NEURAL DRIVE TO NASAL DILATOR MUSCLES - INFLUENCE OF EXERCISE INTENSITY AND ORONASAL FLOW PARTITIONING

Citation
Rf. Fregosi et Rw. Lansing, NEURAL DRIVE TO NASAL DILATOR MUSCLES - INFLUENCE OF EXERCISE INTENSITY AND ORONASAL FLOW PARTITIONING, Journal of applied physiology, 79(4), 1995, pp. 1330-1337
Citations number
25
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
79
Issue
4
Year of publication
1995
Pages
1330 - 1337
Database
ISI
SICI code
8750-7587(1995)79:4<1330:NDTNDM>2.0.ZU;2-T
Abstract
Our aim was to test the following hypotheses: 1) neural drive to the m uscles of the alae nasi (AN) is proportional to nasal airflow and is i ndependent of the overall level of central respiratory drive, and 2) t he 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 corres ponding to the transition from laminar to turbulent airflow was determ ined by measuring the pressure-flow relationship of the nasal airway w ith anterior rhinomanometry. Nasal VI accounted for 70 +/- 11% of tota l ill at rest and 27 +/- 8% (SE) at 90% of the maximal attainable powe r (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 associa ted with a sharp increase in oral QI and with the onset of marked flow turbulence in the nasal airway. The results suggest that during incre mental exercise 1) changes in AN EMG activities are highly correlated with changes in nasal VI, 2) turbulent flow in the nose may be the sti mulus for the switch to oronasal breathing so that total pulmonary res istance is minimized, and 3) the correlation between nasal airflow and neural drive to the AN muscles is probably mediated by mechanisms tha t monitor airway resistance. Although these mechanisms were not identi fied, the most likely possibilities are receptors in the upper and/or lower airways that are sensitive to negative transmural pressure, or t o effort sensations leading to greater corollary motor discharge to na sal dilator muscle motoneurons.