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Acute slow‐paced breathing modulates the pressor and depressor responses following spontaneous oscillations in muscle sympathetic nerve activity
Author(s) -
Vianna Lauro C.,
Fadel Paul J.,
Joyner Michael J.,
Wehrwein Erica A.
Publication year - 2016
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.30.1_supplement.752.8
Subject(s) - microneurography , medicine , blood pressure , heart rate , breathing , anesthesia , respiratory rate , respiratory system , cardiology , baroreflex
Previous studies have indicated that acute slow‐paced breathing (6 breaths/min) significantly decreases arterial blood pressure (BP) in both normotensive and hypertensive individuals. More recent work suggested that muscle sympathetic nerve activity (MSNA) was unchanged during acute slow‐paced breathing, however, the pattern of MSNA firing was altered in that more periods of MSNA quiescence were present. Herein, we examined the ability of MSNA to modulate BP on a beat‐to‐beat basis. We hypothesized that the magnitude of the increase in BP following a burst of MSNA is attenuated during acute slow‐paced breathing contributing to the reduction in BP previously reported. BP (brachial catheter) and MSNA (peroneal microneurography) were continuously measured in 10 young (27 ± 1 years), healthy men during 10 minutes of normal spontaneous breathing (baseline) or paced breathing at six breaths per minute. Signal averaging was used to characterize changes in mean BP for 15 cardiac cycles following heartbeats associated with and without MSNA bursts. MSNA bursts were segregated as either single bursts (directly bordered by ≥1 heartbeat lacking MSNA) or multiple bursts (any burst positioned directly adjacent to another MSNA burst). Respiratory rate was 12 ± 1.1 breaths/min during baseline and 6 ± 0.7 breaths/min during slow‐paced breathing. Compared to baseline, mean BP was decreased during slow‐paced breathing (88±2 vs. 85±2 mmHg, P<0.05), whereas MSNA burst frequency was unchanged (13±2.2 vs. 13±2.4 bursts/min, P>0.05). At baseline, mean BP significantly increased following MSNA bursts (+3.2± 0.2 mmHg, P<0.05) and this increase was augmented during slow‐paced breathing (+5.0± 0.5 mmHg, P<0.05). There was a greater increase in mean BP following single as well as multiple MSNA bursts during slow‐paced breathing. In contrast, cardiac cycles without MSNA bursts (non‐bursts) were associated with a significant decrease in mean BP (−0.7± 0.1 mmHg, P<0.05), which was also augmented during slow‐paced breathing (−1.3± 0.3 mmHg, P<0.05). In summary, the pressor and depressor responses coupled to spontaneous oscillations in MSNA are augmented during slow paced breathing with a net effect of reduced BP. Thus, changes in MSNA firing pattern, without changes in burst frequency, can modulate resting BP. Support or Funding Information Funding: NIH HL‐083947 (MJJ)