Abstract
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.
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References
Eldridge, F. L., D. E. Milhorn, J. P. Kiley and T. G. Waldrop. Stimulation by central command oflocomotion, respiration and circulation during exercise. Respir. Physiol. 59:313–337, 1985.
Wasserman, K., B. J. Whipp, S. N. Koyal, and M. G. Cleary. Effect of Carotid Body Reserection on Ventilatory and Acid-Base Control during Exercise. J. Appl. Physiol. 39:354–358, 1975.
Pan, L. G., H. V. Forster, G. E. Forster, C. L. Murphy, and T. F. Lawry. Independence of exercise hyperpnea and acidosis during high intensity exercise in ponies. J. Appl. Physiol. 60:1016–1024, 1986.
Johnson, B. D., K. W. Saupe and J. A. Dempsey. Mechanical constraints on exercise hyperpnea in endurance athletes. J. Appl. Physiol. 73:874–886, 1992.
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© 1995 Springer Science+Business Media New York
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Dempsey, J.A. (1995). Exercise Hyperpnea. In: Semple, S.J.G., Adams, L., Whipp, B.J. (eds) Modeling and Control of Ventilation. Advances in Experimental Medicine and Biology, vol 393. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1933-1_27
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DOI: https://doi.org/10.1007/978-1-4615-1933-1_27
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