Analysis of Factors Concerned in Regulation of Breathing in Exercise

Grodins, Fred S.

doi:10.1152/physrev.1950.30.2.220

Cited by 98 publications

(49 citation statements)

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“…(1) Grodins (1950), when commenting on the experiments of Asmussen et al (1943), postulated the existence of muscle receptors which respond only to abnormal concentrations of anaerobic products. These might well be activated by direct electrical stimulation.…”

Section: Discussionmentioning

confidence: 99%

The carbon dioxide stimulus to breathing in severe exercise

Bannister¹,

Cunningham²,

Douglas³

1954

The Journal of Physiology

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There has been much speculation for a long time as to the causes of the increased breathing during exercise. In 1905, Haldane & Priestley put forward the theory that it was due to a slight increase in the alveolar CO2 tension (pCO2) and therefore of the arterial pCO2, just as similar increases in alveolar PCO2 induced by CO2 inhalation at rest produced hyperpnoea. Further work showed that whatever might be true for mild exercise, as the work became harder the increase in pCO2 was certainly insufficient to account for the hyperpnoea, and it was clear that some additional factors must come into play. The theory that hydrogen-ion concentration rather than CO2 as such was the stimulus to respiration was more satisfactory since it was known that severe exercise was associated with the accumulation of an excess of lactic acid in the body. Since then, this view has been challenged by many physiologists, and at present there is no agreement as to the main causes of the hyperpnoea. In view of this uncertainty we decided to re-investigate the changes in alveolar C02 during heavy exercise, together with some factors which might modify the response of the respiratory centre to CO2. The current views are partly based on the contention of Krogh & Lindhard (1913c, 1917) that the directly measured alveolar gas tensions do not reflect the gas tensions in the arterial blood during exercise. It is therefore important to the argument presented in this paper that the old controversy between the Danish and Oxford schools of physiology should be re-examined in the light of recent evidence on the alveolar air-arterial blood gas relationships. The arguments used to justify the use of the directly measured alveolar pCO2 as a guide to the arterial pCO2 in exercise are long and intricate and are therefore presented in an appendix to this paper. The conclusions reached are summarized in the main text. METHODSAlveolar air. At rest, alveolar air samples were taken by the Haldane-Priestley method. The values presented in this paper were the means of end-inspiratory and end-expiratory samples.Automatic alveolar air sample8. In exercise, a modification of the method described by Lindhard (1911), and modified by Rahn & Otis (1949), was used (Fig. 1). In this method the last few c.c. of

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Section: Discussionmentioning

confidence: 99%

The carbon dioxide stimulus to breathing in severe exercise

Bannister¹,

Cunningham²,

Douglas³

1954

The Journal of Physiology

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“…Carbon dioxide has been invoked as a major factor on the ground that exercise increases the responsiveness of the respiratory center to this stimulus (22), and the significance of carbon dioxide as a major factor has been denied on the ground that the alveolar carbon dioxide tension remains unchanged or falls during exercise (47). pH change has not been considered of first-line importance by most observers (8,22,41), but its possible importance has recently been asserted (31). Arterial oxygen tension has been dismissed as a regulatory factor because changes in arterial oxygen during exercise are slight, and change in arterial oxygen tension over a considerable range yields little respiratory response at rest (20).…”

Section: Discussionmentioning

confidence: 99%

Respiratory Regulation During Exercise in Unconditioned Subjects 1

Hickam¹,

Pryor²,

Page³

et al. 1951

J. Clin. Invest.

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“…Although the exercise ventilatory response is the largest ventilatory response in our day-to-day lives, our understanding of the primary drive to breathe during exercise has advanced little in more than 50 years (82). On the other hand, we have recently gained an appreciation that at least some degree of plasticity can be observed in the exercise ventilatory response.…”

Section: Exercise-induced Respiratory Plasticity (Adult)mentioning

confidence: 99%

Invited Review: Neuroplasticity in respiratory motor control

Mitchell

Johnson

2003

Journal of Applied Physiology

354

313

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Although recent evidence demonstrates considerable neuroplasticity in the respiratory control system, a comprehensive conceptual framework is lacking. Our goals in this review are to define plasticity (and related neural properties) as it pertains to respiratory control and to discuss potential sites, mechanisms, and known categories of respiratory plasticity. Respiratory plasticity is defined as a persistent change in the neural control system based on prior experience. Plasticity may involve structural and/or functional alterations (most commonly both) and can arise from multiple cellular/synaptic mechanisms at different sites in the respiratory control system. Respiratory neuroplasticity is critically dependent on the establishment of necessary preconditions, the stimulus paradigm, the balance between opposing modulatory systems, age, gender, and genetics. Respiratory plasticity can be induced by hypoxia, hypercapnia, exercise, injury, stress, and pharmacological interventions or conditioning and occurs during development as well as in adults. Developmental plasticity is induced by experiences (e.g., altered respiratory gases) during sensitive developmental periods, thereby altering mature respiratory control. The same experience later in life has little or no effect. In adults, neuromodulation plays a prominent role in several forms of respiratory plasticity. For example, serotonergic modulation is thought to initiate and/or maintain respiratory plasticity following intermittent hypoxia, repeated hypercapnic exercise, spinal sensory denervation, spinal cord injury, and at least some conditioned reflexes. Considerable work is necessary before we fully appreciate the biological significance of respiratory plasticity, its underlying cellular/molecular and network mechanisms, and the potential to harness respiratory plasticity as a therapeutic tool.

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Analysis of Factors Concerned in Regulation of Breathing in Exercise

Cited by 98 publications

References 0 publications

The carbon dioxide stimulus to breathing in severe exercise

The carbon dioxide stimulus to breathing in severe exercise

Respiratory Regulation During Exercise in Unconditioned Subjects 1

Invited Review: Neuroplasticity in respiratory motor control

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