<i>Evidence Against the Existence of Specific Ventilatory Chemoreceptors in the Legs</i>

Dejours, P; Mithoefer, John C.; Raynaud, Julien

doi:10.1152/jappl.1957.10.3.367

Cited by 21 publications

(17 citation statements)

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“…Others also tested the peripheral chemoreflex hypothesis by: (i) perfusing the legs with hypercapnic, acidotic, and hypoxemic blood or venous blood collected previously from exercising legs, (ii) intra-arterial injections of chemical agents that change during exercise, and (iii) vascular occlusion postexercise thereby trapping metabolites in the muscle. The data from these studies do not support a muscle chemoreflex-induced hyperpnea (85,158,176,287). Indeed, the trapping of exercise metabolites in the muscles at the end of exercise results in a return ofV E to resting levels more quickly than normal (Figs.…”

Section: Responses To Electrically Induced Muscle Contractionmentioning

confidence: 83%

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: Responses To Electrically Induced Muscle Contractionmentioning

confidence: 83%

Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

198

203

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“…However, there is also substantial evidence to support a secondary feedback regulation of exercise hypernea (1,3,8,9,18,20,21,28,29,32). This secondary system could serve to finely regulate both respiratory magnitude and frequency and to maintain a close tracking of VII and metabolic events during exercise.…”

Section: Responses During Graded Incremental Exercisementioning

confidence: 99%

“…Conversely, K released from exercising muscle may serve as a peripheral stimulus, invoking activation of yE via stimulation of afferent nerves innervating the active skeletal muscle. It has been observed in cross circulation and bJood-flow occlusion studies that increases in VE can occur without blood from the exercising musculature entering the arterial circulation (8,9,18). It has also been demonstrated that blocking the small myelinated and unmyelinated afferent nerve fibers (Type III and IV) abolishes or significantly reduces the normal increase in VE elicited by electrical stimulation of efferent nerves innervating the hindlimb skeletal muscle of the dog (21,28).…”

Section: Responses During Graded Incremental Exercisementioning

confidence: 99%

Ventilation Parallels Plasma Potassium During Incremental and Continuous Variable Intensity Exercise

Yaspelkis¹,

Anderla²,

Patterson³

et al. 1994

Int J Sports Med

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“…This additional nervous drive to breathe appears to contribute to the rapid increase in ventilation observed after the onset of exercise. The second group is concerned with the nature of the chemical factors involved in the control of breathing and includes a search for chemoreceptors close to the metabolizing tissues (Dejours, Mithoefer & Raynaud, 1957) or in the pulmonary circulation (Cropp & Comroe, 1961) as well as studying the C02 stimulus in terms of oscillations rather than its mean value (Yamamoto, 1960).…”

Section: Introductionmentioning

confidence: 99%

The effect of CO₂ on ventilation and breath‐holding during exercise and while breathing through an added resistance

Clark¹,

Godfrey²

1969

The Journal of Physiology

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SUMMARY1. Ventilation was measured while subjects were made to rebreathe from a bag containing CO2 and 02 in order to expose them to a steadily rising CO2 tension (Pco2). The object of the experiments was to determine the effect of a variety of stimuli upon the increase in ventilation and fall in breath-holding time which occurs in response to the rising PCO2.2. Steady-state exercise at 200 kg.m/min resulted in a small fall in the slope of the ventilation-CO2 response curve (Sv) and a small, though not statistically significant, fall in the PCO2 at which ventilation would be zero by extrapolation (By). There was a marked fall in the slope of the breathholding-CO2 response curve (SBH) and an increase in the Pco0 at which breath-holding time became zero by extrapolation (BBH) 3. These results have been interpreted with the aid of a model of the control of breath-holding and it is suggested that there is no change in CO2 sensitivity on exercise, either during rebreathing or breath-holding.4. An increase in the resistance to breathing caused a marked reduction in S, and Bv, but no change in the breath-holding-CO2 response curve.These findings suggest that the flattening of the ventilation-CO2 response curve is mechanical in origin and acute airway obstruction produces no change in CO2 sensitivity. 5. On the basis of these results, we suggest that more information about CO2 sensitivity can be obtained by a combination of ventilation and breath-holding-CO2 response curves.

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Evidence Against the Existence of Specific Ventilatory Chemoreceptors in the Legs

Cited by 21 publications

References 0 publications

Control of Breathing During Exercise

Control of Breathing During Exercise

Ventilation Parallels Plasma Potassium During Incremental and Continuous Variable Intensity Exercise

The effect of CO₂ on ventilation and breath‐holding during exercise and while breathing through an added resistance

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Evidence Against the Existence of Specific Ventilatory Chemoreceptors in the Legs

Cited by 21 publications

References 0 publications

Control of Breathing During Exercise

Control of Breathing During Exercise

Ventilation Parallels Plasma Potassium During Incremental and Continuous Variable Intensity Exercise

The effect of CO2 on ventilation and breath‐holding during exercise and while breathing through an added resistance

Contact Info

Product

Resources

About

The effect of CO₂ on ventilation and breath‐holding during exercise and while breathing through an added resistance