Abstract
The observation that arterial CO2 tension is regulated (remains at the resting value) under a metabolic CO2 load via exercise, but increases under an airway CO2 load via inspiratory CO2, has motivated numerous theories about the structure of the respiratory controller. This respiratory control system behavior appears to be most consistent with a feedforward/feedback control system structure.1 The peripheral chemoreceptors (carotid body) and indirectly central brain chemoreceptors act as feedback mechanisms with respect to the regulation of arterial CO2 tension. Feedforward mechanisms (signals related to metabolic CO2 production during exercise) are more controversial. Part of this controversy relates to the traditional “search” for a “single” mechanism that will explain the exercise hyperpnea response.2 However, in general, biological systems are characterized by redundancy, suggesting that many “signals” may be combined to form an appropriate feedforward stimulus.
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© 1992 Springer Science+Business Media New York
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Swanson, G.D. (1992). Redundancy Structures in Respiratory Control. In: Honda, Y., Miyamoto, Y., Konno, K., Widdicombe, J.G. (eds) Control of Breathing and Its Modeling Perspective. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9847-0_31
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DOI: https://doi.org/10.1007/978-1-4757-9847-0_31
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