Effects of altitude acclimatization on pulmonary gas exchange during exercise

1989 ◽  
Vol 67 (6) ◽  
pp. 2286-2295 ◽  
Author(s):  
D. E. Bebout ◽  
D. Story ◽  
J. Roca ◽  
M. C. Hogan ◽  
D. C. Poole ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Hemoglobin Concentration ◽  
Barometric Pressure ◽  
Normal Subjects ◽  
Load Cycle ◽  
Constant Load ◽  
Work Rate ◽  
Pulmonary Gas Exchange ◽  
Altitude Acclimatization ◽  
Before And After

Pulmonary gas exchange was studied in eight normal subjects both before and after 2 wk of altitude acclimatization at 3,800 m (12,470 ft, barometric pressure = 484 Torr). Respiratory and multiple inert gas tensions, ventilation, cardiac output (Q), and hemoglobin concentration were measured at rest and during three levels of constant-load cycle exercise during both normoxia [inspired PO2 (PIO2) = 148 Torr] and normobaric hypoxia (PIO2 = 91 Torr). After acclimatization, the measured alveolar-arterial PO2 difference (A-aPO2) for any given work rate decreased (P less than 0.02). The largest reductions were observed during the highest work rates and were 24.8 +/- 1.4 to 19.7 +/- 0.8 Torr (normoxia) and 22.0 +/- 1.1 to 19.4 +/- 0.7 Torr (hypoxia). This could not be explained by changes in ventilation-perfusion inequality or estimated O2 diffusing capacity, which were unaffected by acclimatization. However, Q for any given work rate was significantly decreased (P less than 0.001) after acclimatization. We suggest that the reduction in A-aPO2 after acclimatization is a result of more nearly complete alveolar/end-capillary diffusion equilibration on the basis of a longer pulmonary capillary transit time.

Coupling of ventilation to pulmonary gas exchange during nonsteady-state work in men

1983 ◽  
Vol 54 (2) ◽  
pp. 587-593 ◽  
Author(s):  
D. H. Wasserman ◽  
B. J. Whipp
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Load Cycle ◽  
Constant Load ◽  
Response Dynamics ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Nonsteady State ◽  
End Tidal

During steady-state exercise, ventilation increases in proportion to CO2 output (VCO2), regulating arterial PCO2. To characterize the dynamics of ventilatory coupling to VCO2 and O2 uptake (VO2) in the nonsteady-state phase, seven normal subjects performed constant-load cycle ergometry to a series of subanaerobic threshold work rates. Each bout consisted of eight 6-min periods of alternating loaded and unloaded cycling. Ventilation and gas exchange variables were computed breath by breath, with the time-averaged response dynamics being established off-line. Ventilation increased as a linear function of VCO2 in all cases, the relationship being identical in the steady- and the nonsteady-state phases. Ventilation, however, bore a curvilinear relation to VO2, the kinetics of the latter being more rapid. Owing to the kinetic disparity between expired minute ventilation (VE) and VO2, there was an overshoot in the direction of change in VE/VO2 and end-tidal PO2 during the work-rate transition. In contrast, there was no overshoot in the direction of change in VE/VCO2 and end-tidal PCO2 throughout the nonsteady-state period. These data suggest that the exercise hyperpnea is coupled to metabolism in men via a signal proportional to VCO2 in both the nonsteady and steady states of moderate exercise.

Pulmonary gas exchange in Andean natives with excessive polycythemia--effect of hemodilution

1988 ◽  
Vol 65 (5) ◽  
pp. 2107-2117 ◽  
Author(s):  
G. Manier ◽  
H. Guenard ◽  
Y. Castaing ◽  
N. Varene ◽  
E. Vargas
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
High Altitude ◽  
Barometric Pressure ◽  
Pulmonary Gas Exchange ◽  
Total Blood ◽  
La Paz ◽  
Before And After ◽  
Total Blood Flow ◽  
Mixed Venous

Pulmonary gas exchange in Andean natives (n = 8) with excessive high-altitude (3,600-4,200 m) polycythemia (hematocrit 65.1 +/- 6.6%) and hypoxemia (arterial PO2 45.6 +/- 5.6 Torr) in the absence of pulmonary or cardiovascular disease was investigated both before and after isovolemic hemodilution by use of the inert gas elimination technique. The investigations were carried out in La Paz, Bolivia (3,650 m, 500 mmHg barometric pressure). Before hemodilution, a low ventilation-perfusion (VA/Q) mode (VA/Q less than 0.1) without true shunt accounted for 11.6 +/- 5.5% of the total blood flow and was mainly responsible for the hypoxemia. The hypoventilation with a low mixed venous PO2 value may have contributed to the observed hypoxemia in the absence of an impairment in alveolar capillary diffusion. After hemodilution, cardiac output and ventilation increased from 5.5 +/- 1.2 to 6.9 +/- 1.2 l/min and from 8.5 +/- 1.4 to 9.6 +/- 1.3 l/min, respectively, although arterial and venous PO2 remained constant. VA/Q mismatching fell slightly but significantly. The hypoxemia observed in subjects suffering from high-altitude excessive polycythemia was attributed to an increased in blood flow perfusing poorly ventilated areas, but without true intra- or extrapulmonary shunt. Hypoventilation as well as a low mixed venous PO2 value may also have contributed to the observed hypoxemia.

