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Influence of fitness on the pressor response following spontaneous bursts of muscle sympathetic nerve activity (1172.6)
Author(s) -
Restaino Robert,
Credeur Daniel,
Holwerda Seth,
Fadel Paul
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.1172.6
Subject(s) - microneurography , blood pressure , medicine , beat (acoustics) , reflex , cardiology , mean arterial pressure , baroreflex , heart rate , anesthesia , physics , acoustics
Previous studies suggest that high fit (HF) subjects may exhibit altered vascular responses to reflex mediated increases in muscle sympathetic nerve activity (MSNA). Whether the ability of MSNA to modulate arterial blood pressure (BP) on a beat‐to‐beat basis is affected by fitness is unknown. In 7 HF (VO2 max=67±2 ml/kg/min) and 7 average fit (AF; VO2=44±2 ml/kg/min) young men, MSNA (microneurography) and blood pressure (Finapres) were continuously measured at rest for 10 minutes. Signal averaging was used to characterize beat‐by‐beat changes in mean arterial pressure (MAP) for 10 cardiac cycles following each individual MSNA burst and a peak response calculated. Variations in MSNA burst pattern were considered by comparing single (bordered by >1 heartbeat lacking MSNA) vs. multiple bursts. Changes in MAP were also calculated following heartbeats without MSNA (i.e., non‐bursts). In response to single MSNA bursts, no significant difference was noted in MAP (HF: +2.8±1.2 vs. AF: +1.8±0.34 mmHg, P>0.05); however, multiple bursts produced a significantly greater increase in MAP in HF subjects (HF: +4.8±0.5 vs. AF: +3.4±0.3 mmHg, P<0.05). Also, following non‐bursts, HF subjects tended to have a greater reduction in MAP (HF: ‐1.3±0.3 vs. AF: ‐0.7±0.1, P=0.053). These preliminary findings suggest a greater role for spontaneous MSNA bursts in modulating BP on a beat‐to‐beat basis in HF compared to AF subjects. Grant Funding Source : Supported by NIH Grant RO1 HL093167 (PJF)