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.

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)

Splanchnic blood flow, O2 consumption, removal of lactate, and output of glucose in highlanders

1977 ◽  
Vol 43 (2) ◽  
pp. 204-210 ◽  
Author(s):  
A. Capderou ◽  
J. Polianski ◽  
J. Mensch-Dechene ◽  
L. Drouet ◽  
G. Antezana ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Splanchnic Blood Flow ◽  
O2 Consumption ◽  
Arterial Lactate ◽  
Oxygen Breathing ◽  
Arterial Blood ◽  
Splanchnic Hemodynamics ◽  
Arterial Blood Glucose ◽  
Arteriovenous Difference

An impairment of gluconeogenesis has been proposed to explain the low arterial blood glucose of highlanders. Therefore, we studied splanchnic blood flow, splanchnic uptake of oxygen and lactate, and output of glucose in nine normal and six anemic highlanders at an altitude of 3,750 m. Splanchnic blood flow, arteriovenous difference for oxygen, and oxygen consumption were comparable at rest in both groups and in lowlanders from the literature, whereas splanchnic output of glucose, and uptake of lactate were approximately twice those in lowlanders. After 10 min of mild exercise in 12 subjects (7 normals, 5 anemic), no significant changes in splanchnic hemodynamics and metabolism were found. During 29% oxygen breathing in 8 subjects (5 normals, 3 anemics), arterial lactate, splanchnic uptake of lactate and output of glucose fell to normal sea-level values. We concluded that splanchnic hemodynamics are similar in adapted highlanders and in lowlanders, and that there is no evidence of an impaired gluconeogenesis at the altitude of the present study.

Nonperipheral chemoreceptor stimulation of ventilation by cyanide

1975 ◽  
Vol 39 (2) ◽  
pp. 199-204 ◽  
Author(s):  
S. Levine
Keyword(s):  
Abdominal Aorta ◽  
Minute Ventilation ◽  
Lactate Concentration ◽  
Sodium Cyanide ◽  
Arterial Lactate ◽  
Arterial Blood ◽  
Carotid Bodies ◽  
Peripheral Arterial ◽  
Upper Abdominal ◽  
Stimulation Of

To assess the ventilatory responses elicited by changes of tissue hypoxia, sodium cyanide (0.12 mg/kg-min for 10 min) was infused into the upper abdominal aorta of anesthetized dogs. These infusions produced decreases in oxygen consumption, increases in arterial lactate concentration, and increases in arterial lactate/pyruvate ratio. Coincident with these metabolic changes of hypoxia, minute ventilation (VE) increased 228 +/- SE 36% and arterial PCO2 decreased 21 +/- SE 2 mmHg; therefore, pH increased both in arterial blood in and cisternal cerebrospinal fluid. Following infusion of cyanide into the abdominal aorta, small quantities of cyanide (48 +/- SE 14 mumol/liter) appeared in carotid arterial blood. To evaluate the possibility that the observed increases in VE were due to stimulation of peripheral arterial chemoreceptors by the recirculating cyanide, the carotid and aortic chemoreceptors were denervated in four dogs. Nonetheless, after intra-aortic infusion of sodium cyanide (1.2 mg/kg), ventilation in these chemodenervated animals again increased considerably (154 +/- SE 36%). In order to explore the possibility that cyanide infusion can stimulate ventilation by an extracranial mechanism, heads of vagotomized dogs (including the carotid bodies) were perfused entirely by donor dogs. The intra-aortic infusion of sodium cyanide (0.9 mg/kg) into these head-perfused animals still caused large increases in VE (163 +/- SE 19%). It is concluded that intra-aortic cyanide infusions stimulate VE by an extracranial mechanism other than the carotid and aortic chemoreceptors.

