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.
KeywordsFatigue Lactate Cage Respiration Norepinephrine
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