scholarly journals Relation between Pulmonary Gas Exchange and Closing Volume before and after Substantial Weight Loss in Obese Subjects

BMJ ◽  
1974 ◽  
Vol 3 (5927) ◽  
pp. 391-393 ◽  
Author(s):  
M. J. B. Farebrother ◽  
G. J. R. McHardy ◽  
J. F. Munro
Keyword(s):  
Weight Loss ◽  
Gas Exchange ◽  
Pulmonary Gas Exchange ◽  
Closing Volume ◽  
Before And After ◽  
Obese Subjects

scholarly journals Measuring the efficiency of pulmonary gas exchange using expired gas instead of arterial blood: comparing the “ideal” Po2 of Riley with end-tidal Po2

2020 ◽  
Vol 319 (2) ◽  
pp. L289-L293
Author(s):  
John B. West ◽  
Matthew A. Liu ◽  
Phoebe C. Stark ◽  
G. Kim Prisk
Keyword(s):  
Gas Exchange ◽  
Present Report ◽  
Oxygen Affinity ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Arterial Blood ◽  
The Difference ◽  
End Tidal ◽  
The Ideal

When using a new noninvasive method for measuring the efficiency of pulmonary gas exchange, a key measurement is the oxygen deficit, defined as the difference between the end-tidal alveolar Po2 and the calculated arterial Po2. The end-tidal Po2 is measured using a rapid gas analyzer, and the arterial Po2 is derived from pulse oximetry after allowing for the effect of the Pco2 on the oxygen affinity of hemoglobin. In the present report we show that the values of end-tidal Po2 and Pco2 are highly reproducible, providing a solid foundation for the measurement of the oxygen deficit. We compare the oxygen deficit with the classical ideal alveolar-arterial Po2 difference (A-aDO2) as originally proposed by Riley, and now extensively used in clinical practice. This assumes Riley’s criteria for ideal alveolar gas, namely no ventilation-perfusion inequality, the same Pco2 as arterial blood, and the same respiratory exchange ratio as the whole lung. It transpires that, in normal subjects, the end-tidal Po2 is essentially the same as the ideal value. This conclusion is consistent with the very small oxygen deficit that we have reported in young normal subjects, the significantly higher values seen in older normal subjects, and the much larger values in patients with lung disease. We conclude that this noninvasive measurement of the efficiency of pulmonary exchange is identical in many respects to that based on the ideal alveolar Po2, but that it is easier to obtain.

Ventilation-perfusion relationships during induced normovolemic polycythemia in dogs

1988 ◽  
Vol 65 (4) ◽  
pp. 1686-1692 ◽  
Author(s):  
A. A. Balgos ◽  
D. C. Willford ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Base Line ◽  
Slight Improvement ◽  
Arterial Blood ◽  
The Mean ◽  
Arterial Po2

Previous studies on normal subjects and patients with polycythemia have given conflicting results of the effect of polycythemia on pulmonary gas exchange. We studied acutely induced normovolemic polycythemia in the dog and measured arterial blood gases and ventilation-perfusion (VA/Q) relationships using the multiple inert gas elimination technique. The mean base-line hematocrit of 43 +/- 5% was increased to 57 +/- 4 and 68 +/- 8%, respectively, after two exchange transfusions of packed erythrocytes. Subsequent plasma exchange transfusions returned the mean hematocrit to 44 +/- 4%. Polycythemia caused no significant arterial hypoxemia; indeed there was a slight improvement in the alveolar-arterial PO2 difference. The multiple inert gas elimination measurements showed no increase in VA/Q inhomogeneity with no increase in log SD ventilation (V) or log SD blood flow (Q). There was a shift of mean V and mean Q to high VA/Q areas because of a decrease in cardiac output, presumably caused by increased blood viscosity. This study showed no deleterious effects on pulmonary gas exchange within the hematocrit range of 36-76%.

