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Published online before print November 21, 2007, 10.1183/09031936.00001007
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Eur Respir J 2008; 31:800-806
Copyright ©ERS Journals Ltd 2008

Initiating oral breathing in response to nasal loading: asthmatics versus healthy subjects

M. Hallani1,2, J. R. Wheatley1,2 and T. C. Amis1,2

1 Ludwig Engel Centre for Respiratory Research, and 2 Dept of Respiratory Medicine, Westmead Hospital, Wentworthville, NSW, Australia.

CORRESPONDENCE: T. C. Amis, Dept of Respiratory Research, Westmead Hospital, PO Box 533, Wentworthville, 2145 NSW, Australia. Fax: 61 298457286. E-mail: terence_amis{at}wmi.usyd.edu.au

Keywords: Airway physiology, asthma, perception, upper airway loading

Received: January 3, 2007
Accepted November 7, 2007

Factors influencing nasal versus oral breathing in asthmatics are not well understood. The current authors hypothesised that asthmatic subjects have enhanced perception of nasal threshold loads, and switch from nasal to oral breathing at a lower load than healthy subjects.

In total, 15 mild asthmatic and 20 healthy control subjects breathed nasally via an inspiratory threshold loading device. Nasal loading was progressively increased until subjects switched to oral breathing. Load perception at switching was rated using a Borg scale. Nasal resistance was measured using posterior rhinomanometry. The protocol was repeated before and after nasal decongestant administration in subgroups of 10 healthy control and six asthmatic subjects.

Inspiratory nasal resistance was within normal limits for most subjects and was not significantly different between asthmatics and healthy controls. Compared with controls, asthmatics switched to oral breathing at a significantly lower nasal load but rated "difficulty breathing in" at the same level. Decongestant significantly lowered nasal resistance but did not change the nasal load initiating switching in either subgroup.

Enhanced perception of nasal loading may trigger increased oral breathing in asthmatics, potentially enhancing exposure to nonconditioned inhaled gas and contributing to the occurrence and/or severity of bronchoconstrictive exacerbations.







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Copyright © 2008 by the European Respiratory Society.