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Articles in PresS, published online ahead of print September 6, 2002
J Appl Physiol, 10.1152/jap.00594.2002
Submitted on July 3, 2002
Accepted on September 3, 2002
1 Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA; Pulmonary Department, VA Medical Health Care System, Boston, MA, USA
2 Pulmonary Department, VA Medical Health Care System, Boston, MA, USA; Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Boston, MA, USA
3 Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA; Department of Psychology, University of Arizona, Tucson, AZ, USA
4 Pulmonary Department, VA Medical Health Care System, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA; Pulmonary and Critical Care Unit, Massachusettes General Hosptial, Boston, MA, USA
5 Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA; Pulmonary Department, VA Medical Health Care System, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: smoosavi{at}hsph.harvard.edu.
Anecdotal observations suggest hypoxia does not elicit dyspnea. An opposing view is that any stimulus to medullary respiratory centers generates dyspnea via "corollary discharge" to higher centers; absence of dyspnea during low inspired POO2 may result from increased ventilation and hypocapnia. We hypothesized that, with fixed ventilation, hypoxia and hypercapnia generate equal dyspnea when matched by ventilatory drive. Steady-state levels of hypoxic normocapnia (PETO2=60-40torr) and hypercapnic hyperoxia (PETCO2=40-50torr) were induced in naïve subjects when free-breathing and during fixed mechanical ventilation. In a separate experiment, normocapnic hypoxia and normoxic hypercapnia, 'matched' by ventilation in free-breathing trials, were presented to experienced subjects breathing with constrained rate and tidal volume. 'Air hunger' was rated every 30s on a VAS. Air hunger/PETO2 curves rose sharply at PETO2<50torr. Air hunger was not different between matched stimuli (p>0.05). Hypercapnia had unpleasant non-respiratory effects but was otherwise perceptually indistinguishable from hypoxia. We conclude that hypoxia and hypercapnia have equal potency for air hunger when matched by ventilatory drive. Air hunger may therefore arise via brainstem respiratory drive.
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