Diffusion limitation in normal humans during exercise at sea level and simulated altitude

1985 ◽  
Vol 58 (3) ◽  
pp. 989-995 ◽  
Author(s):  
J. R. Torre-Bueno ◽  
P. D. Wagner ◽  
H. A. Saltzman ◽  
G. E. Gale ◽  
R. E. Moon
Keyword(s):  
Sea Level ◽  
Minute Ventilation ◽  
Inert Gas ◽  
Diffusion Resistance ◽  
Diffusion Limitation ◽  
O2 Concentration ◽  
Normal Humans ◽  
Respiratory Gases ◽  
Arterial Po2 ◽  
Alveolar Capillary

The relative roles of ventilation-perfusion (VA/Q) inequality, alveolar-capillary diffusion resistance, postpulmonary shunt, and gas phase diffusion limitation in determining arterial PO2 (PaO2) were assessed in nine normal unacclimatized men at rest and during bicycle exercise at sea level and three simulated altitudes (5,000, 10,000, and 15,000 ft; barometric pressures = 632, 523, and 429 Torr). We measured mixed expired and arterial inert and respiratory gases, minute ventilation, and cardiac output. Using the multiple inert gas elimination technique, PaO2 and the arterial O2 concentration expected from VA/Q inequality alone were compared with actual values, lower measured PaO2 indicating alveolar-capillary diffusion disequilibrium for O2. At sea level, alveolar-arterial PO2 differences were approximately 10 Torr at rest, increasing to approximately 20 Torr at a metabolic consumption of O2 (VO2) of 3 l/min. There was no evidence for diffusion disequilibrium, similar results being obtained at 5,000 ft. At 10 and 15,000 ft, resting alveolar-arterial PO2 difference was less than at sea level with no diffusion disequilibrium. During exercise, alveolar-arterial PO2 difference increased considerably more than expected from VA/Q mismatch alone. For example, at VO2 of 2.5 l/min at 10,000 ft, total alveolar-arterial PO2 difference was 30 Torr and that due to VA/Q mismatch alone was 15 Torr. At 15,000 ft and VO2 of 1.5 l/min, these values were 25 and 10 Torr, respectively. Expected and actual PaO2 agreed during 100% O2 breathing at 15,000 ft, excluding postpulmonary shunt as a cause of the larger alveolar-arterial O2 difference than accountable by inert gas exchange.

Pulmonary gas exchange in humans during exercise at sea level

1986 ◽  
Vol 60 (5) ◽  
pp. 1590-1598 ◽  
Author(s):  
M. D. Hammond ◽  
G. E. Gale ◽  
K. S. Kapitan ◽  
A. Ries ◽  
P. D. Wagner
Keyword(s):  
Gas Exchange ◽  
Sea Level ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
O2 Uptake ◽  
Heavy Exercise ◽  
Blood Temperature ◽  
O2 Diffusion

Previous studies have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during exercise at simulated altitude and suggested that similar changes could occur even at sea level. We used the multiple-inert gas-elimination technique to further study gas exchange during exercise in healthy subjects at sea level. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate, minute ventilation, respiratory rate, and blood temperature were recorded at rest and during steady-state exercise in the following order: rest, minimal exercise (75 W), heavy exercise (300 W), heavy exercise breathing 100% O2, repeat rest, moderate exercise (225 W), and light exercise (150 W). Alveolar-to-arterial O2 tension difference increased linearly with O2 uptake (VO2) (6.1 Torr X min-1 X 1(-1) VO2). This could be fully explained by measured VA/Q inequality at mean VO2 less than 2.5 l X min-1. At higher VO2, the increase in alveolar-to-arterial O2 tension difference could not be explained by VA/Q inequality alone, suggesting the development of diffusion limitation. VA/Q inequality increased significantly during exercise (mean log SD of perfusion increased from 0.28 +/- 0.13 at rest to 0.58 +/- 0.30 at VO2 = 4.0 l X min-1, P less than 0.01). This increase was not reversed by 100% O2 breathing and appeared to persist at least transiently following exercise. These results confirm and extend the earlier suggestions (8, 21) of increasing VA/Q inequality and O2 diffusion limitation during heavy exercise at sea level in normal subjects and demonstrate that these changes are independent of the order of performance of exercise.

