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.

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.

Effect of inspiratory resistive loading on control of ventilation during progressive exercise

1987 ◽  
Vol 62 (1) ◽  
pp. 134-140 ◽  
Author(s):  
A. D. D'Urzo ◽  
K. R. Chapman ◽  
A. S. Rebuck
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Work Load ◽  
Cycle Ergometer ◽  
Resistive Load ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Resistive Loading ◽  
End Tidal ◽  
Arterial O2 Saturation

Eight healthy volunteers performed gradational tests to exhaustion on a mechanically braked cycle ergometer, with and without the addition of an inspiratory resistive load. Mean slopes for linear ventilatory responses during loaded and unloaded exercise [change in minute ventilation per change in CO2 output (delta VE/delta VCO2)] measured below the anaerobic threshold were 24.1 +/- 1.3 (SE) = l/l of CO2 and 26.2 +/- 1.0 l/l of CO2, respectively (P greater than 0.10). During loaded exercise, decrements in VE, tidal volume, respiratory frequency, arterial O2 saturation, and increases in end-tidal CO2 tension were observed only when work loads exceeded 65% of the unloaded maximum. There was a significant correlation between the resting ventilatory response to hypercapnia delta VE/delta PCO2 and the ventilatory response to VCO2 during exercise (delta VE/delta VCO2; r = 0.88; P less than 0.05). The maximal inspiratory pressure generated during loading correlated with CO2 sensitivity at rest (r = 0.91; P less than 0.05) and with exercise ventilation (delta VE/delta VCO2; r = 0.83; P less than 0.05). Although resistive loading did not alter O2 uptake (VO2) or heart rate (HR) as a function of work load, maximal VO2, HR, and exercise tolerance were decreased to 90% of control values. We conclude that a modest inspiratory resistive load reduces maximum exercise capacity and that CO2 responsiveness may play a role in the control of breathing during exercise when airway resistance is artificially increased.

Parameters of ventilatory and gas exchange dynamics during exercise

1982 ◽  
Vol 52 (6) ◽  
pp. 1506-1513 ◽  
Author(s):  
B. J. Whipp ◽  
S. A. Ward ◽  
N. Lamarra ◽  
J. A. Davis ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Constant Load ◽  
Moderate Intensity ◽  
Second Phase ◽  
Base Line ◽  
O2 Uptake ◽  
Moderate Intensity Exercise ◽  
Exponential Behavior ◽  
Co2 Output ◽  
Nonsteady State

To determine the precise nonsteady-state characteristics of ventilation (VE), O2 uptake (VO2), and CO2 output (VCO2) during moderate-intensity exercise, six subjects each underwent eight repetitions of 100-W constant-load cycling. The tests were preceded either by rest or unloaded cycling (“0” W). An early component of VE, VO2, and VCO2 responses, which was obscured on any single test by the breath-to-breath fluctuations, became apparent when the several repetitions were averaged. These early responses were abrupt when the work was instituted from rest but were much slower and smaller from the 0-W base line and corresponded to the phase of cardiodynamic gas exchange. Some 20 s after the onset of the work a further monoexponential increase to steady state occurred in all three variables, the time constants of which did not differ between the two types of test. Consequently, the exponential behavior of VE, VO2, and VCO2 in response to moderate exercise is best described by a model that incorporates only the second phase of the response.

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.

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 and occlusion pressure responses to helium breathing

1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu
Keyword(s):  
Breathing Circuit ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Mouth Pressure ◽  
Partial Pressure Of Co2 ◽  
Lung Resistance ◽  
Balloon Technique ◽  
Resistive Loads ◽  
End Tidal ◽  
Airway Tone

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.

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.

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.

Control of breathing at the start of exercise as influenced by posture

1983 ◽  
Vol 55 (5) ◽  
pp. 1460-1466 ◽  
Author(s):  
D. Weiler-Ravell ◽  
D. M. Cooper ◽  
B. J. Whipp ◽  
K. Wasserman
Keyword(s):  
Stroke Volume ◽  
Phase I ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Initial Increase ◽  
Base Line ◽  
Co2 Output ◽  
End Tidal ◽  
Response To Exercise ◽  
Initial Change

It has been suggested that the initial phase of the ventilatory response to exercise is governed by a mechanism which responds to the increase in pulmonary blood flow (Q)--cardiodynamic hyperpnea. Because the initial change in stroke volume and Q is less in the supine (S) than in the upright (U) position at the start of exercise, we hypothesized that the increase in ventilation would also be less in the first 20 s (phase I) of S exercise. Ten normal subjects performed cycle ergometry in the U and S positions. Inspired ventilation (VI), O2 uptake (VO2), CO2 output (VCO2), corrected for changes in lung gas stores, and end-tidal O2 and CO2 tensions were measured breath by breath. Heart rate (HR) was determined beat by beat. The phase I ventilatory response was markedly different in the two positions. In the U position, VI increased abruptly by 81 +/- 8% (mean +/- SE) above base line. In the S position, the phase I response was significantly attenuated (P less than 0.001), the increase in VI being 50 +/- 6%. Similarly, the phase I VO2 and VO2/HR responses reflecting the initial increase in Q and stroke volume, were attenuated (P less than 0.001) in the S posture, compared with that for U; VO2 increased 49 +/- 5.3 and 113 +/- 14.7% in S and U, respectively, and VO2/HR increased 16 +/- 3.0 and 76 +/- 7.1% in the S and U, respectively. The increase in VI correlated well with the increase in VO2, (r = 0.80, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Immediate effects of cigarette smoking on cardiorespiratory responses to exercise

1985 ◽  
Vol 58 (6) ◽  
pp. 1975-1981 ◽  
Author(s):  
G. L. Hirsch ◽  
D. Y. Sue ◽  
K. Wasserman ◽  
T. E. Robinson ◽  
J. E. Hansen
Keyword(s):  
Gas Exchange ◽  
Cigarette Smoking ◽  
Pulse Pressure ◽  
Minute Ventilation ◽  
Cardiovascular Responses ◽  
Co2 Production ◽  
Blood Levels ◽  
Maximal Aerobic Capacity ◽  
Arterial Blood ◽  
End Tidal

To determine the acute action of cigarette smoking on cardiorespiratory function under stress, the immediate effects of cigarette smoking on the ventilatory, gas exchange, and cardiovascular responses to exercise were studied in nine healthy male subjects. Each subject performed an incremental exercise test to exhaustion on two separate days, one without smoking (control) and one after smoking 3 cigarettes/h for 5 h. The order of the two tests was randomized. Arterial blood gases and pH were measured during rest and all levels of exercise; CO blood levels confirmed the absorption of cigarette smoke. In addition, minute ventilation (VE), end-tidal PCO2 and PO2, O2 uptake (VO2), CO2 production, directly measured blood pressure, electrocardiogram, and heart rate (HR) were recorded every 30 s. The dead space-to-tidal volume ratio (VD/VT), maximal aerobic capacity (VO2max), and anaerobic threshold (AT) were determined from the gas exchange data. Cigarette smoking resulted in a significantly lower VO2max, AT, and VO2/HR (O2 pulse) and a significantly higher HR, pulse-pressure product, and pulse pressure (P less than 0.05) compared with the control. Additionally, a trend toward a higher VD/VT and arterial-end-tidal PCO2 difference was found during exercise after smoking. We conclude that cigarette smoking causes immediate detrimental effects on cardiovascular function during exercise, including tachycardia, increased pulse-pressure product, and impaired O2 delivery. The acute effects on respiratory function were less striking and primarily limited to abnormalities reflecting ventilation-perfusion mismatching.

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