Determinants of gas exchange kinetics during exercise in the dog

1979 ◽  
Vol 46 (6) ◽  
pp. 1054-1060 ◽  
Author(s):  
R. Casaburi ◽  
M. L. Weissman ◽  
D. J. Huntsman ◽  
B. J. Whipp ◽  
K. Wasserman
Keyword(s):  
Co2 Exchange ◽  
Appreciable Effect ◽  
O2 Uptake ◽  
Arterial Pco2 ◽  
Co2 Output ◽  
Exercise Onset ◽  
Anesthetized Dogs ◽  
Time Courses ◽  
End Tidal ◽  
Gas Exchange Kinetics

Following exercise onset, CO2 output (VCO2) and O2 uptake (VO2) increase exponentially, but with appreciably different time constants. To determine the sensitivity of the time courses of these variables to altered ventilatory kinetics, rhythmic exercise was induced abruptly in anesthetized dogs by bilateral stimulation of the peripheral ends of the cut sciatic and femoral nerves. This increased the metabolic rate by 83 +/- 25 (SD) %. The dogs were ventilated with a constant-volume pump, the frequency of which was changed exponentially from the start of the exercise up to the ventilation that returned arterial CO2 and O2 pressure (PCO2 and PO2) in the steady state to resting levels. The time constant (tau) of the increase in ventilation (VE) was varied among trials. VCO2, VO2, end-tidal PCO2 and PO2, and arterial PCO2 were measured breath by breath. tauVO2 was constant at approximately 18 s regardless of alterations in tauVE. In contrast, tauVCO2 was strongly dependent on tauVE, apparently due to the larger body stores for CO2; the transitions were isocapnic when tau VE was approximately 40 s. We conclude that ventilatory dynamics can markedly influence the dynamics of CO2 exchange during exercise, but has no appreciable effect on O2 uptake dynamics.

Regulation of arterial PCO2 during intravenous CO2 loading

1975 ◽  
Vol 38 (4) ◽  
pp. 651-656 ◽  
Author(s):  
K. Wasserman ◽  
B. J. Whipp ◽  
R. Casaburi ◽  
D. J. Huntsman ◽  
J. Castagna ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Response Curve ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Control Value ◽  
Co2 Output ◽  
Anesthetized Dogs ◽  
Co2 Flow ◽  
Co2 Response Curve

Increased CO2 flow to the lung produced by increasing cardiac output (with constant PVCO2) results in hyperpnea with arterial PCO2 maintained at its control value (J. Appl. Physiol. 36: 457, 1974). To study if arterial PCO2 could be similarly regulated when CO2 flow was elevated by increasing PVCO2 (without changing cardiac output), we produced graded increases in PVCO2 (up to a mean of 69 mmHg) using an extracorporeal gas exchanger in five chloralose-urethan-anesthetized dogs. CO2 output increased up to fourfold. Ventilation increased in proportion to the additional CO2 flow to the lung with consequent regulation of arterial PCO2 at its control value. Comparable increases in VE produced by “conventional” airway loading resulted in arterial hypercapnia. The resulting CO2 response curve was similar to that found in unanesthetized dogs. We conclude that intravenous delivery of CO2 to the lung results in infinite “sensitivity” when computed as Delta VE/Delta paco2. These results provide evidence for a CO2-linked hyperpnea which is not mediated by measurable increases in mean arterial PCO2.

Difference between end-tidal and arterial PCO2 in exercise

1979 ◽  
Vol 47 (5) ◽  
pp. 954-960 ◽  
Author(s):  
N. L. Jones ◽  
D. G. Robertson ◽  
J. W. Kane
Keyword(s):  
Carbon Dioxide ◽  
Carbon Dioxide Tension ◽  
Infrared Analysis ◽  
Arterial Carbon Dioxide Tension ◽  
Arterial Pco2 ◽  
Response Characteristics ◽  
Co2 Output ◽  
End Tidal Carbon Dioxide ◽  
Power Outputs ◽  
End Tidal

The relation between end-tidal carbon dioxide tension (PETCO2) measured by infrared analysis and arterial carbon dioxide tension (PaCO2) during exercise was systematically examined in five healthy adults at two power outputs (25 and 50% VO2max) and at three frequencies of breathing (15, 30, and 45 breaths/min). PETCO2-PaCO2 varied between -2.5 and +9.1 Torr, was inversely related to the frequency of breathing (r = 0.475), and directly related to tidal volume (VT; r = 0.791) and CO2 output (r = 0.627). An equation was obtained by multiple regression analysis, to predict PaCO2 from PETCO2: PaCO2 = 5.5 +0.90 PETCO2 -0.0021 VT (r = 0.915). The equation was applied to measurements of PETCO2 obtained in two previous studies in 10 subjects in which PaCO2 had been measured, and was found to predict PaCO2 to within 1.04 Torr (+/- SD) for PaCO2 between 25 and 58 Torr (n = 56; r = 0.962). The effect of the response characteristics of the CO2 analyzer on the measurement of PETCO2 was also systematically examined by comparison with a fast-responding respiratory mass spectrometer.

