E.Fiona Bailey

E.Fiona Bailey

Professor, Physiology
Professor, Evelyn F Mcknight Brain Institute
Professor, Speech/Language and Hearing
Professor, BIO5 Institute
Member of the General Faculty
Member of the Graduate Faculty
Primary Department
Department Affiliations
Contact
(520) 626-8299

Research Interest

My research focus is the neural control of breathing in human and nonhuman mammals. My earlier work assessed the role of pulmonary stretch receptors and central chemoreceptors in the genesis and relief of dyspnea or shortness of breath in healthy adults. These studies led to studies in the mammalian (rodent) airway that explored the modulation of upper airway muscles activities by chemical and pulmonary afferent feedback and the potential for selective electrical stimulation of the cranial nerve XII to alter airway geometry and volume (NIH/NIDCD RO3). Beginning in 2005, with the support of an NIH/NIDCD K23 I began work in neural control of upper airway muscles using tungsten microelectrodes to record from single motor units in adult human subjects. This work led in turn, to studies of regional (or segmental) muscle and motor unit activities in human subjects under volitional, state-dependent (i.e., wake/sleep) and chemoreceptor drives, in health and disease (NIH/NIDCD RO1). On the basis of the experimental work in muscle and motor units I have pursued additional lines of enquiry focused on clinical respiratory dysfunction in two specific populations a) infants at risk for SIDS and b) adults diagnosed with obstructive sleep apnea (OSA). Both lines of enquiry are highly innovative and have diagnostic and clinical applications. One recent line of enquiry explores the potential for a non-pharmacologic intervention daily to lower blood pressure and to improve sleep in patients diagnosed with mild-moderate obstructive sleep apnea. This training protocol shows promise as a cheap, effective and safe means of lowering blood pressure and improving autonomic-cardiovascular dysfunction in patients who are unwilling or unable to use the standard CPAP therapy.

Publications

Vranish, J. R., & Bailey, E. F. (2015). Daily respiratory training with large intrathoracic pressures, but not large lung volumes, lowers blood pressure in normotensive adults. Respiratory physiology & neurobiology, 216, 63-9.

Inspiratory muscle training holds promise as a non-pharmacologic treatment that can improve respiratory muscle strength, reduce blood pressure, and improve autonomic balance in hypertensive patients. There is a gap in knowledge regarding the specific respiratory stimulus that gives rise to these favorable outcomes. We implemented five respiratory training protocols that differed in the magnitude and direction of the lung volumes and/or intrathoracic pressures generated by subjects in training. Normotensive adults were randomly assigned to each group and trained daily for 6 weeks. Pre-post and weekly measures of blood pressure showed significant declines in systolic [-8.96 mmHg (95% CI, 7.39-10.53)] and diastolic [-5.25 mmHg (95% CI, 3.67-6.83)] blood pressures for subjects who trained with large positive or negative intrathoracic pressures. Subjects who trained with modest intrathoracic pressures or large lung volumes saw no improvement in blood pressure (P > 0.3). Large intra-thoracic pressures are the specific respiratory stimulus underpinning breathing training related improvements in blood pressure.

DeLucia, C. M., De Asis, R. M., & Bailey, E. F. (2017). Daily inspiratory muscle training lowers blood pressure and vascular resistance in healthy men and women. Experimental physiology.

What is the central question of this study? What impact does inspiratory muscle training have on systemic vascular resistance, cardiac output and baroreflex sensitivity in adult men and women? What is the main finding and its importance? Inspiratory muscle training exerts favorable effects on blood pressure, vascular resistance and perception of stress. This exercise format is well-tolerated and equally effective whether implemented in men or women.

Bailey, E. F. (2008). A tasty morsel: the role of the dorsal vagal complex in the regulation of food intake and swallowing. Focus on "BDNF/TrkB signaling interacts with GABAergic system to inhibit rhythmic swallowing in the rat," by Bariohay et al. American journal of physiology. Regulatory, integrative and comparative physiology, 295(4), R1048-9.
Bailey, E. F., Janssen, P. L., & Fregosi, R. F. (2005). PO2-dependent changes in intrinsic and extrinsic tongue muscle activities in the rat. American journal of respiratory and critical care medicine, 171(12), 1403-7.

Historically, respiratory-related research in sleep apnea has focused exclusively on the extrinsic tongue muscles (i.e., genioglossus, hyoglossus, and styloglossus). Until recently, the respiratory control and function of intrinsic tongue muscles (i.e., inferior and superior longitudinalis, transverses, and verticalis), which comprise the bulk of the tongue, were unknown.

Bailey, E. F., & Fregosi, R. F. (2003). Pressure-volume behaviour of the rat upper airway: effects of tongue muscle activation. The Journal of physiology, 548(Pt 2), 563-8.

Our hypothesis was that the simultaneous activation of tongue protrudor and retractor muscles (co-activation) would constrict and stiffen the pharyngeal airway more than the independent activation of tongue protrudor muscles. Upper airway stiffness was determined by injecting known volumes of air into the sealed pharyngeal airway of the anaesthetized rat while measuring nasal pressure under control (no-stimulus) and stimulus conditions (volume paired with hypoglossal (XII) nerve stimulation). Stimulation of the whole XII nerves (co-activation) or the medial XII branches (protrudor activation) effected similar increases in total pharyngeal airway stiffness. Importantly, co-activation produced volume compression (airway narrowing) at large airway volumes (P 0.05), but had no effect on airway dimension at low airway volumes. In comparison, protrudor activation resulted in significant volume expansion (airway dilatation) at low airway volumes and airway narrowing at high airway volumes (P 0.05). In conclusion, both co-activation and independent protrudor muscle activation increase airway stiffness. However, their effects on airway size are complex and depend on the condition of the airway at the time of activation.