Decreased reliance on lactate during exercise after acclimatization to 4,300 m

1991 ◽  
Vol 71 (1) ◽  
pp. 333-341 ◽  
Author(s):  
G. A. Brooks ◽  
G. E. Butterfield ◽  
R. R. Wolfe ◽  
B. M. Groves ◽  
R. S. Mazzeo ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Blood Lactate ◽  
Lactate Concentration ◽  
Acute Exposure ◽  
O2 Consumption ◽  
Arterial Lactate ◽  
Healthy Men ◽  
Subsequent Decrease ◽  
Appearance Rate

We hypothesized that the increased exercise arterial lactate concentration on arrival at high altitude and the subsequent decrease with acclimatization were caused by changes in blood lactate flux. Seven healthy men [age 23 +/- 2 (SE) yr, wt 72.2 +/- 1.6 kg] on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6–2D]glucose (Brooks et al. J. Appl. Physiol. 70:919–927, 1991) and [3–13C]lactate 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 sea level peak O2 consumption (VO2peak; 65 +/- 2% of both acute altitude and acclimatization). During rest at sea level, lactate appearance rate (Ra) was 0.52 +/- 0.03 mg.kg-1.min-1; this increased sixfold during exercise to 3.24 +/- 0.19 mg.kg-1.min-1. On acute exposure, resting lactate Ra rose from sea level values to 2.2 +/- 0.2 mg.kg-1.min-1. During exercise on acute exposure, lactate Ra rose to 18.6 +/- 2.9 mg.kg-1.min-1. Resting lactate Ra after acclimatization (1.77 +/- 0.25 mg.kg-1.min-1) was intermediate between sea level and acute exposure values. During exercise after acclimatization, lactate Ra (9.2 +/- 0.7 mg.kg-1.min-1) rose from resting values but was intermediate between sea level and acute exposure values. The increased exercise arterial lactate concentration response on arrival at high altitude and subsequent decrease with acclimatization are due to changes in blood lactate appearance.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscle accounts for glucose disposal but not blood lactate appearance during exercise after acclimatization to 4,300 m

1992 ◽  
Vol 72 (6) ◽  
pp. 2435-2445 ◽  
Author(s):  
G. A. Brooks ◽  
E. E. Wolfel ◽  
B. M. Groves ◽  
P. R. Bender ◽  
G. E. Butterfield ◽  
...  
Keyword(s):  
Blood Glucose ◽  
High Altitude ◽  
Sea Level ◽  
Blood Lactate ◽  
Lactate Concentration ◽  
Acute Exposure ◽  
Glucose Disposal ◽  
O2 Uptake ◽  
Arterial Lactate ◽  
Subsequent Decrease

We hypothesized that the increased blood glucose disappearance (Rd) observed during exercise and after acclimatization to high altitude (4,300 m) could be attributed to net glucose uptake (G) by the legs and that the increased arterial lactate concentration and rate of appearance (Ra) on arrival at altitude and subsequent decrease with acclimatization were caused by changes in net muscle lactate release (L). To evaluate these hypotheses, seven healthy males [23 +/- 2 (SE) yr, 72.2 +/- 1.6 kg], on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6–D2]glucose (Brooks et al., J. Appl. Physiol. 70: 919–927, 1991) and [3–13C]lactate (Brooks et al., J. Appl. Physiol. 71:333–341, 1991) 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 sea level peak O2 uptake (65 +/- 2% of both acute altitude and acclimatization peak O2 uptake). Glucose and lactate arteriovenous differences across the legs and arms and leg blood flow were measured. Leg G increased during exercise compared with rest, at altitude compared with sea level, and after acclimatization. Leg G accounted for 27–36% of Rd at rest and essentially all glucose Rd during exercise. A shunting of the blood glucose flux to active muscle during exercise at altitude is indicated. With acute altitude exposure, at 5 min of exercise L was elevated compared with sea level or after acclimatization, but from 15 to 45 min of exercise the pattern and magnitude of L from the legs varied and followed neither the pattern nor the magnitude of responses in arterial lactate concentration or Ra. Leg L accounted for 6–65% of lactate Ra at rest and 17–63% during exercise, but the percent Ra from L was not affected by altitude. Tracer-measured lactate extraction by legs accounted for 10–25% of lactate Rd at rest and 31–83% during exercise. Arms released lactate under all conditions except during exercise with acute exposure to high altitude, when the arms consumed lactate. Both active and inactive muscle beds demonstrated simultaneous lactate extraction and release. We conclude that active skeletal muscle is the predominant site of glucose disposal during exercise and at high altitude but not the sole source of blood lactate during exercise at sea level or high altitude.