Hypocapnic-hypoglycemic interactions on cerebral high-energy phosphates and pH in dogs

1992 ◽  
Vol 263 (6) ◽  
pp. H1864-H1871 ◽  
Author(s):  
F. E. Sieber ◽  
S. A. Derrer ◽  
S. M. Eleff ◽  
R. C. Koehler ◽  
R. J. Traystman
Keyword(s):  
Glucose Uptake ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
O2 Uptake ◽  
Arterial Pco2 ◽  
Eeg Abnormalities ◽  
Active Regulation ◽  
Venous Pco2 ◽  
Anesthetized Dogs

With a level of hypoglycemia (1–1.5 mM) that does not alter cerebral O2 uptake and glucose uptake in dogs, induction of hypocapnia may cause severe electroencephalographic (EEG) abnormalities. The aim of this study was to determine the effect of hypoglycemia (blood glucose = 1.1 +/- 0.1 mM) and hypocapnia (arterial PCO2 = 15 +/- 1 mmHg) on cerebral ATP, phosphocreatine, and intracellular pH (pHi; 31P magnetic resonance spectroscopy), cerebral blood flow (CBF; radiolabeled microspheres), global O2 uptake, and glucose uptake in anesthetized dogs. Neither hypoglycemia nor hypocapnia alone altered brain high-energy phosphates, pHi, O2 or glucose uptake or caused major EEG abnormalities. Hypocapnia alone decreased CBF to 62 +/- 4% of control. The combination of hypoglycemia and hypocapnia did not decrease CBF (85 +/- 6% of control), and O2 and glucose uptake were unchanged. During hypocapnic hypoglycemia, isoelectric EEG was seen in 40% of animals, ATP and phosphocreatine decreased to 38 +/- 12 and 43 +/- 12% of control, respectively, while pHi increased from 7.13 +/- 0.05 to 7.43 +/- 0.09. The increase in pHi was related reciprocally to the decrease in venous PCO2, indicating little change in intracellular bicarbonate concentration ([HCO3-]i). With normoglycemic hypocapnia, in contrast, estimated [HCO3-]i decreased 57 +/- 1%. These data suggest that active regulation of pHi during normoglycemic hypocapnia is impaired during hypoglycemic hypocapnia associated with decreased ATP.

Role of VCO2 in control of breathing of awake exercising dogs

1984 ◽  
Vol 56 (5) ◽  
pp. 1335-1339 ◽  
Author(s):  
F. M. Bennett ◽  
R. D. Tallman ◽  
F. S. Grodins
Keyword(s):  
Directional Statistics ◽  
Direct Signal ◽  
Arterial Pco2 ◽  
Average Decrease ◽  
Ventilatory Responses ◽  
Co2 Output ◽  
Exercise Hyperpnea ◽  
Co2 Flow ◽  
End Tidal

Steady-state ventilatory responses to CO2 inhalation, intravenous CO2 loading (loading), and intravenous CO2 unloading (unloading) were measured in chronic awake dogs while they exercised on an air-conditioned treadmill at 3 mph and 0% grade. End-tidal PO2 was maintained at control levels by manipulation of inspired gas. Responses obtained in three dogs demonstrated that the response to CO2 loading [average increase in CO2 output (Vco2) of 216 ml/min or 35%] was a hypercapnic hyperpnea in every instance. Also, the response to CO2 unloading [average decrease in Vco2 of 90 ml/min or 15% decrease] was a hypocapnic hypopnea in every case. Also, the analysis of the data by directional statistics indicates that there was no difference in the slopes of the responses (change in expiratory ventilation divided by change in arterial Pco2) for loading, unloading, and inhalation. These results indicate that the increased CO2 flow to the lung that occurs in exercise does not provide a direct signal to the respiratory controller that accounts for the exercise hyperpnea. Therefore, other mechanisms must be important in the regulation of ventilation during exercise.

