Respiratory oscillations in arterial carbon dioxide tension as a control signal in exercise

Band, D. M.; Wolff, Christopher B.; Ward, Jane; Cochrane, G. M.; Prior, J G

doi:10.1038/283084a0

Cited by 61 publications

(40 citation statements)

References 2 publications

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“…The information which Yamamoto (1960) Band, Wolff, Ward, Cochrane & Prior (1980) showed, (at least for one subject), that this information can reach the arterial blood stream in the form of P.,co2 oscillations. The P. Co3 oscillation rate of change increased as expected from the alveolar gas studies reported here.…”

Section: Methodsmentioning

confidence: 99%

The rate of rise of alveolar carbon dioxide pressure during expiration in man.

Cochrane¹,

Newstead²,

Nowell³

et al. 1982

The Journal of Physiology

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SUMMARY1. The purpose of the study was to see whether the rate of rise of alveolar Pco, (PA, co2) in expiration was directly proportional to the rate of pulmonary elimination of C02 ( Vco2) in man in the steady state.2. Alveolar ventilation at rest and during exercise in man was calculated from the difference between total ventilation and dead space ventilation, and from the ratio of the rate of pulmonary C02 elimination to the mean expired alveolar C02 (total) fraction. The results were indistinguishable. In agreement with other workers' findings alveolar ventilation changed in direct proportion to the rate of carbon dioxide elimination, confirming the isocapnia of exercise ventilation in man.3. The rate of rise of expiratory alveolar PCO2 in individual breaths has been obtained by two methods. In the first, a pattern of respiration with constant expiratory flow in each breath brought expiratory alveolar profiles to the outermost end of the airway. In the second method, the early part of the alveolar PCO2 during normal expiration was calculated from airway PCO2 and expired volume.4. The data obtained with both methods show that, in the steady state, expiratory alveolar PCO2 rises at a rate which is directly proportional to the rate of C02 production.

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Section: Methodsmentioning

confidence: 99%

The rate of rise of alveolar carbon dioxide pressure during expiration in man.

Cochrane¹,

Newstead²,

Nowell³

et al. 1982

The Journal of Physiology

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“…When the first increase of breathing occurs around the third breath this assumption is no longer tenable, for dpH/dtjmax is a potential humoral signal at this time. Band et al (1980) have recorded a change in dpH/dt on the downstroke of the pH oscillation in the brachial artery of man by the second breath of exercise. This rapid development of a chemical signal in the arterial blood is presumably due to an abrupt increase in cardiac output at the start of exercise.…”

Section: Comparison Of the Present Experiments With Other 8tudie8mentioning

confidence: 99%

The pH oscillations in arterial blood during exercise; a potential signal for the ventilatory response in the dog

Cross¹,

Davey²,

Guz³

et al. 1982

The Journal of Physiology

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SUMMARY1. The effect of electrically induced 'exercise' on the respiratory oscillation of arterial pH was studied in chloralose-anaesthetized dogs with spinal cord transaction at T8/9 (dermatome level T6/7).2. Respiratory oscillations of arterial pH (presumed to be due to oscillations of arterial Pco2) were sensed with a fast-responding electrode in one carotid artery.Breath-by-breath estimates of the maximum rate of change of pH of the downstroke of the pH oscillation (dpH/dtjmax) were obtained by differentiating the pH signal.3. Consistent with the findings of the previous paper (Cross et al. 1982), the ventilatory response to exercise could not be explained on the basis of sensitivity to C02; the A T4/APaco, was significantly greater for 'exercise' than for CO2 inhalation.4. On average, the amplitude of the pH oscillations decreased during 'exercise'.The change in the phase relationship (0) between respiratory and pH cycles, although significant from the second breath onwards, was not thought to be responsible for the increased ventilation V,; the direction of the change was opposite to that previously found to increase VI. 14 and dpH/dtjmax were also linearly related during the on-transient, although the same relationship did not hold true throughout 'exercise'.6. The dpH/dtjmax was related to CO2 production (1rco,) lending support to the prediction that the slope of the downstroke of the pH oscillation is a function of TCo2.7. It was concluded that the dpH/dtimax (dpCO2/dttmax) is a potential humoral signal in 'exercise' and could account totally for the shortening of te. Since there was a late rise in VI (due to an increase in tidal volume VT) in the absence of a change in dpH/dtjmax, it was considered unlikely that the dpH/dtjmax was the only humoral signal present during 'exercise'.

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“…They found increases in the amplitude and the slope of pH oscillation (4pH/dt) with intravenous C02 administration while both amplitude and the slope decreased during C02 inhalation. It has also been shown in man using a left brachial artery cannula that during exercise both amplitude and the slope of pH oscillation increased with Vcp2 (BAND et al, 1980). CROSS et al (1982) found a logarithmic relationship between the maximum slope of the downstroke of pH oscillation ((d pH/dt)~mag) and V00, during on-transient of electrically induced exercise in the dog.…”

Section: Discussionmentioning

confidence: 99%

Open-loop analysis of Pax(x=CO2) oscillation in the dog.

1984

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Venous C02 loading and/or unloading using an artificial lung was performed on dogs to evaluate whether changes in the rate of carbon dioxide output (V002) can be involved in the control of respiration. As the signal providing J'2 information, small fluctuations in arterial Pco2 (4Paco2) which synchronized with the respiratory cycle were estimated from both the mean Pa002 and the fluctuations in arterial pH (4pH) measured with a catheter tip ISFET (ion sensitive field-effect transistor) pH sensor inserted in the common carotid artery. The open-loop method was used to analyze the effects of various respiratory parameters such as j02, tidal volume, and respiratory frequency on the changes in dpH and 4Paco2. Findings are: (1) 4Paco2 was linearly proportional to VC02 while the correlation between 4pH and VC02 was less linear, (2) magnitude of 4pH was dependent on the changes in tidal volume while 4Pa0O2 was not, (3) both the amplitude and the positive slope of Pa002 oscillation were functions of respiratory frequency. These results suggest the possibility that if Vco2 itself takes part in the control of ventilation, it will be C02 oscillation which links ventilation with Vco2.

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Respiratory oscillations in arterial carbon dioxide tension as a control signal in exercise

Cited by 61 publications

References 2 publications

The rate of rise of alveolar carbon dioxide pressure during expiration in man.

The rate of rise of alveolar carbon dioxide pressure during expiration in man.

The pH oscillations in arterial blood during exercise; a potential signal for the ventilatory response in the dog

Open-loop analysis of Pax(x=CO2) oscillation in the dog.

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