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 ◽  
...  

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)

2004 ◽  
Vol 286 (1) ◽  
pp. E20-E24 ◽  
Author(s):  
C. M. Maresh ◽  
W. J. Kraemer ◽  
D. A. Judelson ◽  
J. L. VanHeest ◽  
L. Trad ◽  
...  

High-altitude exposure changes the distribution of body water and electrolytes. Arginine vasopressin (AVP) may influence these alterations. The purpose of this study was to examine the effect of a 24-h water deprivation trial (WDT) on AVP release after differing altitude exposures. Seven healthy males (age 22 ± 1 yr, height 176 ± 2 cm, mass 75.3 ± 1.8 kg) completed three WDTs: at sea level (SL), after acute altitude exposure (2 days) to 4,300 m (AA), and after prolonged altitude exposure (20 days) to 4,300 m (PA). Body mass, standing and supine blood pressures, plasma osmolality (Posm), and plasma AVP (PAVP) were measured at 0, 12, 16, and 24 h of each WDT. Urine volume was measured at each void throughout testing. Baseline Posm increased from SL to altitude (SL 291.7 ± 0.8 mosmol/kgH2O, AA 299.6 ± 2.2 mosmol/kgH2O, PA 302.3 ± 1.5 mosmol/kgH2O, P < 0.05); however, baseline PAVP measurements were similar. Despite similar Posm values, the maximal PAVP response during the WDT (at 16 h) was greater at altitude than at SL (SL 1.7 ± 0.5 pg/ml, AA 6.4 ± 0.7 pg/ml, PA 8.7 ± 0.9 pg/ml, P < 0.05). In conclusion, hypoxia appeared to alter AVP regulation by raising the osmotic threshold and increasing AVP responsiveness above that threshold.


1976 ◽  
Vol 41 (6) ◽  
pp. 848-858 ◽  
Author(s):  
C. M. Blatteis ◽  
L. O. Lutherer

The thermoregulatory responses to 10 degrees C (for 3 h) were investigated in 1) 12 natives from sea level (lowlanders) at 150 m, and on arrival at 3,350 and 4,340 m; 2) 6 of these during a 6-wk sojourn at 4,360 m, and on return to sea level; and 3) 5 natives from each of the two altitudes (highlanders) in their respective habitat, and after descent to 150 m. The cold-induced increase in the rate of O2 consumption (Vo2) of the lowlanders was significantly smaller at both altitudes than at sea level. It did not recover substantially during the 6 wk at altitude, but was restored to its initial rate on return to sea level. By contrast, visible shivering activity was augmented on arrival at altitude. It persisted throughout the 6 wk there, but was greatly depressed on return to sea level, despite the increased Vo2. Mean skin temperatures (Tsk) stabilized in the cold at significantly higher values at altitude. Rectal temperature (Tre) decreased similarly at all altitudes. Vo2 of the highlanders in the cold was significantly greater at sea level than at their resident altitudes, although shivering activity was less intense; Tsk stabilized at significantly lower levels at 150 m than at either altitude. These results indicate that altitude exposure reduces the calorigenic response of man to cold, and that this effect is not moderated by acclimatization to altitude, yet is reversible immediately on descent to sea level. The component of cold thermogenesis which appeared to be reduced by altitude exposure was nonshivering thermogenesis rather than visible shivering.


1983 ◽  
Vol 244 (6) ◽  
pp. R882-R887 ◽  
Author(s):  
S. S. Crandell ◽  
P. A. Palma ◽  
F. H. Morriss

Umbilical glucose and lactate extractions were determined in previously instrumented pregnant ewes into some of which D-glucose was infused to produce graded levels of maternal hyperglycemia as great as 20 mM. While fetal arterial glucose concentration continued to increase linearly as a function of maternal arterial glucose concentration during maternal hyperglycemia, the umbilical venoarterial difference in blood glucose concentration did not, and umbilical glucose extraction approached a plateau at approximately 0.063 mmol X min-1 X kg fetus-1 at maternal glucose concentrations greater than approximately 8 mM. The observed plateau in glucose extraction is consistent with saturation at high maternal glucose concentrations of the carrier mechanism for transport of glucose from the maternal to the fetal aspects of the trophoblast. The observed value of the plateau in umbilical extraction of glucose is slightly less than the maximum extraction predicted from previously published equations for this species, but the maternal blood glucose concentration at which the observed maximum occurred agrees closely with the value predicted by those equations. Umbilical lactate extraction, 0.031 +/- 0.021 mmol X min-1 X kg fetus-1, was independent of maternal arterial blood glucose and lactate concentrations and was independent of umbilical glucose extraction.


1994 ◽  
Vol 76 (1) ◽  
pp. 26-32 ◽  
Author(s):  
S. R. Colberg ◽  
G. A. Casazza ◽  
M. A. Horning ◽  
G. A. Brooks

To evaluate the hypothesis that smoking increases the dependence on blood glucose as a fuel, seven male smokers [28.7 +/- 1.7 (SE) yr. 77.7 +/- 4.3 kg] and seven nonsmokers (NS; 29.1 +/- 0.9 yr, 78.7 +/- 5.3 kg) were studied in the postabsorptive condition. NS received a primed continuous infusion of [6,6–2H]glucose and [1–13C]glucose during 90 min of rest and 60 min of exercise at 49.7 +/- 0.8% of peak O2 consumption on one occasion; chronic smokers continued their overnight abstinence from smoking (CS) for one trial but, on another occasion, acutely smoked (AS) two cigarettes immediately before resting measurements and another cigarette before exercise. Plasma glucose levels were similar among all groups at all times during the trials; however, the glucose rates of appearance (Ra) at rest in CS (1.96 +/- 0.14 mg.kg-1 x min-1) and AS (2.02 +/- 0.14) were higher than in NS (1.41 +/- 0.15, P < 0.05). With exercise, the glucose Ra values rose in all groups above resting values but were significantly greater in CS (4.76 +/- 0.50) and AS (4.71 +/- 0.53) than in NS (3.31 +/- 0.16). Glucose oxidation during exercise was elevated in smokers (2.31 +/- 0.37 mg.kg-1 x min-1 in CS and 2.18 +/- 0.34 in AS) compared with NS (1.09 +/- 0.18, P < 0.05). Nicotine levels correlated with the glucose Ra in AS (r = 0.93, P < 0.01). In conclusion, the results indicate that long-term smoking, independent of acute smoking, increases the dependence on blood glucose as a fuel during rest and sustained submaximal exercise.


1991 ◽  
Vol 71 (1) ◽  
pp. 333-341 ◽  
Author(s):  
G. A. Brooks ◽  
G. E. Butterfield ◽  
R. R. Wolfe ◽  
B. M. Groves ◽  
R. S. Mazzeo ◽  
...  

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)


1992 ◽  
Vol 24 (Supplement) ◽  
pp. S89
Author(s):  
Amy C. Roberts ◽  
G. A. Brooks ◽  
G. E. Butterfield ◽  
A. Cymerman ◽  
R. S. Mazzeo ◽  
...  

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