Beta-adrenergic blockade does not prevent the lactate response to exercise after acclimatization to high altitude

1994 ◽  
Vol 76 (2) ◽  
pp. 610-615 ◽  
Author(s):  
R. S. Mazzeo ◽  
G. A. Brooks ◽  
G. E. Butterfield ◽  
A. Cymerman ◽  
A. C. Roberts ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Blood Lactate ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Arterial O2 Saturation ◽  
Response To Exercise ◽  
Peak Blood

We examined the extent to which epinephrine influences blood lactate adjustments to exercise during both acute (AC) and chronic (CH) high-altitude exposure. Eleven male sea level residents were divided into a control group (n = 5) receiving a placebo or a drug group (n = 6) receiving 240 mg/day of propranolol. All subjects were studied at rest and during 45 min of submaximal exercise (approximately 50% of sea level maximal O2 uptake) at sea level (SL) and within 4 h of exposure to and after 3 wk residence at 4,300 m (summit of Pikes Peak). Blood samples were collected from the femoral artery for epinephrine and lactate concentration. Exercising blood lactate concentration was significantly different across all altitude conditions such that AC > CH > SL (P < 0.05). For a given arterial O2 saturation, mean exercising blood lactates were lower for the beta-blocked group compared with controls; however, both groups demonstrated similar patterns across all conditions. Epinephrine levels during exercise followed a similar pattern to that of lactate, averaging 0.67, 0.43, and 0.29 ng/ml for AC, CH, and SL, respectively. The correlation between lactate and epinephrine was 0.93 and 0.84 for control and beta-blocked subjects, respectively. Whereas during exercise epinephrine was consistently higher for the beta-blocked group than controls, this difference was only significant during CH exposure. The epinephrine response was related to the extent of hypoxia in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased exercise muscle lactate release after high altitude acclimatization

1989 ◽  
Vol 67 (4) ◽  
pp. 1456-1462 ◽  
Author(s):  
P. R. Bender ◽  
B. M. Groves ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
L. Trad ◽  
...  
Keyword(s):  
High Altitude ◽  
Lactate Concentration ◽  
Ambient Air ◽  
Venous Blood Flow ◽  
O2 Consumption ◽  
Arterial Lactate ◽  
Lactate Release ◽  
Altitude Acclimatization ◽  
Arterial Blood ◽  
Arterial Concentration

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.

A STUDY OF VARIOUS INDICES OF ADRENOCORTICAL ACTIVITY DURING 23 DAYS AT HIGH ALTITUDE

1963 ◽  
Vol 26 (4) ◽  
pp. 555-566 ◽  
Author(s):  
P. C. B. MACKINNON ◽  
M. E. MONK-JONES ◽  
K. FOTHERBY
Keyword(s):  
Length Of Stay ◽  
High Altitude ◽  
Sea Level ◽  
Acute Exposure ◽  
Adrenocorticotrophic Hormone ◽  
Adrenocortical Activity

SUMMARY 1. Four men and three women ascended by télépherique and helicopter from 1000 to 4333 m. where they remained for 23 days. 2. Measurements of urinary 17-hydroxycorticosteroids, 17-oxosteroids, pregnanediol and pregnanetriol and circulating eosinophils were made at sea level and at high altitude. 3. An attempt was also made to measure changes in emotional activity by means of the palmar sweat index (PSI). This index was assessed at intervals throughout the day at sea level and at high altitude, and in response to adrenocorticotrophic hormone (ACTH) and a self-imposed stress. 4. Within 24 hr. of acute exposure to high altitude urinary 17-hydroxycorticosteroids increased whilst circulating eosinophils decreased; by the 5th day both were returning to sea-level values. The output of 17-oxosteroids was lower by the 5th day at high altitude and subsequently increased; pregnanediol and pregnanetriol levels remained unchanged. 5. PSIs throughout the day become progressively lower as the length of stay at altitude increased. The response to ACTH at sea level and high altitude appeared to be similar but the response to a self-imposed stress was longer in duration at high altitude than at sea level.