Effect of change in P50 on exercise tolerance at high altitude: a theoretical study

1982 ◽  
Vol 53 (6) ◽  
pp. 1487-1495 ◽  
Author(s):  
H. Z. Bencowitz ◽  
P. D. Wagner ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Exercise Tolerance ◽  
Theoretical Study ◽  
Dissociation Curve ◽  
Diffusion Limitation ◽  
Rightward Shift ◽  
Arterial Po2 ◽  
O2 Dissociation Curve ◽  
Very High ◽  
Alveolar Capillary

Acclimatization to altitude often results in a rightward shift of the O2 dissociation curve (ODC). However, a left-shifted ODC is reported to increase exercise tolerance in humans at medium altitude and increase survival in rats breathing hypoxic gas mixtures. We examined this paradox using a computer model of pulmonary gas exchange. A Bohr integration procedure allowed for alveolar-capillary diffusion. When diffusion equilibration was complete, mixed venous (PVO2) and arterial PO2 fell as O2 consumption (VO2) was increased, but PVO2 approached a plateau. Under these conditions a right-shifted ODC is advantageous (higher PVO2) at all but very high altitudes. However, diffusion limitation of O2 transfer may occur at any altitude if VO2 is increased sufficiently. If this occurs, a left-shifted ODC results in higher calculated VO2max (compared with the standard ODC). Further, diffusion limitation always occurs at a lower VO2 with a right-shifted ODC than with a left-shifted ODC. We conclude that whether a leftward or rightward shift in the ODC is advantageous to gas exchange at altitude depends on the presence or absence of diffusion limitation.

Ventilation-perfusion inequality in normal humans during exercise at sea level and simulated altitude

1985 ◽  
Vol 58 (3) ◽  
pp. 978-988 ◽  
Author(s):  
G. E. Gale ◽  
J. R. Torre-Bueno ◽  
R. E. Moon ◽  
H. A. Saltzman ◽  
P. D. Wagner
Keyword(s):  
Blood Flow ◽  
High Altitude ◽  
Sea Level ◽  
Statistical Significance ◽  
Barometric Pressure ◽  
Bicycle Ergometer ◽  
Lung Model ◽  
Inert Gas ◽  
Topographical Distribution ◽  
Normal Humans

To investigate the effects of both exercise and acute exposure to high altitude on ventilation-perfusion (VA/Q) relationships in the lungs, nine young men were studied at rest and at up to three different levels of exercise on a bicycle ergometer. Altitude was simulated in a hypobaric chamber with measurements made at sea level (mean barometric pressure = 755 Torr) and at simulated altitudes of 5,000 (632 Torr), 10,000 (523 Torr), and 15,000 ft (429 Torr). VA/Q distributions were estimated using the multiple inert gas elimination technique. Dispersion of the distributions of blood flow and ventilation were evaluated by both loge standard deviations (derived from the VA/Q 50-compartment lung model) and three new indices of dispersion that are derived directly from inert gas data. Both methods indicated a broadening of the distributions of blood flow and ventilation with increasing exercise at sea level, but the trend was of borderline statistical significance. There was no change in the resting distributions with altitude. However, with exercise at high altitude (10,000 and 15,000 ft) there was a significant increase in dispersion of blood flow (P less than 0.05) which implies an increase in intraregional inhomogeneity that more than counteracts the more uniform topographical distribution that occurs. Since breathing 100% O2 at 15,000 ft abolished the increased dispersion, the greater VA/Q mismatching seen during exercise at altitude may be related to pulmonary hypertension.