Gas exchange abnormalities after pneumonectomy in conditioned foxhounds

1990 ◽  
Vol 68 (1) ◽  
pp. 94-104 ◽  
Author(s):  
C. C. Hsia ◽  
J. I. Carlin ◽  
P. D. Wagner ◽  
S. S. Cassidy ◽  
R. L. Johnson
Keyword(s):  
Gas Exchange ◽  
Exercise Capacity ◽  
Lung Tissue ◽  
Minute Ventilation ◽  
Hemoglobin Concentration ◽  
Work Load ◽  
O2 Consumption ◽  
Diffusion Limitation ◽  
Before And After ◽  
O2 Delivery

Loss of a major portion of lung tissue has been associated with impaired exercise capacity, but the underlying mechanisms are not well defined. We studied the alterations in gas exchange during exercise before and after left pneumonectomy in three conditioned foxhounds. After pneumonectomy, minute ventilation and O2 consumption at comparable submaximal work loads were unchanged but arterial PCO2 at any work load was higher, implying that ventilatory response to CO2 was impaired. Arterial hypoxemia and an elevated alveolar-arterial O2 tension difference (AaDO2) developed during heavy exercise. Using the multiple inert gas elimination technique, we determined the distributions of ventilation-perfusion (VA/Q) ratios postpneumonectomy. Significant increase in VA/Q inequality developed during exercise while the foxhounds were breathing room air, accounting for an average of 42% of the total increase in AaDO2 while diffusion limitation accounted for 58%. While the animals were breathing hypoxic gas mixture, diffusion limitation accounted for an average of 88% of the total increase AaDO2. Cardiac output and O2 delivery were reduced at a given O2 consumption after pneumonectomy. After pneumonectomy, the animals reached O2 consumptions close to the maximum expected for normal dogs. Compensation for the impairment in O2 delivery post-pneumonectomy occurred mainly by an increase in hemoglobin concentration. Training probably played an important role in returning exercise capacity toward prepneumonectomy levels. We conclude that significant abnormalities in gas exchange develop during exercise after loss of 42% of lung tissue, but the animals demonstrate a remarkable ability to compensate for these changes.

Intensity-dependent tolerance to exercise after attaining V̇o2 max in humans

2003 ◽  
Vol 95 (2) ◽  
pp. 483-490 ◽  
Author(s):  
Edward M. Coats ◽  
Harry B. Rossiter ◽  
James R. Day ◽  
Akira Miura ◽  
Yoshiyuki Fukuba ◽  
...  
Keyword(s):  
High Intensity ◽  
Critical Power ◽  
Load Cycle ◽  
Constant Load ◽  
Cycle Ergometer ◽  
Work Rate ◽  
Hyperbolic Function ◽  
Exercise Tests ◽  
Ergometer Exercise

The tolerable duration of high-intensity, constant-load cycle ergometry is a hyperbolic function of power, with an asymptote termed critical power (CP) and a curvature constant (W′) with units of work. It has been suggested that continued exercise after exhaustion may only be performed below CP, where predominantly aerobic energy transfer can occur and W′ can be partially replenished. To test this hypothesis, six volunteers each performed cycle-ergometer exercise with breath-by-breath determination of ventilatory and pulmonary gas exchange variables. Initially, four exercise tests to exhaustion were made: 1) a ramp-incremental and 2) three high-intensity constant-load bouts at different work rates, to estimate lactate (θ̂L) and CP thresholds, W′, and maximum oxygen uptake (V̇o2 max). Subsequently, subjects cycled to the limit of tolerance (for ∼360 s) on three occasions, each followed by a work rate reduction to 1) 110% CP, 2) 90% CP, and 3) 80% θ̂L for a 20-min target. W′ averaged 20.9 ± 2.35 kJ or 246 ± 30 J/kg. After initial fatigue, 110% CP was tolerated for only 30 ± 12 s. Each subject completed 20 min at 80% θ̂L, but only two sustained 20 min at 90% CP; the remaining four subjects fatigued at 577 ± 306 s, with oxygen consumption at 89 ± 8% V̇o2 max. The results support the suggestion that replenishing W′ after fatigue necessitates a sub-CP work rate. The variation in subjects' responses during 90% CP was unexpected but consistent with mechanisms such as reduced CP consequent to prior high-intensity exercise, variation in lactate handling, and/or regional depletion of energy substrates, e.g., muscle glycogen.