Disposal of blood [1-13C]lactate in humans during rest and exercise

1986 ◽  
Vol 60 (1) ◽  
pp. 232-241 ◽  
Author(s):  
R. S. Mazzeo ◽  
G. A. Brooks ◽  
D. A. Schoeller ◽  
T. F. Budinger
Keyword(s):  
Blood Lactate ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Curvilinear Relationship ◽  
O2 Consumption ◽  
Lactate Oxidation ◽  
Respiratory Parameters ◽  
Steady Rate ◽  
Lactate Levels

Lactate irreversible disposal (RiLa) and oxidation (RoxLa) rates were studied in six male subjects during rest (Re), easy exercise [EE, 140 min of cycling at 50% of maximum O2 consumption (VO2max)] and hard exercise (HE, 65 min at 75% VO2max). Twenty minutes into each condition, subjects received a Na+-L(+)-[1–13C]lactate intravenous bolus injection. Blood was sampled intermittently from the contralateral arm for metabolite levels, acid-base status, and enrichment of 13C in lactate. Expired air was monitored continuously for determination of respiratory parameters, and aliquots were collected for determination of 13C enrichment in CO2. Steady-rate values for O2 consumption (VO2) were 0.33 +/- 0.01, 2.11 +/- 0.03, and 3.10 +/- 0.03 l/min for Re, EE, and HE, respectively. Corresponding values of blood lactate levels were 0.84 +/- 0.01, 1.33 +/- 0.05, and 4.75 +/- 0.28 mM in the three conditions. Blood lactate disposal rates were significantly correlated to VO2 (r = 0.78), averaging 123.4 +/- 20.7, 245.5 +/- 40.3, and 316.2 +/- 53.7 mg X kg-1 X h-1 during Re, EE, and HE, respectively. Lactate oxidation rate was also linearly related to VO2 (r = 0.81), and the percentage of RiLa oxidized increased from 49.3% at rest to 87.0% during exercise. A curvilinear relationship was found between RiLa and blood lactate concentration. It was concluded that, in humans, 1) lactate disposal (turnover) rate is directly related to the metabolic rate, 2) oxidation is the major fate of lactate removal during exercise, and 3) blood lactate concentration is not an accurate indicator of lactate disposal and oxidation.

Iron deficiency anemia and steady-state work performance at high altitude

1988 ◽  
Vol 64 (5) ◽  
pp. 1878-1884 ◽  
Author(s):  
J. L. Beard ◽  
J. D. Haas ◽  
D. Tufts ◽  
H. Spielvogel ◽  
E. Vargas ◽  
...  
Keyword(s):  
High Altitude ◽  
Lactate Concentration ◽  
Work Load ◽  
Molar Ratio ◽  
Deficiency Anemia ◽  
Arterial Lactate ◽  
Population Mean ◽  
Relationship Of ◽  
The Relationship ◽  
Maximal Effort

Thirty-seven young adult male highland residents at 3,600–4,100 m in La Paz, Bolivia, performed short-duration cycle ergometry at 60, 80, and 100% of maximal voluntary O2 consumption (VO2max). Three groups of subjects representing the high-altitude population mean hemoglobin (Hb), the 10th percentile Hb, and below the 1st percentile were examined to test the hypothesis that the relationship of exercise performance to Hb concentration is similar to those relationships established at low altitude. Anemic individuals (n = 8) had 23% lower voluntary VO2max and 28% lower maximal work loads compared with controls (n = 17) or marginally anemic subjects (n = 12) although the relationship of VO2 to work load was similar. Anemic individuals maintained significantly higher arterial O2 partial pressures and Hb saturations during heavy exercise (90 +/- 0.5 vs. 85 +/- 0.6%) in conjunction with a greater heart rate up to maximal effort. A significantly decreased erythrocyte 2,3-diphosphoglycerate (2,3-DPG)-to-Hb molar ratio (0.70 +/- 0.04 vs. 1.12 +/- 0.06), suggestive of a left-shifted dissociation curve in anemics, is in contrast to the expected right-shifted curve. Moderate anemics were similar to controls. Anemic individuals did not differ in arterial lactate concentration from controls at absolute work loads; anemics had significantly lower arterial lactate concentrations at maximal effort than controls with no differences in the work load-to-lactate relationship. In conclusion, O2 transport during exercise at high altitude seems unaffected by the Hb concentrations as low as the 10th percentile of the population mean.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Altitude Cardiomyopathy Is Associated With Impaired Stress Electrocardiogram and Increased Circulating Inflammation Makers