Ventilation-perfusion relationships in the lung during head-out water immersion

1992 ◽  
Vol 72 (1) ◽  
pp. 64-72 ◽  
Author(s):  
T. Derion ◽  
H. J. Guy ◽  
K. Tsukimoto ◽  
W. Schaffartzik ◽  
R. Prediletto ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Standard Deviation ◽  
Minute Ventilation ◽  
Water Immersion ◽  
Inert Gas ◽  
Closing Volume ◽  
O2 Uptake ◽  
Tidal Breathing ◽  
Normal Males ◽  
Arterial Po2

Water immersion can cause airways closure during tidal breathing, and his may result in areas of low ventilation-perfusion (VA/Q) ratios (VA/Q less than or equal to 0.1) and/or shunt and, ultimately, hypoxemia. We studied this in 12 normal males: 6 young (Y; aged 20–29 yr) with closing volume (CV) less than expiratory reserve volume (ERV), and six older (O; aged 40–54 yr) with CV greater than ERV during seated head-out immersion. Arterial and expired inert gas concentrations and dye-dilution cardiac output (Q) were measured before and at 2, 5, 10, 15, and 20 min in 35 degrees C water. During immersion, Y showed increases in expired minute ventilation (VE; 8.3–10.3 l/min), Q (6.1–8.2 l/min), and arterial PO2 (PaO2; 91–98 Torr; P less than or equal to 0.05). However, O2 uptake (VO2), shunt, amount of low-VA/Q areas (% of Q), and the log standard deviation of the perfusion distribution (log SDQ) were unchanged. During immersion, O showed increases in shunt (0.6–1.8% of Q), VE (8.5–11.4 l/min), and VO2 (0.31–0.40 l/min) but showed no change in low-VA/Q areas, log SDQ, Q, or PaO2. Throughout, O showed more VA/Q inequality (greater log SDQ) than Y (O, 0.69 vs. Y, 0.47).(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of exercise-induced hypoxemia in horses

1989 ◽  
Vol 66 (3) ◽  
pp. 1227-1233 ◽  
Author(s):  
P. D. Wagner ◽  
J. R. Gillespie ◽  
G. L. Landgren ◽  
M. R. Fedde ◽  
B. W. Jones ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Treadmill Exercise ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
O2 Uptake ◽  
Heavy Exercise ◽  
Physiological Basis ◽  
Blood Temperature ◽  
Exercise Induced ◽  
Arterial Po2

Arterial hypoxemia has been reported in horses during heavy exercise, but its mechanism has not been determined. With the use of the multiple inert gas elimination technique, we studied five horses, each on two separate occasions, to determine the physiological basis of the hypoxemia that developed during horizontal treadmill exercise at speeds of 4, 10, 12, and 13–14 m/s. Mean, blood temperature-corrected, arterial PO2 fell from 89.4 Torr at rest to 80.7 and 72.1 Torr at 12 and 13–14 m/s, respectively, whereas corresponding PaCO2 values were 40.3, 40.3, and 39.2 Torr. Alveolar-arterial PO2 differences (AaDO2) thus increased from 11.4 Torr at rest to 24.9 and 30.7 Torr at 12 and 13–14 m/s. In 8 of the 10 studies there was no change in ventilation-perfusion (VA/Q) relationships with exercise (despite bronchoscopic evidence of airway bleeding in 3) and total shunt was always less than 1% of the cardiac output. Below 10 m/s, the AaDO2 was due only to VA/Q mismatch, but at higher speeds, diffusion limitation of O2 uptake was increasingly evident, accounting for 76% of the AaDO2 at 13–14 m/s. Most of the exercise-induced hypoxemia is thus the result of diffusion limitation with a smaller contribution from VA/Q inequality and essentially none from shunting.

Mechanism of improvement in pulmonary gas exchange during growth in awake piglets

1988 ◽  
Vol 65 (3) ◽  
pp. 1055-1061 ◽  
Author(s):  
P. J. Escourrou ◽  
B. P. Teisseire ◽  
R. A. Herigault ◽  
M. O. Vallez ◽  
A. J. Dupeyrat ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Pressure Difference ◽  
Age Groups ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
Significant Difference ◽  
Arterial Po2 ◽  
And Diffusion

