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.

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.

scholarly journals Pulmonary gas exchange during exercise in pigs

1999 ◽  
Vol 86 (1) ◽  
pp. 93-100 ◽  
Author(s):  
S. R. Hopkins ◽  
C. M. Stary ◽  
E. Falor ◽  
H. Wagner ◽  
P. D. Wagner ◽  
...  
Keyword(s):  
Animal Model ◽  
Treadmill Exercise ◽  
Systematic Difference ◽  
Inert Gases ◽  
Inert Gas ◽  
Blood Gas ◽  
Diffusion Limitation ◽  
Heavy Exercise ◽  
Direct Examination ◽  
Pig Animal Model

Increased ventilation-perfusion (V˙a/Q˙) inequality is observed in ∼50% of humans during heavy exercise and contributes to the widening of the alveolar-arterial O2 difference (A-[Formula: see text]). Despite extensive investigation, the cause remains unknown. As a first step to more direct examination of this problem, we developed an animal model. Eight Yucatan miniswine were studied at rest and during treadmill exercise at ∼30, 50, and 85% of maximal O2 consumption (V˙o 2 max). Multiple inert-gas, blood-gas, and metabolic data were obtained. The A-[Formula: see text]increased from 0 ± 3 (SE) Torr at rest to 14 ± 2 Torr during the heaviest exercise level, but arterial[Formula: see text]([Formula: see text]) remained at resting levels during exercise. There was normalV˙a/Q˙inequality [log SD of the perfusion distribution (log[Formula: see text]) = 0.42 ± 0.04] at rest, and moderate increases (log[Formula: see text] = 0.68 ± 0.04, P < 0.0001) were observed with exercise. This result was reproducible on a separate day. TheV˙a/Q˙inequality changes are similar to those reported in highly trained humans. However, in swine, unlike in humans, there was no inert gas evidence for pulmonary end-capillary diffusion limitation during heavy exercise; there was no systematic difference in the measured[Formula: see text] and the[Formula: see text] as predicted from the inert gases. These data suggest that the pig animal model is well suited for studying the mechanism of exercise-inducedV˙a/Q˙inequality.

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)

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)

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.

Free dopamine in dog plasma: lack of relationship with sympathoadrenal activity

1985 ◽  
Vol 58 (3) ◽  
pp. 763-769 ◽  
Author(s):  
J. M. Pequignot ◽  
R. Favier ◽  
D. Desplanches ◽  
L. Peyrin ◽  
R. Flandrois
Keyword(s):  
Treadmill Exercise ◽  
Activity Levels ◽  
O2 Uptake ◽  
Arterial Partial Pressure ◽  
Combined Exercise ◽  
Dog Plasma ◽  
Sympathoadrenal Activity ◽  
Submaximal Work ◽  
Exercise Induced ◽  
The Relationship

To investigate the relationship between dopamine (DA) released into the bloodstream and sympathoadrenal activity, levels of free DA, norepinephrine (NE), and epinephrine (E) in plasma were recorded in four dogs subjected to three tests: treadmill exercise at two work levels [55 and 75% maximal O2 uptake; 15 min], normobaric hypoxia (12% O2; 1 h), combined exercise and hypoxia. Normoxic exercise induced slight nonsignificant decreases in the arterial partial pressure of O2 (PaO2), increases in NE [median values and ranges during submaximal work vs. rest: 1086 (457–1,637) vs. 360 (221–646) pg/ml; P less than 0.01] and E [277 (151–461) vs. 166 (95–257) pg/ml; P less than 0.05], but it failed to alter the DA level. Hypoxia elicited large decreases in PaO2 [hypoxia vs. normoxia: 42.8 (40.3–50.0) vs. 97.6 (83.2–117.6) Torr; P less than 0.01], increases in DA [230 (105–352) vs. 150 (85–229) pg/ml; P less than 0.01] and NE [383 (219–1,165) vs. 358 (210–784) pg/ml; P less than 0.05], but it failed to alter the E level. Combined exercise and hypoxia further increased NE levels but did not alter the DA response to hypoxia alone. The data indicate that free DA in plasma may vary independently of the sympathoadrenal activity.

Circulatory response to arterial hyperoxia

1979 ◽  
Vol 46 (5) ◽  
pp. 973-977 ◽  
Author(s):  
Y. Cassuto ◽  
L. E. Farhi
Keyword(s):  
Cardiac Output ◽  
Lactic Acidosis ◽  
The Other ◽  
O2 Uptake ◽  
Right Heart ◽  
Arterial Pco2 ◽  
Circulatory Response ◽  
Systemic Artery ◽  
The Right ◽  
Arterial Po2

We have studied the circulatory response to 100% O2 at 1 and 3 atm, using unanesthetized rabbits in which a systemic artery and the right heart had been cannulated previously. One group of animals served as controls; the other was infused with a flurocarbon emulsion that boosted blood O2 solubility to approximately 5 ml.100 ml-1.atm-1. Exposure to hyperoxia caused an identical sustained rise in arterial PO2 in both groups. O2 uptake was measured during normobaric exposure to 100% O2 and was found to be the same as in control conditions. There was an immediate rise in right heart PO2, more marked in infused animals, but this increase was only temporary, and PO2 dropped, while the right heart-arterial PCO2 difference rose, indicating a gradual fall in cardiac output. This readjustment occurred at a faster rate in the infused animals, a difference that led us to conclude that the peripheral response to hyperoxia is influenced by factors other than arterial PO2. The pronounced decrease in cardiac output seen in infused rabbits was accompanied by lactic acidosis, implying that some of the animals' tissues were becoming hypoxic in the presence of arterial hyperoxia.

