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Departments of Internal Medicine and Physiology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Richmond 23249; and Medical College of Virginia at Virginia Commonwealth University, Richmond, Virginia 23284
Clinicians and experimentalists routinely estimate
vagal-cardiac nerve traffic from respiratory sinus arrhythmia. However, evidence suggests that sympathetic mechanisms may also modulate respiratory sinus arrhythmia. Our study examined modulation of respiratory sinus arrhythmia by sympathetic outflow. We measured R-R
interval spectral power in 10 volunteers that breathed sequentially at
13 frequencies, from 15 to 3 breaths/min, before and after
-adrenergic blockade. We fitted changes of respiratory frequency R-R
interval spectral power with a damped oscillator model:
frequency-dependent oscillations with a resonant frequency, generated
by driving forces and modified by damping influences.
-Adrenergic
blockade enhanced respiratory sinus arrhythmia at all frequencies (at
some, fourfold). The damped oscillator model fit experimental
data well (39 of 40 ramps; r = 0.86 ± 0.02).
-Adrenergic blockade increased respiratory sinus arrhythmia by
amplifying respiration-related driving forces (P < 0.05), without altering resonant frequency or damping influences. Both
spectral power data and the damped oscillator model indicate that
cardiac sympathetic outflow markedly reduces heart period oscillations
at all frequencies. This challenges the notion that respiratory sinus
arrhythmia is mediated simply by vagal-cardiac nerve activity. These
results have important implications for clinical and experimental
estimation of human vagal cardiac tone.
autonomic nervous system; heart rate variability; vagus
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