Previous studies have shown a lower arterial PO2 (PaO2) in infants and young animals than in adults. To investigate the mechanism of this impairment of gas exchange we studied 13 piglets from 12 to 65 days of age. Two days after instrumentation we measured the distribution of ventilation-perfusion ratios (VA/Q) by use of the multiple inert gas technique on awake animals. We showed that PaO2 is lower in young animals, increasing from 72 +/- 11.5 Torr before 2 wk to 102 Torr at 2 mo. This hypoxemia is due to an enlarged alveolar-arterial O2 pressure difference that significantly decreases with age. This impairment in gas exchange is not due to shunting (0.6 +/- 1.3%). Mean dead space (36 +/- 11%) was not related to age. Mean modes of perfusion and ventilation did not differ significantly between age groups. However, the dispersion of perfusion as expressed by its logSD decreased significantly with age, whereas dispersion of ventilation remained constant. Furthermore, in the young animals only, a significant difference was evidenced between measured alveolar-arterial PO2 gradient and the value predicted by the inert gas model. We therefore conclude that the impairment of gas exchange in piglets is due to two mechanisms: VA/Q mismatch and diffusion limitation for O2.

Pulmonary gas exchange in humans during normobaric hypoxic exercise

1986 ◽  
Vol 61 (5) ◽  
pp. 1749-1757 ◽  
Author(s):  
M. D. Hammond ◽  
G. E. Gale ◽  
K. S. Kapitan ◽  
A. Ries ◽  
P. D. Wagner
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Barometric Pressure ◽  
Normal Subjects ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
Heavy Exercise ◽  
Blood Temperature ◽  
O2 Partial Pressure ◽  
Hypoxic Exercise

Previous studies (J. Appl. Physiol. 58: 978–988 and 989–995, 1985) have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during heavy exercise at sea level and during hypobaric hypoxia in a chamber [fractional inspired O2 concentration (FIO2) = 0.21, minimum barometric pressure (PB) = 429 Torr, inspired O2 partial pressure (PIO2) = 80 Torr]. We used the multiple inert gas elimination technique to compare gas exchange during exercise under normobaric hypoxia (FIO2 = 0.11, PB = 760 Torr, PIO2 = 80 Torr) with earlier hypobaric measurements. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate (HR), minute ventilation, respiratory rate (RR), and blood temperature were recorded at rest and during steady-state exercise in 10 normal subjects in the following order: rest, air; rest, 11% O2; light exercise (75 W), 11% O2; intermediate exercise (150 W), 11% O2; heavy exercise (greater than 200 W), 11% O2; heavy exercise, 100% O2 and then air; and rest 20 minutes postexercise, air. VA/Q inequality increased significantly during hypoxic exercise [mean log standard deviation of perfusion (logSDQ) = 0.42 +/- 0.03 (rest) and 0.67 +/- 0.09 (at 2.3 l/min O2 consumption), P less than 0.01]. VA/Q inequality was improved by relief of hypoxia (logSDQ = 0.51 +/- 0.04 and 0.48 +/- 0.02 for 100% O2 and air breathing, respectively). Diffusion limitation for O2 was evident at all exercise levels while breathing 11% O2.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary gas exchange in humans exercising at sea level and simulated altitude

1986 ◽  
Vol 61 (1) ◽  
pp. 260-270 ◽  
Author(s):  
P. D. Wagner ◽  
G. E. Gale ◽  
R. E. Moon ◽  
J. R. Torre-Bueno ◽  
B. W. Stolp ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Arterial Pressure ◽  
Sea Level ◽  
Pulmonary Arterial Pressure ◽  
Minute Ventilation ◽  
Statistical Significance ◽  
Random Order ◽  
Normal Subjects ◽  
Simulated Altitude ◽  
Pulmonary Arterial