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)

Alveolar gas composition and exchange during deep breath-hold diving and dry breath holds in elite divers

1991 ◽  
Vol 70 (2) ◽  
pp. 794-802 ◽  
Author(s):  
G. Ferretti ◽  
M. Costa ◽  
M. Ferrigno ◽  
B. Grassi ◽  
C. Marconi ◽  
...  
Keyword(s):  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Breath Hold ◽  
O2 Consumption ◽  
Gas Composition ◽  
Arterial Blood ◽  
Co2 Output ◽  
Before And After ◽  
Volume Blood ◽  
End Tidal

End tidal O2 and CO2 (PETCO2) pressures, expired volume, blood lactate concentration ([Lab]), and arterial blood O2 saturation [dry breath holds (BHs) only] were assessed in three elite breath-hold divers (ED) before and after deep dives and BH and in nine control subjects (C; BH only). After the dives (depth 40-70 m, duration 88-151 s), end-tidal O2 pressure decreased from approximately 140 Torr to a minimum of 30.6 Torr, PETCO2 increased from approximately 25 Torr to a maximum of 47.0 Torr, and expired volume (BTPS) ranged from 1.32 to 2.86 liters. Pulmonary O2 exchange was 455-1,006 ml. CO2 output approached zero. [Lab] increased from approximately 1.2 mM to at most 6.46 mM. Estimated power output during dives was 513-929 ml O2/min, i.e. approximately 20-30% of maximal O2 consumption. During BH, alveolar PO2 decreased from approximately 130 to less than 30 Torr in ED and from 125 to 45 Torr in C. PETCO2 increased from approximately 30 to approximately 50 Torr in both ED and C. Contrary to C, pulmonary O2 exchange in ED was less than resting O2 consumption, whereas CO2 output approached zero in both groups. [Lab] was unchanged. Arterial blood O2 saturation decreased more in ED than in C. ED are characterized by increased anaerobic metabolism likely due to the existence of a diving reflex.

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.

Uptake of lactate by dog skeletal muscle in vivo and the effect of free fatty acids

1975 ◽  
Vol 229 (2) ◽  
pp. 255-259 ◽  
Author(s):  
RB Dunn ◽  
JB Critz
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Lactate Concentration ◽  
Sodium Pentobarbital ◽  
Arterial Lactate ◽  
Arterial Blood

These experiments were designed to determine: 1) if lactate can be extracted from the arterial blood and utilized by resting skeletal muscle of the dog, and 2) if lactate uptake or production by skeletal muscle is influenced by the level of circulating free fatty acids. Skeletal muscle arteriovenous differences in lactate were measured at several arterial lactate and free fatty acid concentrations. With sodium pentobarbital anesthesia and a low concentration of free fatty acids, arterial lactate concentrations of 1-2 mM were associated with extraction of lactate; however, when circulating free fatty acids were elevated (greater than 1 mM), no extraction of lactate occurred at these lactate concentrations. The relationship between arterial free fatty acids and uptake or release of lactate demonstrated in these in vivo studies suggest that the inhibition of free fatty acid release from adipose tissue that occurs when the arterial lactate concentration increases may function facilitate the metabolism of lactate by skeletal muscle.

Effects of glucose-insulin-potassium on intestinal hemodynamics and substrate utilization during endotoxemia

1986 ◽  
Vol 251 (3) ◽  
pp. G341-G348
Author(s):  
C. H. Lang ◽  
R. J. Alteveer
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Aerobic Glycolysis ◽  
Lactate Concentration ◽  
Intestinal Blood Flow ◽  
Whole Body ◽  
Constant Infusion ◽  
Metabolic Pattern ◽  
Lactate Release ◽  
Arterial Blood

This study examined the effects of endotoxin on small intestinal hemodynamics and metabolism with and without an infusion of glucose-insulin-potassium (GIK). Glucose uptake and lactate release were determined by arteriovenous differences across a segment of canine ileum, which was vascularly isolated in vivo, and by the direct measurement of intestinal blood flow. Free fatty acid (FFA) utilization by intestinal tissue was assessed by the constant infusion of albumin-bound [14C]palmitate and [3H]oleate. Endotoxemic dogs showed a sustained reduction of mean arterial blood pressure (MABP) and intestinal blood flow. In contrast, endotoxemic dogs infused with GIK demonstrated a decreased intestinal vascular resistance and an increased blood flow (two-fold), whereas MABP was transiently improved. Intestinal glucose uptake was not different from control values in endotoxemic animals; however, a sixfold increase was seen in shocked dogs treated with GIK. The endotoxin-induced increase in the plasma lactate concentration and intestinal lactate release was similar between dogs infused with saline or GIK. After endotoxin, the arterial FFA concentration remained unchanged and whole-body FFA turnover was decreased. FFA uptake by the gut was reduced, but FFA oxidation was not altered. Similar changes in FFA metabolism were seen in endotoxemic animals infused with GIK. The metabolic pattern after endotoxin suggests an elevated rate of aerobic glycolysis by the gut that increases the availability of lactate to the liver. Compared with saline-infused endotoxemic animals, GIK produced an elevation in glucose uptake without a further increase in lactate output, suggesting an increased storage of glucose by this tissue.

