title: Slow and deep respiration suppresses steady-state sympathetic nerve activity in patients with chronic heart failure: from modeling to clinical application.
abstract: Influences of slow and deep respiration on steady-state sympathetic nerve activity remain controversial in humans and could vary depending on disease conditions and basal sympathetic nerve activity. To elucidate the respiratory modulation of steady-state sympathetic nerve activity, we modeled the dynamic nature of the relationship between lung inflation and muscle sympathetic nerve activity (MSNA) in 11 heart failure patients with exaggerated sympathetic outflow at rest. An autoregressive exogenous input model was utilized to simulate entire responses of MSNA to variable respiratory patterns. In another 18 patients, we determined the influence of increasing tidal volume and slowing respiratory frequency on MSNA; 10 patients underwent a 15-min device-guided slow respiration and the remaining 8 had no respiratory modification. The model predicted that a 1-liter, step increase of lung volume decreased MSNA dynamically; its nadir (-33 ± 22%) occurred at 2.4 s; and steady-state decrease (-15 ± 5%), at 6 s. Actually, in patients with the device-guided slow and deep respiration, respiratory frequency effectively fell from 16.4 ± 3.9 to 6.7 ± 2.8/min (P < 0.0001) with a concomitant increase in tidal volume from 499 ± 206 to 1,177 ± 497 ml (P < 0.001). Consequently, steady-state MSNA was decreased by 31% (P < 0.005). In patients without respiratory modulation, there were no significant changes in respiratory frequency, tidal volume, and steady-state MSNA. Thus slow and deep respiration suppresses steady-state sympathetic nerve activity in patients with high levels of resting sympathetic tone as in heart failure.
authors.affiliation: The Cardiology Division, Imizu City Hospital, Imizu City, Toyama, Japan; and.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Harada
authors.affiliation: The Cardiology Division, Imizu City Hospital, Imizu City, Toyama, Japan; and hasanoi@kmh.biglobe.ne.jp.
authors.forename: Hidetsugu
authors.initials: H
authors.lastname: Asanoi
authors.affiliation: The Cardiology Division, Imizu City Hospital, Imizu City, Toyama, Japan; and.
authors.forename: Junya
authors.initials: J
authors.lastname: Takagawa
authors.affiliation: The Cardiology Division, Imizu City Hospital, Imizu City, Toyama, Japan; and.
authors.forename: Hisanari
authors.initials: H
authors.lastname: Ishise
authors.affiliation: The Cardiology Division, Imizu City Hospital, Imizu City, Toyama, Japan; and.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ueno
authors.affiliation: The Cardiology Division, Toyama University Hospital, Toyama City, Toyama, Japan.
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Oda
authors.affiliation: The Cardiology Division, Toyama University Hospital, Toyama City, Toyama, Japan.
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Goso
authors.affiliation: The Cardiology Division, Toyama University Hospital, Toyama City, Toyama, Japan.
authors.forename: Shuji
authors.initials: S
authors.lastname: Joho
authors.affiliation: The Cardiology Division, Toyama University Hospital, Toyama City, Toyama, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Inoue
mesh_terms: D000328:Adult; D000368:Aged; D001945:Breathing Exercises; D016022:Case-Control Studies; D005260:Female; D006333:Heart Failure / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D008959:Models, Neurological; D012119:Respiration; D012132:Respiratory Muscles / Q000294:innervation / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology*
keywords: broad-band respiration; chronic heart failure; lung inflation reflex; sympathetic nerve activity; system identification