In a previous study of normal subjects exercising at sea level and simulated altitude, ventilation-perfusion (VA/Q) inequality and alveolar-end-capillary O2 diffusion limitation (DIFF) were found to increase on exercise at altitude, but at sea level the changes did not reach statistical significance. This paper reports additional measurements of VA/Q inequality and DIFF (at sea level and altitude) and also of pulmonary arterial pressure. This was to examine the hypothesis that VA/Q inequality is related to increased pulmonary arterial pressure. In a hypobaric chamber, eight normal subjects were exposed to barometric pressures of 752, 523, and 429 Torr (sea level, 10,000 ft, and 15,000 ft) in random order. At each altitude, inert and respiratory gas exchange and hemodynamic variables were studied at rest and during several levels of steady-state bicycle exercise. Multiple inert gas data from the previous and current studies were combined (after demonstrating no statistical difference between them) and showed increasing VA/Q inequality with sea level exercise (P = 0.02). Breathing 100% O2 did not reverse this increase. When O2 consumption exceeded about 2.7 1/min, evidence for DIFF at sea level was present (P = 0.01). VA/Q inequality and DIFF increased with exercise at altitude as found previously and was reversed by 100% O2 breathing. Indexes of VA/Q dispersion correlated well with mean pulmonary arterial pressure and also with minute ventilation. This study confirms the development of both VA/Q mismatch and DIFF in normal subjects during heavy exercise at sea level. However, the mechanism of increased VA/Q mismatch on exercise remains unclear due to the correlation with both ventilatory and circulatory variables and will require further study.

Influence of ventilation and hypocapnia on sympathetic nerve responses to hypoxia in normal humans

1989 ◽  
Vol 67 (5) ◽  
pp. 2095-2100 ◽  
Author(s):  
V. K. Somers ◽  
A. L. Mark ◽  
D. C. Zavala ◽  
F. M. Abboud
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inhibitory Influence ◽  
Sympathetic Response ◽  
Normal Humans ◽  
Breathing Room ◽  
Baroreceptor Activation ◽  
Voluntary Apnea

The sympathetic response to hypoxia depends on the interaction between chemoreceptor stimulation (CRS) and the associated hyperventilation. We studied this interaction by measuring sympathetic nerve activity (SNA) to muscle in 13 normal subjects, while breathing room air, 14% O2, 10% O2, and 10% O2 with added CO2 to maintain isocapnia. Minute ventilation (VE) and blood pressure (BP) increased significantly more during isocapnic hypoxia (IHO) than hypocapnic hypoxia (HHO). In contrast, SNA increased more during HHO [40 +/- 10% (SE)] than during IHO (25 +/- 19%, P less than 0.05). To determine the reason for the lesser increase in SNA with IHO, 11 subjects underwent voluntary apnea during HHO and IHO. Apnea potentiated the SNA responses to IHO more than to HHO. SNA responses to IHO were 17 +/- 7% during breathing and 173 +/- 47% during apnea whereas SNA responses to HHO were 35 +/- 8% during breathing and 126 +/- 28% during apnea. During ventilation, the sympathoexcitation of IHO (compared with HHO) is suppressed, possibly for two reasons: 1) because of the inhibitory influence of activation of pulmonary afferents as a result of a greater increase in VE, and 2) because of the inhibitory influence of baroreceptor activation due to a greater rise in BP. Thus in humans, the ventilatory response to chemoreceptor stimulation predominates and restrains the sympathetic response. The SNA response to chemoreceptor stimulation represents the net effect of the excitatory influence of the chemoreflex and the inhibitory influence of pulmonary afferents and baroreceptor afferents.

Digital Simulation of the Chemical Control of Ventilation

1973 ◽  
Vol 95 (3) ◽  
pp. 335-339
Author(s):  
H. T. Milhorn ◽  
W. J. Reynolds
Keyword(s):  
Computer Model ◽  
Respiratory System ◽  
Digital Computer ◽  
Chemical Control ◽  
Minute Ventilation ◽  
Digital Simulation ◽  
Transient Responses ◽  
O2 Concentration ◽  
Lower Oxygen ◽  
Series Of Experiments

Experimental human data, obtained for the development and evaluation of a digital computer model of the human respiratory system, are presented. The data are from two series of experiments. In the first series the transient responses of tidal volume, respiratory frequency, minute ventilation, alveolar Pco2 and alveolar Po2 were obtained for several inspired CO2 concentrations (3, 5, 6, and 7 percent). In the second series, transient responses of the same variables were obtained for steps of inspired O2 concentration from room air to several lower oxygen levels (9, 8, and 7 percent). An example of the use of the data for the development and evaluation of a model is indicated.

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