2021 ◽  
Vol 12 ◽  
Author(s):  
Ya-Jun Shi ◽  
Jin-Li Wang ◽  
Ling Gao ◽  
Dong-Lin Wen ◽  
Qing Dan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Altitude ◽  
Sea Level ◽  
Exercise Intensity ◽  
Exercise Tolerance ◽  
Acute Mountain Sickness ◽  
Young Men ◽  
Acute Exposure ◽  
Physiological Variables ◽  
Metabolic Equivalents

Many sea-level residents suffer from acute mountain sickness (AMS) when first visiting altitudes above 4,000 m. Exercise tolerance also decreases as altitude increases. We observed exercise capacity at sea level and under a simulated hypobaric hypoxia condition (SHHC) to explore whether the response to exercise intensity represented by physiological variables could predict AMS development in young men. Eighty young men from a military academy underwent a standard treadmill exercise test (TET) and biochemical blood test at sea level, SHHC, and 4,000-m altitude, sequentially, between December 2015 and March 2016. Exercise-related variables and 12-lead electrocardiogram parameters were obtained. Exercise intensity and AMS development were investigated. After exposure to high altitude, the count of white blood cells, alkaline phosphatase and serum albumin were increased (P &lt; 0.05). There were no significant differences in exercise time and metabolic equivalents (METs) between SHHC and high-altitude exposures (7.05 ± 1.02 vs. 7.22 ± 0.96 min, P = 0.235; 9.62 ± 1.11 vs. 9.38 ± 1.12, P = 0.126, respectively). However, these variables were relatively higher at sea level (8.03 ± 0.24 min, P &lt; 0.01; 10.05 ± 0.31, P &lt; 0.01, respectively). Thus, subjects displayed an equivalent exercise tolerance upon acute exposure to high altitude and to SHHC. The trends of cardiovascular hemodynamics during exercise under the three different conditions were similar. However, both systolic blood pressure and the rate–pressure product at every TET stage were higher at high altitude and under the SHHC than at sea level. After acute exposure to high altitude, 19 (23.8%) subjects developed AMS. Multivariate logistic regression analysis showed that METs under the SHHC {odds ratio (OR) 0.355 per unit increment [95% confidence intervals (CI) 0.159−0.793], P = 0.011}, diastolic blood pressure (DBP) at rest under SHHC [OR 0.893 per mmHg (95%CI 0.805−0.991), P = 0.030], and recovery DBP 3 min after exercise at sea level [OR 1.179 per mmHg (95%CI 1.043−1.333), P = 0.008] were independently associated with AMS. The predictive model had an area under the receiver operating characteristic curve of 0.886 (95%CI 0.803−0.969, P &lt; 0.001). Thus, young men have similar exercise tolerance in acute exposure to high altitude and to SHHC. Moreover, AMS can be predicted with superior accuracy using characteristics easily obtainable with TET.

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

1991 ◽  
Vol 70 (2) ◽  
pp. 919-927 ◽  
Author(s):  
G. A. Brooks ◽  
G. E. Butterfield ◽  
R. R. Wolfe ◽  
B. M. Groves ◽  
R. S. Mazzeo ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Continuous Infusion ◽  
Sea Level ◽  
Glucose Concentration ◽  
O2 Consumption ◽  
Vo2 Max ◽  
Altitude Exposure ◽  
Appearance Rate ◽  
Arterial Glucose ◽  
Healthy Males

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)

Maximal lactic capacity at altitude: effect of bicarbonate loading

1993 ◽  
Vol 75 (3) ◽  
pp. 1070-1074 ◽  
Author(s):  
B. Kayser ◽  
G. Ferretti ◽  
B. Grassi ◽  
T. Binzoni ◽  
P. Cerretelli
Keyword(s):  
Sea Level ◽  
Blood Lactate ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Altitude Effect ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Arterial Blood Lactate ◽  
Arterial Blood Lactate Concentration ◽  
Blood Lactate Accumulation

