Ventilatory Response to Exercise and to Co2 Rebreathing in Normal Subjects

1972 ◽  
Vol 43 (6) ◽  
pp. 861-867 ◽  
Author(s):  
A. S. Rebuck ◽  
N. L. Jones ◽  
E. J. M. Campbell
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
O2 Uptake ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Progressive Exercise ◽  
Response To Exercise ◽  
Rebreathing Method ◽  
Ventilatory Response To Co2

1. Changes in ventilation during progressive exercise were measured in eleven normal subjects. Ventilatory response to carbon dioxide at rest was measured in the same subjects using a rebreathing method. 2. The range of ventilatory response to exercise was 16·6–32·0 litres min−1 (litres CO2 min−1)−1 (mean 22·7; SD 5·35); response to O2 uptake was 17·0–43·9 litres min−1 (litres O2 min−1)−1 (mean 29·02; SD 9·07). Ventilatory response to CO2 (Sco2) ranged from 0·81 to 3·22 litre min−1 mmHg−1 (mean 1·87; SD 0·62). 3. There was a highly significant (P < 0·001) correlation between the changes in response to increasing CO2 output or O2 uptake, and Sco2. 4. The results are compatible with the suggestion that ventilation during exercise in normal subjects is directly related to their chemosensitivity to CO2, those having the highest sensitivity showing the greatest exercise ventilation.

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)

Patterns of Ventilatory Response to Carbon Dioxide during Recovery from Severe Asthma

1971 ◽  
Vol 41 (1) ◽  
pp. 13-21 ◽  
Author(s):  
A. S. Rebuck ◽  
John Read
Keyword(s):  
Carbon Dioxide ◽  
Lower Limit ◽  
Severe Asthma ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Normal Range ◽  
Clinical Recovery ◽  
Time Of Presentation ◽  
Ventilatory Response To Co2

1. Ventilatory response to CO2 was measured regularly by a rebreathing technique in nineteen patients with severe asthma from the day of presentation to the time of clinical recovery. 2. Ventilatory response to CO2 increased during recovery in sixteen patients and the increased ventilatory response correlated well with increase of FEV1. Among these sixteen patients only one showed elevation of arterial CO2 tension at the time of presentation. 3. Ventilatory response to CO2 failed to increase during recovery in three patients despite increases in FEV1. All three patients showed elevation of arterial CO2 tension at the time of presentation. 4. In five patients (including three of the four with initial hypercapnia) ventilatory response to CO2 after recovery remained below the previously reported lower limit for normal subjects. The limits of normality were explored by examining ventilatory response to CO2 in seventeen outstanding athletic performers. Values for ventilatory response to CO2 both above and below the previously defined ‘normal range’ were found. The normal ventilatory response to CO2 covers a 14-fold range from 0.57 to 8.17 1 min−1 mmHg−1Pco2.

The Ventilatory Response to CO2 of Patients with Diffuse Pulmonary Infiltrations or Fibrosis

1972 ◽  
Vol 43 (1) ◽  
pp. 55-69 ◽  
Author(s):  
J. M. S. Patton ◽  
S. Freedman
Keyword(s):  
Ventilatory Response ◽  
Normal Subjects ◽  
Work Rate ◽  
Mechanical Work ◽  
Respiratory Response ◽  
Co2 Sensitivity ◽  
Venous Pco2 ◽  
Pulmonary Infiltration ◽  
Rebreathing Method ◽  
Ventilatory Response To Co2

1. We have used the rebreathing method to examine the respiratory response to CO2 in five normal subjects and twelve patients with diffuse pulmonary infiltration or fibrosis. The response to CO2 was measured in terms of both ventilation and mechanical work rate. 2. The response to CO2 was, on average, reduced in the patients compared with the normals but the patients had to perform more mechanical work to achieve a given level of ventilation. 3. Six patients had an abnormally low resting mixed venous Pco2 and four of these also had an abnormally low response to CO2. 4. The pattern of breathing was identical in patients and normals. 5. The results indicate that the reduced ventilatory response represents a true loss of CO2 sensitivity and is not simply due to mechanical limitation; but the paradox in some patients of resting hyperventilation and a low level of CO2 responsiveness is unexplained.