Gas-to-blood PCO2 differences during severe hypercapnia

1979 ◽  
Vol 47 (1) ◽  
pp. 67-71 ◽  
Author(s):  
G. H. Gurtner ◽  
R. J. Traystman
Keyword(s):  
Blood Cells ◽  
Carbonic Acid ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Charged Membrane ◽  
Intracellular Compartments ◽  
Anesthetized Dogs ◽  
The Mean ◽  
End Tidal

Five anesthetized dogs were made severely hypercapnic by stepwise addition of CO2 to their inspired air. Blood PCO2 levels greater than 400 Torr were reached. During hypercapnia, the steady-state end-tidal PCO2 (PaCO2) was always higher than the simultaneous measured arterial PCO2 (PaCO2). The mean ratio PaCO2/PACO2 was 0.861 +/- 0.01. These results are consistent with the predictions of the Charged Membrane Hypothesis, that gas-to-blood PCO2 differences should be directly proportional to the blood H+ activity. The results cannot be explained by delayed equilibration of CO2 between plasma and red blood cells. The latter hypothesis predicts that, under the conditions of these experiments, the PCO2 of arterial blood should be higher than the PCO2 of end-tibal gas. The blood HCO3- during hypercapnia did not increase as much as would be predicted if the blood were exposed to CO2 in vitro. This may reflect movement of blood HCO3- generated by the buffering of carbonic acid into intracellular compartments during hypercapnia.

scholarly journals Relationship between hyperventilation and excessive CO2 output during recovery from repeated cycling sprints

2009 ◽  
pp. 529-535 ◽  
Author(s):  
T Yano ◽  
T Yunoki ◽  
R Matsuura ◽  
T Arimitsu
Keyword(s):  
Blood Lactate ◽  
O2 Uptake ◽  
Repeated Cycle ◽  
Passive Recovery ◽  
Co2 Output ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Repeated Cycling

The purpose of the present study was to examine whether excessive CO2 output (VCO2excess) is dominantly attributable to hyperventilation during the period of recovery from repeated cycling sprints. A series of four 10-sec cycling sprints with 30-sec passive recovery periods was performed two times. The first series and second series of cycle sprints (SCS) were followed by 360-sec passive recovery periods (first recovery and second recovery). Increases in blood lactate (DeltaLa) were 11.17+/-2.57 mM from rest to 5.5 min during first recovery and 2.07+/-1.23 mM from the start of the second SCS to 5.5 min during second recovery. CO2 output (VCO2) was significantly higher than O2 uptake (VO2) during both recovery periods. This difference was defined as VCO2excess. VCO2excess was significantly higher during first recovery than during second recovery. VCO2excess was added from rest to the end of first recovery and from the start of the second SCS to the end of second recovery (CO2excess). DeltaLa was significantly related to CO2excess (r=0.845). However, ventilation during first recovery was the same as that during second recovery. End-tidal CO2 pressure (PETCO2) significantly decreased from the resting level during the recovery periods, indicating hyperventilation. PETCO2 during first recovery was significantly higher than that during second recovery. It is concluded that VCO2excess is not simply determined by ventilation during recovery from repeated cycle sprints.

Effect of interbreath fluctuations on characterizing exercise gas exchange kinetics

1987 ◽  
Vol 62 (5) ◽  
pp. 2003-2012 ◽  
Author(s):  
N. Lamarra ◽  
B. J. Whipp ◽  
S. A. Ward ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Least Squares ◽  
Kinetic Parameters ◽  
Nonlinear Least Squares ◽  
Cycle Ergometer ◽  
Gaussian Stochastic Process ◽  
Co2 Output ◽  
Nonsteady State ◽  
Exchange Kinetics ◽  
Gas Exchange Kinetics

Breathing has inherent irregularities that produce breath-to-breath fluctuations (“noise”) in pulmonary gas exchange. These impair the precision of characterizing nonsteady-state gas exchange kinetics during exercise. We quantified the effects of this noise on the confidence of estimating kinetic parameters of the underlying physiological responses and hence of model discrimination. Five subjects each performed eight transitions from 0 to 100 W on a cycle ergometer. Ventilation, CO2 output, and O2 uptake were computed breath by breath. The eight responses were interpolated uniformly, time aligned, and averaged for each subject; and the kinetic parameters of a first-order model (i.e., the time constant and time delay) were then estimated using three methods: linear least squares, nonlinear least squares, and maximum likelihood. The breath-by-breath noise approximated an uncorrelated Gaussian stochastic process, with a standard deviation that was largely independent of metabolic rate. An expression has therefore been derived for the number of square-wave repetitions required for a specified parameter confidence using methods b and c; method a being less appropriate for parameter estimation of noisy gas exchange kinetics.