Endurance training of older men: responses to submaximal exercise

1992 ◽  
Vol 73 (2) ◽  
pp. 452-457 ◽  
Author(s):  
M. J. Poulin ◽  
D. H. Paterson ◽  
D. Govindasamy ◽  
D. A. Cunningham
Keyword(s):  
Heart Rate ◽  
Oxygen Uptake ◽  
Training Program ◽  
Performance Test ◽  
Older Men ◽  
Constant Load ◽  
Submaximal Exercise ◽  
Work Rate ◽  
Performance Time ◽  
Before And After

The purpose of this study was to quantify the exercise response of older subjects on a time-to-fatigue (TTF) submaximal performance test before and after a training program. Eight older men (67.4 +/- 4.8 yr) performed two maximal treadmill tests to determine maximum oxygen uptake (VO2max) and ventilation threshold (TVE) and a constant-load submaximal exercise treadmill test that required an oxygen uptake (VO2) between TVE and VO2max. The submaximal test, performed at the same absolute work rate before and after the training program, was performed to volitional fatigue to measure endurance time. The men trained under supervision at an individualized pace representing approximately 70% of VO2max (80% maximum heart rate) for 1 h, four times per week for 9 wk. Significant increases were demonstrated for VO2max (ml.kg-1.min-1; 10.6%); maximal ventilation (VE, l/min; 11.6%), and TVE (l/min; 9.8%). Weight decreased 2.1%. Performance time on the TTF test increased by 180% (7.3 +/- 3.0 to 20.4 +/- 13.5 min). The similar end points for VO2, VE, and heart rate during the TTF and maximal treadmill tests established that the TTF test was stopped because of physiological limitations. The increase in performance time among the subjects was significantly correlated with improvements in VO2max and TVE, with the submaximal work rate representing a VO2 above TVE by 88% of the difference between TVE and VO2max pretraining and 73% of this difference on posttraining values.

scholarly journals Noninvasive measurement of pulmonary gas exchange: comparison with data from arterial blood gases

2019 ◽  
Vol 316 (1) ◽  
pp. L114-L118 ◽  
Author(s):  
John B. West ◽  
Daniel L. Wang ◽  
G. Kim Prisk ◽  
Janelle M. Fine ◽  
Amy Bellinghausen ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Noninvasive Method ◽  
Arterial Blood Gases ◽  
Noninvasive Technique ◽  
Arterial Blood ◽  
End Tidal

A new noninvasive method was used to measure the impairment of pulmonary gas exchange in 34 patients with lung disease, and the results were compared with the traditional ideal alveolar-arterial Po2 difference (AaDO2) calculated from arterial blood gases. The end-tidal Po2 was measured from the expired gas during steady-state breathing, the arterial Po2 was derived from a pulse oximeter if the [Formula: see text] was 95% or less, which was the case for 23 patients. The difference between the end-tidal and the calculated Po2 was defined as the oxygen deficit. Oxygen deficit was 42.7 mmHg (SE 4.0) in this group of patients, much higher than the means previously found in 20 young normal subjects measured under hypoxic conditions (2.0 mmHg, SE 0.8) and 11 older normal subjects (7.5 mmHg, SE 1.6) and emphasizes the sensitivity of the new method for detecting the presence of abnormal gas exchange. The oxygen deficit was correlated with AaDO2 ( R2 0.72). The arterial Po2 that was calculated from the noninvasive technique was correlated with the results from the arterial blood gases ( R2 0.76) and with a mean bias of +2.7 mmHg. The Pco2 was correlated with the results from the arterial blood gases (R2 0.67) with a mean bias of −3.6 mmHg. We conclude that the oxygen deficit as obtained from the noninvasive method is a very sensitive indicator of impaired pulmonary gas exchange. It has the advantage that it can be obtained within a few minutes by having the patient simply breathe through a tube.

Cardiac output increase and gas exchange at start of exercise

1982 ◽  
Vol 52 (1) ◽  
pp. 236-244 ◽  
Author(s):  
M. L. Weissman ◽  
P. W. Jones ◽  
A. Oren ◽  
N. Lamarra ◽  
B. J. Whipp ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Free Breathing ◽  
Cycle Ergometer ◽  
Work Rate ◽  
Pulmonary Gas Exchange ◽  
Controlled Ventilation ◽  
Output Increase ◽  
Exercise Onset ◽  
Exercise Transitions

To determine the rapidity of increased gas exchange resulting from increased cardiac output (Q) following exercise onset, subjects performed multiple rest-exercise transitions on a cycle ergometer: the early dynamics of pulmonary gas exchange were measured during 1) rhythmic breathing with ventilation kept constant at the resting level (controlled ventilation) and 2) prolonged constant airflow exhalation. With controlled ventilation, PACO2 increased and PAO2 decreased, typically beginning in the first exercise breath. After 15 s, PACO2 had increased and PAO2 decreased by 4.5–6.2 and 8.7–12.1 Torr, respectively, graded within these narrow ranges as functions of work rate (0–100 W). Exercise starting during a prolonged exhalation caused the slopes of the alveolar phases for O2 and CO2 to increase immediately or within 2–5 s following exercise onset. Work rate had little effect on the delay or the change of alveolar gas tension slope during the subsequent 10–15 s. Thus, increased gas exchange due to increasing Q occurred very rapidly following exercise onset so that it would coincide with the first or second breath of exercise in free-breathing subjects.

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