Hypoxic ventilatory response and arterial desaturation during heavy work

1989 ◽  
Vol 67 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie
Keyword(s):  
Maximal Exercise ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Ideal Gas ◽  
Respiratory Drive ◽  
O2 Uptake ◽  
Arterial Blood ◽  
Arterial Desaturation ◽  
Exercise Ventilation ◽  
Arterial O2 Saturation

Arterial desaturation in athletes during intense exercise has been reported by several authors, yet the etiology of this phenomenon remains obscure. Inadequate pulmonary ventilation, due to a blunted respiratory drive, has been implicated as a factor. To investigate the relationship between the ventilatory response to hypoxia, exercise ventilation, and arterial desaturation, 12 healthy male subjects [age, 23.8 +/- 3.6 yr; height, 181.6 +/- 5.6 cm; weight, 73.7 +/- 6.2 kg; and maximal O2 uptake (VO2max), 63.0 +/- 2.2 ml.kg-1 min-1] performed a 5-min treadmill test at 100% of VO2max, during which arterial blood samples and ventilatory data were collected every 15 s. Alveolar PO2 (PAO2) was determined using the ideal gas equation. On a separate occasion the ventilatory response to isocapnic hypoxia was measured. Arterial PO2 decreased by an average of 29 Torr during the test, associated with arterial desaturation [arterial O2 saturation (SaO2) 92.0%]. PAO2 was maintained; however, alveolar-arterial gas pressure difference increased progressively to greater than 40 Torr. Minimal hypocapnia was observed, despite marked metabolic acidosis. There was no significant correlation observed between hypoxic drives and ventilation-to-O2 uptake ratio or SaO2 (r = 0.1 and 0.06, respectively, P = NS). These data support the conclusions that hypoxic drives are not related to maximal exercise ventilation or to the development of arterial desaturation during maximal exercise.

Effect of obesity on ventilatory adjustment to exercise

1963 ◽  
Vol 18 (1) ◽  
pp. 19-24 ◽  
Author(s):  
J. Howland Auchincloss ◽  
John Sipple ◽  
Robert Gilbert
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Treadmill Exercise ◽  
Ventilatory Response ◽  
Carbon Dioxide Production ◽  
Exercise Ventilation ◽  
Expired Gas ◽  
Obese Subjects ◽  
Oxygen Tensions ◽  
Alveolar Oxygen

The ventilatory response to treadmill exercise was studied in normal and obese subjects, with an analysis of both the steady and unsteady states of exercise. Ventilation, oxygen consumption, carbon dioxide production, respiratory quotient, and alveolar and mixed expired gas concentrations were measured directly or computed. During the steady state of exercise obese subjects increased their ventilation sufficiently to maintain normal alveolar carbon dioxide tensions. During the first 2 min of exercise hypoventilation was more pronounced in obese subjects and in certain individuals resulted in mild reductions in alveolar oxygen tensions. Obese individuals exercised less efficiently than nonobese as manifested by excessive energy expenditure in relation to weight. Steady-state exercise PaCoCo2 values were higher in those subjects previously shown to be relatively insensitive to inhalation of 5% CO2 but failed to correlate with the speed of ventilatory responsiveness.

The effect of Airway Anaesthesia on the Control of Breathing and the Sensation of Breathlessness in Man

1985 ◽  
Vol 68 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
S. A. Shea ◽  
C. Knott ◽  
A. Guz
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Cough Reflex ◽  
Before And After ◽  
Median Diameter ◽  
Receptor Block ◽  
Normal Man ◽  
End Tidal ◽  
Ventilatory Response To Co2

1. The effect on ventilation of airway anaesthesia, produced by the inhalation of a 5% bupivacaine aerosol (aerodynamic mass median diameter = 4.77 μm), was studied in 12 normal subjects. 2. The dose and distribution of the aerosol were determined from lung scans after the addition to bupivacaine of 99mTc. Bupivacaine labelled in this way was deposited primarily in the central airways. The effectiveness and duration of airway anaesthesia were assessed by the absence of the cough reflex to the inhalation of three breaths of a 5% citric acid aerosol. Airway anaesthesia always lasted more than 20 min. 3. Resting ventilation was measured, by respiratory inductance plethysmography, before and after inhalation of saline and bupivacaine aerosols. The ventilatory response to maximal incremental exercise and, separately, to CO2 inhalation was studied after the inhalation of saline and bupivacaine aerosols. Breathlessness was quantified by using a visual analogue scale (VAS) during a study and by questioning on its completion. 4. At rest, airway anaesthesia had no effect on mean tidal volume (VT), inspiratory time (Ti), expiratory time (Te) or end-tidal Pco2, although the variability of tidal volume was increased. On exercise, slower deeper breathing was produced and breathlessness was reduced. The ventilatory response to CO2 was increased. 5. The results suggest that stretch receptors in the airways modulate the pattern of breathing in normal man when ventilation is stimulated by exercise; their activation may also be involved in the genesis of the associated breathlessness. 6. A hypothesis in terms of a differential airway/alveolar receptor block, is proposed to explain the exaggerated ventilatory response to CO2.

