) a 2-wk lead-in phase, followed by 2) 4 wk of supervised training at sea level; and 3) 4 wk of field training camp randomized to three groups: "high-low" (n = 13), living at moderate altitude (2,500 m) and training at low altitude (1,250 m); "high-high" (n = 13), living and training at moderate altitude (2,500 m); or "low-low" (n = 13), living and training in a mountain environment at sea level (150 m). A 5,000-m time trial was the primary measure of performance; laboratory outcomes included maximal O2 uptake (VO2 max), anaerobic capacity (accumulated O2 deficit), maximal steady state (MSS; ventilatory threshold), running economy, velocity at VO2 max, and blood compartment volumes. Both altitude groups significantly increased VO2 max (5%) in direct proportion to an increase in red cell mass volume (9%; r = 0.37, P < 0.05), neither of which changed in the control. Five-kilometer time was improved by the field training camp only in the high-low group (13.4 +/- 10 s), in direct proportion to the increase in VO2 max (r = 0.65, P < 0.01). Velocity at VO2 max and MSS also improved only in the high-low group. Four weeks of living high-training low improves sea-level running performance in trained runners due to altitude acclimatization (increase in red cell mass volume and VO2 max) and maintenance of sea-level training velocities, most likely accounting for the increase in velocity at VO2 max and MSS.

Acclimatization↗