Exercise Hyperpnea

Chairman’s Introduction
  • J. A. Dempsey
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 393)


As judged by the number of presentations at this meeting dealing with this topic, exercise hyperpnea continues to be a popular focus of research-although its primary mechanisms remain a dilemma. To summarize recent trends, this reviewer’s bias is that little if any support remains for the traditional “CO2 flow” hypothesis. The normal ventilatory response to steady-state exercise in the lung/heart transplant patient have added the final piece of negative evidence (in humans) against this hypotheses. Similarly, cardiopulmonary afferents from working locomotor muscles probably play only a minor reflex role in hyperpnea. Based on studies of chemoreceptor denervation, it is also unlikely that these types of time-dependent influences play a significant role in hyperpnea. Finally, a role for traditional carotid and/or medullary chemoreceptors in hyperpnea continues to be advanced with the evidence that arterial H+ is tightly correlated with the hyperpnea during progressive increases in work rate (see W. Stringer); but as has been the case so often in the past, it seems just as likely that the ventilatory response is dictating the change in arterial H+rather than vice versa. The kinetics of the ventilatory response to exercise onset may involve mechanisms which are masked during steady-state periods. Several studies in this conference dealt with this topic (see M. Walsh et al., A. Datta et al.). Some suggested-based on indirect evidence -that carotid chemoreceptors might play some stabilizing role for ventilation during these transient phases of exercise.


Carotid Body Ventilatory Response Heavy Exercise Locomotor Muscle Carotid Sinus Nerve 
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Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • J. A. Dempsey
    • 1
  1. 1.Department of Preventive MedicineUniversity of Wisconsin-MadisonMadisonUSA

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