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Effect of device guided slow deep breathing on central sympathetic outflow and arterial baroreflex sensitivity in young healthy individuals (1170.4)
Author(s) -
Shantsila Alena,
Adlan Ahmed M,
Lip Gregory,
Pickering Anthony,
Paton Julian,
Fisher James
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1170.4
Subject(s) - microneurography , baroreflex , medicine , heart rate , blood pressure , anesthesia , cardiology , heart rate variability , respiratory rate , interquartile range
We sought to investigate whether device guided slow deep breathing (SDB; RESPeRATE © ) influences muscle sympathetic nerve activity (MSNA) and spontaneous baroreflex sensitivity in young healthy individuals. Following a 10 min supine baseline period, 9 men (29±7 years, body mass index 24±2 kg/m 2 ; mean±SD) undertook 10 min of SDB while respiratory frequency (strain gauge pneumobelt), partial pressure of end‐tidal carbon dioxide (P ET CO 2 ), blood pressure (BP; finger photoplethymography), heart rate (HR; ECG) and MSNA (microneurography) were continuously monitored. Indices of arterial baroreflex control of the heart (sequence technique) and MSNA burst incidence were calculated. Respiratory rate was reduced from 12±2 to 6.2±0.7 breaths/min (P<0.001) during SDB, while P ET CO 2 (P=0.50), and mean BP (P=0.40) were unchanged. SDB significantly reduced MSNA burst incidence (i.e., percentage of cardiac cycles associated with a MSNA burst) from 25 (20‐38) to 20 (18‐33) (median and interquartile range; P=0.04). Neither cardiac (systolic BP‐RR interval; P=0.26) or sympathetic (P=0.95) baroreflex sensitivity were changed with SDB. Thus, reductions in MSNA burst incidence with device guided SDB in young healthy individuals appear not to be secondary to a change in baroreflex sensitivity, but may reflect an increase in lung inflation afferent input and/or a reduction in central respiratory‐sympathetic coupling. Grant Funding Source : Supported by British Heart Foundation