Ventilatory control during experimental maldistribution of VA/Q in the dog

1982 ◽  
Vol 52 (1) ◽  
pp. 245-253 ◽  
Author(s):  
C. E. Juratsch ◽  
B. J. Whipp ◽  
D. J. Huntsman ◽  
M. M. Laks ◽  
K. Wasserman
Keyword(s):  
Steady State ◽  
Early Phase ◽  
Main Pulmonary Artery ◽  
State Regulation ◽  
Balloon Inflation ◽  
Peripheral Chemoreceptors ◽  
Arterial Pco2 ◽  
Bilateral Carotid ◽  
End Tidal ◽  
Transient Elevation

To determine the role of the peripheral chemoreceptors in mediating the hyperpnea associated with acute, nonocclusive inflation of a balloon in the main pulmonary artery of the conscious dog, we performed balloon inflations in awake and lightly anesthetized (chloralose-urethan) dogs before and after a) bilateral carotid body resection (CBR), b) cervical vagotomy (V), and c) after both CBR and V. In the intact awake state, balloon inflation increased VE from a mean of 4.91 to 7.16 1/min, usually within 1.5–2.0 min. Mean arterial PO2 decreased from 82 to 71 Torr and end-tidal PCO2 was reduced by 6 Torr. Arterial PCO2 and pH were unchanged in the steady state (as evidenced by discrete blood samples), even in those dogs in which VE increased up to 7.5 1/min. However, an indwelling PCO2 electrode in the femoral artery demonstrated a consistent transient elevation of arterial PCO2 prior to the steady state regulation. Vagotomy alone did not impair the ability to regulate PCO2 during balloon inflation. In some cases with CBR alone, arterial PCO2 was regulated at control levels in the steady state, but the transient increase during the early phase of balloon inflation was more marked (mean increase, 2 Torr). We conclude that the peripheral chemoreceptors are responsible for a significant component of the dynamic ventilatory behavior during this early phase (1.5–2.0 min) of acute maldistribution of VA/Q.

Infrared end-tidal CO2 measurement does not accurately predict arterial CO2 values or end-tidal to arterial PCO2, gradients in rabbits with lung injury

1994 ◽  
Vol 17 (3) ◽  
pp. 189-196 ◽  
Author(s):  
Andrew O. Hopper ◽  
Gerald A. Nystrom ◽  
Douglas D. Deming ◽  
Wesley R. Brown ◽  
Joyce L. Peabody
Keyword(s):  
Lung Injury ◽  
Arterial Pco2 ◽  
End Tidal ◽  
End Tidal Co2

Gas exchange in nonperfused dog lungs

1981 ◽  
Vol 51 (5) ◽  
pp. 1261-1267 ◽  
Author(s):  
J. W. Shepard ◽  
V. D. Minh ◽  
G. F. Dolan
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Left Lung ◽  
Co2 Concentration ◽  
Gas Transfer ◽  
O2 Uptake ◽  
Tissue Metabolism ◽  
End Tidal

Gas exchange was studied under conditions of zero perfusion both in situ and in vitro. Six dogs, anesthetized with pentobarbital sodium, underwent surgical interruption of both pulmonary and bronchial circulations to the left lung. Despite the absence of perfusion, O2 uptake for the left lung ranged from 0.76 to 0.98 ml/min, whereas CO2 elimination greatly exceeded O2 uptake ranging from 1.68 to 4.34 ml/min. In addition, CO2 output was observed to vary directly with the level of minute ventilation (VE) and inversely with end-tidal CO2 concentration. To investigate the mechanisms responsible for these findings we studied 20 excised, ventilated, but nonperfused dog lungs to evaluate the relative roles of tissue metabolism and transpleural diffusion to gas exchange. The results obtained with these excised lungs under conditions of varying VE and extrapleural gas concentrations indicate that the high respiratory exchange ratios observed in situ can be explained by the greater rate with which CO2 diffuses through the pleura, and that reduced ventilation decreases total gas transfer by decreasing the transpleural partial pressure driving gradient. Our data further document that the concentration of CO2 in alveolar gas may differ significantly from that present in inspired gas under conditions of ventilation-perfusion ratio equal to infinity, and that tissue metabolism as well as transpleural diffusion contribute to gas exchange in nonperfused lung.

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