Carbon dioxide and venous return and their interaction as stimuli to ventilation in the cat

Ponte, J; Purves, M. J.

doi:10.1113/jphysiol.1978.sp012160

Cited by 46 publications

(15 citation statements)

References 38 publications

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“…In several studies on anesthetized animals, it was claimed thatV E changed in proportion to the change in CO 2 delivery to maintain homeostasis of PaCO 2 (206,214,274,314,338). In contrast, in an equal number of studies, there was a change in PaCO 2 sufficient to account for the hyperpnea or hypopnea during CO 2 loading and unloading (39,118,138,171,209,277,284,300). Similar studies on awake sheep found that venous CO 2 loading that increased pulmonary CO 2 excretion up to 350% also increasedV E to the same extent as exercise induced increases in CO 2 excretion (275).…”

Section: Venous Co 2 Content As a Signal For The Exercise Hyperpneamentioning

confidence: 88%

“…Several investigators have studied whether receptors sensing pulmonary blood and CO 2 flow mediate the exercise hyperpnea (142,173,277,298,300). These studies used an extracorporeal gas exchange system to alter either CO 2 content, blood flow, or both to the lung independent of arterial CO 2 and blood flow.…”

Section: Pulmonary Blood and Co 2 Flow As A Signal For The Exercise Hmentioning

confidence: 99%

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Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

198

203

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During exercise by healthy mammals, alveolar ventilation and alveolar-capillary diffusion increase in proportion to the increase in metabolic rate to prevent PaCO2 from increasing and PaO2 from decreasing. There is no known mechanism capable of directly sensing the rate of gas exchange in the muscles or the lungs; thus, for over a century there has been intense interest in elucidating how respiratory neurons adjust their output to variables which can not be directly monitored. Several hypotheses have been tested and supportive data were obtained, but for each hypothesis, there are contradictory data or reasons to question the validity of each hypothesis. Herein, we report a critique of the major hypotheses which has led to the following conclusions. First, a single stimulus or combination of stimuli that convincingly and entirely explains the hyperpnea has not been identified. Second, the coupling of the hyperpnea to metabolic rate is not causal but is due to of these variables each resulting from a common factor which link the circulatory and ventilatory responses to exercise. Third, stimuli postulated to act at pulmonary or cardiac receptors or carotid and intracranial chemoreceptors are not primary mediators of the hyperpnea. Fourth, stimuli originating in exercising limbs and conveyed to the brain by spinal afferents contribute to the exercise hyperpnea. Fifth, the hyperventilation during heavy exercise is not primarily due to lactacidosis stimulation of carotid chemoreceptors. Finally, since volitional exercise requires activation of the CNS, neural feed-forward (central command) mediation of the exercise hyperpnea seems intuitive and is supported by data from several studies. However, there is no compelling evidence to accept this concept as an indisputable fact.

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Section: Venous Co 2 Content As a Signal For The Exercise Hyperpneamentioning

confidence: 88%

Section: Pulmonary Blood and Co 2 Flow As A Signal For The Exercise Hmentioning

confidence: 99%

Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

198

203

View full text Add to dashboard Cite

show abstract

“…The demonstration of isocapnic hyperpnea in response to venous CO2 loading has been extrapolated to imply that the isocapnic hyperpnea of exercise may also be attributable solely to the associated increase in Vco2. However, an equally large number of other studies have been unable to demonstrate isocapnic hyperpnea in response to venous CO2 loading; and have therefore concluded that an increase in Vco2 alone cannot account for the isocapnic hyperpnea of exercise (21)(22)(23)(24)(25)(26).…”

Section: Introductionmentioning

confidence: 99%

Role of metabolic CO2 production in ventilatory response to steady-state exercise.

Phillipson¹,

Bowes²,

Townsend³

et al. 1981

J. Clin. Invest.

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A B S T R A C T We examined the role of metabolic CO2 production in the hyperpnea of muscular exercise by comparing the response of alveolar ventilation to moderate levels ofexercise with the response to venous infusion of CO2 at rest. Studies were performed in four awake sheep that were trained to run on a treadmill. The sheep had been cannulated for veno-venous extracorporeal perfusion so that CO2 could be infused into the peripheral venous blood through membrane lungs in the perfusion circuit. The sheep breathed room air through an endo-tracheal tube inserted through a tracheostomy, and samples of expired gas were collected for measurement of the rates of CO2 production and 02 consumption. All measurements were made in the steady state. In each of the four sheep, the relationship between alveolar ventilation and the rate of CO2 production could be described by a single linear function (r > 0.99; P < 0.001), regardless of whether CO2 production was increased by exercise, venous CO2 infusion, or combinations of both procedures. This relationship applied for values of CO2 production up to 350% of control. In contrast, no unique relationship was found between the rate of alveolar ventilation and either the rate of 02 consumption, cardiac output, or mixed venous blood gas pressures. The findings indicate that the hyperpnea of mild to moderate steady-state exercise can be attributed to the associated increase in the rate of CO2 production. Therefore, there is no need to invoke obligatory nonmetabolic stimuli to account for the ventilatory response to steady-state exercise.

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“…However, if factors more directly related to venous return were involved, the exercise-induced hyperpnoea should be attenuated in similar proportion during partial or total occlusion (Yamamoto & Edwards, 1960;Sylvester et nl. 1973;Ponte & Purves, 1978;Jones et a/. 1982;Huszczuk et al 1986).…”

mentioning

confidence: 99%

Control of breathing and muscle perfusion in humans

Haouzi

Chenuel

Chalon

2001

Experimental Physiology

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Very brief and intense exercise triggers a biphasic metabolic and respiratory response with a second phase that occurs after the cessation of the muscular activity. The effects on minute ventilation (VE) produced by manipulation of the peripheral circulation in metabolically active muscles could thus be studied without the confounding effects of painful contractions. The second phase of breath-by-breath ft and pulmonary gas exchange responses to a brief change in work rate (400 W for 12 s) were studied in six healthy male subjects on four occasions (24 tests). An upper thigh cuff inflation was randomly applied either above or below the systolic blood pressure (200 or 90 Torr, respectively) for 90 s just after the cessation of the contractions prior to the delayed rise in pulmonary gas exchange (eight tests in each subject). Total occlusion produced a significant reduction in the delayed rise in T & (-29 ? 3 %) which normally occurred 20-25 s after the cessation of the contractions. In contrast, cuff inflation at a level predominantly impeding venous return while partially maintaining the arterial supply reduced the rise in pulmonary gas exchange in similar proportion to that during total obstruction but with a slight but not significant reduction in ventilation (-9 f 5%). ft during partial occlusion was if anything higher than in control tests with similar oxygen uptake (280 W), despite a higher blood pressure (BP) during occlusion (+7 Torr). It is concluded that the factors resulting from a reduction in venous return or from the involvement of the arterial baroreflex are not responsible for the changes in ft produced by the obstruction of the circulation to and from metabolically active muscles. It is proposed that factors related to the level of the perfusion pressure in hyperaemic muscles, possibly located at the venular end of the microcirculation, could account for the changes in J& observed.

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Carbon dioxide and venous return and their interaction as stimuli to ventilation in the cat

Cited by 46 publications

References 38 publications

Control of Breathing During Exercise

Control of Breathing During Exercise

Role of metabolic CO2 production in ventilatory response to steady-state exercise.

Control of breathing and muscle perfusion in humans

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