Key result
Arterial chemoreceptors substantially drive exercise ventilation, potentially excited by sympathetic innervation and raised potassium.
Why the study?
The role and stimulus-response characteristics of carotid body chemoreceptors in generating exercise hyperpnea and their activation mechanisms remain to be clarified.
This review highlights the role of carotid body chemoreceptors in exercise hyperpnea, proposing sympathetic activation and elevated potassium as key stimuli.
Does not support practice changes in exercise testing; leaves open interventional studies on chemoreceptor modulation.
This short review considers the essential structure and stimulus-response characteristics of the carotid body chemoreceptors and attempts to relate the latter to their role in the generation of exercise hyperpnea. It shows that the arterial chemoreceptors do contribute substantially to the drive to breathe in exercising man and it suggests that this extra drive results from an increase in discharge which occurs in spite of the fact that the classical stimuli to its discharge, do not change. The possibility that in exercise the carotid body is excited by activation of its sympathetic innervation, and by raised arterial potassium, is considered. The idea that breath-by-breath oscillations of arterial blood gas tension convey accurate information about the whole body rate of carbon dioxide production is described and found wanting.
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P. C. G. Nye (1994) conducted a review in Exercise hyperpnea. Peripheral chemoreceptor stimuli was evaluated. Arterial chemoreceptors contribute substantially to the drive to breathe during exercise, potentially excited by sympathetic innervation and raised arterial potassium rather than blood gas oscillations.
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