Luft's syndrome: O2 cost of exercise and chemical control of breathing

1975 ◽  
Vol 39 (5) ◽  
pp. 857-859 ◽  
Author(s):  
N. H. Edelman ◽  
T. V. Santiago ◽  
H. L. Conn
Keyword(s):  
Chemical Control ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Control Of Breathing ◽  
O2 Consumption ◽  
Arterial Blood ◽  
Skeletal Muscle Mitochondria ◽  
Ventilatory Response To Co2

The oxygen cost of exercise and chemical control of breathing were studied in a subject with Luft's syndrome, a disorder in which skeletal muscle mitochondria have a high “resting” O2 consumption which is imcreased only slightly by stimulation with excess phosphate acceptor, but a normal P/O ratio. The O2 consumption was more than three times normal (1.05 1/min) at rest but could be doubled when stimulated by maximal exercise. The O2 cost of exercise was similar to that of normal subjects. At rest, arterial blood PCO2 and ventilatory response to CO2 were normal, while ventilatory response to hypoxia was four times the predicted value. The data 1) confirm, in vivo, the normal respiratory efficiency of skeletal muscles in this disorder; 2) suggest that in vitro estimates of the extent to which mitochondrial respiration can be stimulated may not correlate with in vivo determinations; and 3) suggests that hypermetabolism per se can cause the ventilatory adjustments which are associated with exercise in normal subjects.

Effect of endurance exercise training on ventilatory function in older individuals

1985 ◽  
Vol 58 (3) ◽  
pp. 791-794 ◽  
Author(s):  
J. E. Yerg ◽  
D. R. Seals ◽  
J. M. Hagberg ◽  
J. O. Holloszy
Keyword(s):  
Endurance Training ◽  
Maximal Exercise ◽  
Ventilatory Response ◽  
Submaximal Exercise ◽  
Older Individuals ◽  
Ventilatory Function ◽  
O2 Uptake ◽  
Exercise Ventilation ◽  
Ventilatory Equivalent ◽  
Sedentary Subjects

To evaluate the effect of endurance training on ventilatory function in older individuals, 1) 14 master athletes (MA) [age 63 +/- 2 yr (mean +/- SD); maximum O2 uptake (VO2max) 52.1 +/- 7.9 ml . kg-1 . min-1] were compared with 14 healthy male sedentary controls (CON) (age 63 +/- 3 yr; VO2max of 27.6 +/- 3.4 ml . kg-1 . min-1), and 2) 11 sedentary healthy men and women, age 63 +/- 2 yr, were reevaluated after 12 mo of endurance training that increased their VO2max 25%. MA had a significantly lower ventilatory response to submaximal exercise at the same O2 uptake (VE/VO2) and greater maximal voluntary ventilation (MVV), maximal exercise ventilation (VEmax), and ratio of VEmax to MVV than CON. Except for MVV, all of these parameters improved significantly in the previously sedentary subjects in response to training. Hypercapnic ventilatory response (HCVR) at rest and the ventilatory equivalent for CO2 (VE/VCO2) during submaximal exercise were similar for MA and CON and unaffected by training. We conclude that the increase in VE/VO2 during submaximal exercise observed with aging can be reversed by endurance training, and that after training, previously sedentary older individuals breathe at the same percentage of MVV during maximal exercise as highly trained athletes of similar age.

The Ventilatory Response to CO2 after Administration of Frusemide in Normal Man

1972 ◽  
Vol 43 (1) ◽  
pp. 47-54 ◽  
Author(s):  
H. W. Iff ◽  
D. C. Flenley
Keyword(s):  
Ventilatory Response ◽  
Normal Subjects ◽  
Oxygen Balance ◽  
Co2 Response ◽  
Small Shift ◽  
Normal Man ◽  
Slight Rise ◽  
End Tidal ◽  
The Right ◽  
Ventilatory Response To Co2

1. We have determined the ventilatory response to CO2 inhaled in 30% oxygen (balance nitrogen) in eight normal subjects (1) before and during 4 days of 80 mg of oral frusemide daily and (2) within 55–75 min of 80 mg of frusemide orally. 2. Over 4 days the drug decreased serum potassium concentrations, but increased end tidal (and arterial) Pco2 and serum bicarbonate, thus inducing a mild metabolic alkalosis with an appropriate but small shift in CO2 response to the right without a significant change in the slope of the response. The CO2 response was unaltered by oral frusemide 55–75 min earlier. 3. This slight rise in Pco2 during 4 days of frusemide therapy contrasts with the absence of rise in Pco2 after treatment with thiazide diuretics, as reported by others. 4. We discuss possible implications of these results for the selection of an appropriate diuretic in patients with CO2 retention at various phases of their illness.

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.

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