The aim of the present study was to test the hypothesis that the net maximal blood lactate accumulation ([La]max) during heavy exercise in lowlanders acclimatized to chronic hypoxia may be limited by the reduced bicarbonate stores. Six men [age 32 +/- 4 (SD) yr] performed supramaximal exercise until voluntary exhaustion at sea level (204 +/- 54 W) and after sojourning for 1 mo at 5,050 m (175 +/- 23 W), without (C) and with (B) oral sodium-bicarbonate loading (0.3 g/kg body wt). Exhaustion time, arterial blood lactate concentration, arterial pH (pHa), arterial PCO2, and intramuscular pH were measured at rest and after exercise. At sea level, exhaustion time increased from 6.5 +/- 2.8 min in C to 7.5 +/- 2.7 min in B (P < 0.05). At altitude, exhaustion times were similar to the sea level C values and the same in C and B. At sea level, resting pHa increased from 7.41 +/- 0.02 in C to 7.46 +/- 0.03 in B (P < 0.001); the corresponding values at altitude were 7.46 +/- 0.04 and 7.55 +/- 0.03 (P < 0.001). Postexercise pHa at sea level was 7.22 +/- 0.02 in C and 7.25 +/- 0.08 in B (NS). After exercise at altitude, pHa was 7.32 +/- 0.04 and 7.44 +/- 0.03 in C and B, respectively (P < 0.001). [La]max increased from 12.86 +/- 1.45 mM in C to 16.63 +/- 1.76 mM in B (P < 0.01) at sea level and from 6.85 +/- 1.40 mM in C to 7.95 +/- 1.74 mM in B (NS) at altitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Peak blood lactate and blood lactate vs. workload during acclimatization to 5,050 m and in deacclimatization

1996 ◽  
Vol 80 (2) ◽  
pp. 685-692 ◽  
Author(s):  
B. Grassi ◽  
M. Marzorati ◽  
B. Kayser ◽  
M. Bordini ◽  
A. Colombini ◽  
...  
Keyword(s):  
Sea Level ◽  
Blood Lactate ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Acid Base ◽  
Acid Base Status ◽  
Per Se ◽  
The Right ◽  
Peak Blood ◽  
Peak Blood Lactate

Peak blood lactate ([Labl]peak) and blood lactate concentration ([Labl]) vs. workload (W) relationships during acclimatization to altitude and in the deacclimatization were evaluated in 10 Caucasian lowlanders at sea level (SL0); after approximately 1 wk (Alt1wk), 3 wk (Alt3wk), and 5 wk (Alt5wk) at 5,050 m; and weekly during the first 5 wk after return to sea level (SL1wk-SL5wk). Incremental bicycle ergometer exercises (30 W added every 4 min up to exhaustion) were performed. At Alt1wk and at Alt5wk, the experiments were repeated in hypobaric normoxia (Alt1wk-O2 and Alt5wk-O2). [Labl] was determined at rest and during the last approximately 30 s of each W. [Labl]peak was taken as the highest [Labl] during recovery. Acid-base status (pH and concentration of HCO-3 in arterialized capillary blood) was determined at rest. Mean [Labl]peak values were 11.5 (SL0), 8.0 (Alt1wk), 6.4 (Alt3wk), 6.3 (Alt5wk), 8.0 (SL1wk), 9.4 (SL2wk), 10.8 (SL3wk), 11.3 (SL4wk), and 11.6 (SL5wk) mM. At Alt1wk-O2 and Alt5wk-O2, peak W increased, compared with Alt1wk and Alt5wk, whereas no changes were observed for [Labl]peak. [Labl] vs. W was shifted to the left (i.e., higher [Labl] values were found for the same W) at Alt1wk compared with SL0 and partially shifted back to the right (i.e., lower [Labl] values were found for the same W) at Alt3wk and Alt5wk. At Alt1wk-O2 and Alt5wk-O2, [Labl] vs. W values were superimposed on that at SL0. At SL1wk-SL5wk, [Labl] vs. W values were shifted to the right compared with that at SL0. At Alt1wk, a condition of respiratory alkalosis was found, which was only partially compensated for during acclimatization. At SL1wk, the acid-base status was back to normal. We conclude that 1) the reduced [Labl]peak at altitude is still present for 2-3 wk after return from altitude; is not attributable to reduced peak W nor to hypoxia per se, nor to a reduced buffer capacity; alternatively, it could be related to some central determinants of fatigue. 2) The [Labl] vs. W leftward shift at altitude was due to hypoxia per se. 3) The factor(s) responsible for the [Labl] vs. W partial rightward shift during acclimatization could still be effective during the first weeks after return to sea level.

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