Effect of hemoglobin concentration on critical cardiac output and oxygen transport

1989 ◽  
Vol 256 (2) ◽  
pp. H527-H532 ◽  
Author(s):  
F. Heusser ◽  
J. T. Fahey ◽  
G. Lister
Keyword(s):  
Cardiac Output ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Hemoglobin Concentration ◽  
Base Line ◽  
O2 Consumption ◽  
Arterial Blood ◽  
O2 Transport ◽  
O2 Extraction ◽  
The Right

We previously found limited tolerance to acute reduction in cardiac output in lambs at the nadir of their physiological anemia [Am. J. Physiol. 253 (Heart Cir. Physiol. 12): H100-H106, 1987]. To determine the effect of hemoglobin concentration [Hb] on critical cardiac output, critical systemic O2 transport, and peripheral O2 extraction, we performed 31 experiments in 12 one-mo-old lambs at four [Hb] (means +/- SD in g/dl): 7.4 +/- 0.6, 10.5 +/- 0.5, 14.5 +/- 0.5, and 16.5 +/- 0.6. Desired [Hb] was obtained by exchange transfusion with packed red cells or plasma. Cardiac output was reduced by inflation of a balloon-tipped catheter in the right atrium, and critical levels were defined at the point where O2 consumption decreased and/or arterial blood lactate concentration increased in response. With lower [Hb], cardiac output was unchanged, systemic O2 transport was reduced, and fractional O2 extraction was increased, keeping O2 consumption constant at base line. As [Hb] was reduced, critical cardiac output was significantly higher, whereas critical systemic O2 transport was independent of [Hb], as were fractional O2 extraction and mixed venous PO2 at the critical point. Thus peripheral O2 extraction was not affected by changes in [Hb] during progressive decreases in cardiac output. We conclude that 4-wk-old lambs have decreased tolerance to reductions in cardiac output and systemic O2 transport because their relative anemia provides them with a base-line cardiac output and systemic O2 transport close to the critical level.

Changes in alveolar and arterial gas tensions as related to altitude and age

1964 ◽  
Vol 19 (1) ◽  
pp. 21-24 ◽  
Author(s):  
James W. Terman ◽  
Jerry L. Newton
Keyword(s):  
High Altitude ◽  
Pulmonary Ventilation ◽  
Research Station ◽  
Age Changes ◽  
Altitude Acclimatization ◽  
Ventilation Perfusion Ratio ◽  
Early Phases ◽  
Chilean Andes

In the summer of 1962 at the White Mountain Research Station the early phases of altitude acclimatization were studied in six of the surviving eight members of the 1935 expedition to the Chilean Andes; they were from 58 to 71 years of age. Alveolar and arterial Po2 and Pco2 were determined for each man a few hours after arrival at 3,093 m and at 3,800 and 4,343 m over the next few days. The effects of age were superimposed on the classical responses to high altitude. The arterial and alveolar Pco2 values showed no significant gradient; the alveolar Pco2 was found to be lower for a given altitude than 27 years before. For example, their average alveolar Pco2 at 4,700 m in 1935 was 27.7 mm Hg as opposed to 25.1 mm Hg at 4,343 m in 1962. The case of Hall was exceptional: his alveolar Pco2 ranged from 21 to 24 mm Hg regardless of altitude for his sojourn of 22 days. In 1935 these six men had a mean A-a Po2 gradient of +3.0 mm Hg at 4,700 m, while in 1962 the gradient over the three altitudes was +12.4 mm Hg. These findings would likely be explained partially by age changes in the pulmonary ventilation-perfusion ratio. acclimatization; pulmonary ventilation-perfusion ratio; alveolar-arterial Po2 and Pco2 gradients; alveolar hyperventilation; aging and altitude Submitted on February 19, 1963

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