Ventilation-perfusion inequality during normoxic and hypoxic exercise in the emu

2002 ◽  
Vol 93 (6) ◽  
pp. 1980-1986 ◽  
Author(s):  
P. M. Schmitt ◽  
F. L. Powell ◽  
S. R. Hopkins
Keyword(s):  
Cardiac Output ◽  
Standard Deviation ◽  
Treadmill Exercise ◽  
Hypoxic Condition ◽  
Avian Species ◽  
Inert Gas ◽  
Intrapulmonary Shunt ◽  
The Stability ◽  
Hypoxic Exercise

Many avian species exhibit an extraordinary ability to exercise under hypoxic condition compared with mammals, and more efficient pulmonary O2 transport has been hypothesized to contribute to this avian advantage. We studied six emus ( Dromaius novaehollandaie, 4–6 mo old, 25–40 kg) at rest and during treadmill exercise in normoxia and hypoxia (inspired O2 fraction ≈ 0.13). The multiple inert gas elimination technique was used to measure ventilation-perfusion (V˙/Q˙) distribution of the lung and calculate cardiac output and parabronchial ventilation. In both normoxia and hypoxia, exercise increased arterial Po 2 and decreased arterial Pco 2, reflecting hyperventilation, whereas pH remained unchanged. The V˙/Q˙ distribution was unimodal, with a log standard deviation of perfusion distribution = 0.60 ± 0.06 at rest; this did not change significantly with either exercise or hypoxia. Intrapulmonary shunt was <1% of the cardiac output in all conditions. CO2 elimination was enhanced by hypoxia and exercise, but O2 exchange was not affected by exercise in normoxia or hypoxia. The stability of V˙/Q˙ matching under conditions of hypoxia and exercise may be advantageous for birds flying at altitude.

Cardiac output of dogs exercising in the heat

1984 ◽  
Vol 247 (1) ◽  
pp. R124-R126
Author(s):  
L. W. Chapman ◽  
M. A. Baker
Keyword(s):  
Cardiac Output ◽  
Ambient Temperature ◽  
High Ambient Temperature ◽  
Moderate Exercise ◽  
Heavy Exercise ◽  
Blood Temperature ◽  
Cool Conditions

We measured cardiac output and central blood temperature in five large dogs (27 kg mean body wt) running at 7.5 km/h for 30 min at two work loads and at low and high ambient temperature (Ta). Each animal ran on a level treadmill (O2 cost about 4 times that of resting) at 25 and 35 degrees C Ta and at a 20% slope (O2 cost about 10 times that of resting) at 25 and 35 degrees C Ta. Cardiac output (CO) was the same at 15 and 30 min of exercise at both work loads and both TaS. CO was higher at 35 degrees C Ta at both work loads. Blood temperature rose 0.6 degrees C during exercise on the level treadmill at 25 degrees C and stabilized after the 15th min of exercise. On the level treadmill at 35 degrees C, blood temperature increased by 1.9 degrees C after 30 min. During 30 min of running at 20% slope, blood temperature increased by 3.2 degrees C at 25 degrees C and by 4.6 degrees C at 35 degrees C. At these work loads the dog is able to increase CO during exercise in the heat. This response is similar to that of humans doing moderate exercise in the heat but is in contrast to that of humans doing heavy exercise in the heat, in whom CO shows a drop or no change compared with cool conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial blood flow during exercise after gradual coronary occlusion in the dog

1983 ◽  
Vol 245 (1) ◽  
pp. H131-H138 ◽  
Author(s):  
R. J. Bache ◽  
J. S. Schwartz
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Occlusion ◽  
Treadmill Exercise ◽  
Radioactive Microspheres ◽  
Heavy Exercise ◽  
Normal Response ◽  
Exercise Load ◽  
Exercise Induced ◽  
Severe Degree

Myocardial blood flow was studied with radioactive microspheres in 14 dogs 1 mo after placement of an Ameroid constrictor on either the left circumflex or the left anterior descending coronary artery to result in total coronary occlusion without myocardial infarction, as well as in 7 normal control dogs. Measurements were performed during quiet resting conditions and during two levels of treadmill exercise to achieve heart rates of approximately 180 (light exercise) and 230 beats/min (heavy exercise). During resting conditions myocardial blood flow in the collateral-dependent area was normal in all dogs. Three different patterns of response occurred during treadmill exercise in the animals with coronary occlusion. In five dogs, both the volume and transmural distribution of myocardial blood flow behaved similarly to the normal dogs at both exercise levels. In five dogs, blood flow behaved normally during light exercise, but during heavy exercise a transmural redistribution of perfusion occurred in the collateralized area to result in subendocardial underperfusion. Finally, in four dogs even light exercise resulted in subendocardial underperfusion in the collateral-dependent area, whereas further increasing the exercise load resulted in an actual decrease of subendocardial blood flow below the resting level. These data demonstrated that although resting myocardial blood flow was normal in the collateral-dependent area 1 mo after Ameroid implantation, a markedly heterogeneous response occurred during exercise, ranging from a completely normal response to a severe degree of exercise-induced subendocardial underperfusion.

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