Journal of Applied Physiology, Vol 79, Issue 4 1330-1337, Copyright © 1995 by American Physiological Society

ARTICLES

Neural drive to nasal dilator muscles: influence of exercise intensity and oronasal flow partitioning

R. F. Fregosi and R. W. Lansing
Department of Physiology, University of Arizona, Tucson 85721-0093, USA.

Our aim was to test the following hypotheses: 1) neural drive to the muscles of the alae nasi (AN) is proportional to nasal airflow and is independent of the overall level of central respiratory drive, and 2) the switch from nasal to oronasal breathing corresponds to the onset of marked flow turbulence in the nasal airway. Total and nasal inspired ventilation rates (VI) and the electromyogram (EMG) of the AN muscles were measured in seven subjects during progressive-intensity bicycling exercise. In separate experiments in six subjects the nasal VI corresponding to the transition from laminar to turbulent airflow was determined by measuring the pressure-flow relationship of the nasal airway with anterior rhinomanometry. Nasal VI accounted for 70 +/- 11% of total VI at rest and 27 +/- 8% (SE) at 90% of the maximal attainable power (max). Nasal VI and integrated AN EMG activities increased linearly with exercise intensity up to 60% of the max power, but both variables plateaued at this level even though total VI (and central respiratory drive) began to increase exponentially as exercise intensity increased to 90% max. The onset of the exponential rise in total VI was associated with a sharp increase in oral VI and with the onset of marked flow turbulence in the nasal airway. The results suggest that during incremental exercise 1) changes in AN EMG activities are highly correlated with changes in nasal VI, 2) turbulent flow in the nose may be the stimulus for the switch to oronasal breathing so that total pulmonary resistance is minimized, and 3) the correlation between nasal airflow and neural drive to the AN muscles is probably mediated by mechanisms that monitor airway resistance. Although these mechanisms were not identified, the most likely possibilities are receptors in the upper and/or lower airways that are sensitive to negative transmural pressure, or to effort sensations leading to greater corollary motor discharge to nasal dilator muscle motoneurons.

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