Sympathetic restraint of respiratory sinus arrhythmia: implications for vagal-cardiac tone assessment in humans

Abstract

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 beta-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. beta-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). beta-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.

Baroreflex mechanisms in major depression

“…The observed reduction of the high frequency component of heart rate variability in the patients may not be related parasympathetic tone withdrawal, but to the centrally restricted range of baroreflex gain by sympathetic arousal or cardiac sympathetic nerve tonic hyperactivity (a part of general sympathetic hyperarousal), which restrains vagally mediated heart period oscillations (Cohen and Taylor, 2002;Taylor et al, 2001). This is supported by the finding that the efferent 'parasympathetic' component of the baroreflex loop was not affected in the depressed patients compared to controls.…”

Effects of aerobic training intensity on resting, exercise and post-exercise blood pressure, heart rate and heart-rate variability

“…46 Moreover, the extent to which measurements of HRV and HF reflect parasympathetic tonic activity has still not been clearly established. 47 It is thus possible that there exists differences in tonic parasympathetic activity, but that this is not adequately captured by the assessment of HR modulations such as HRV.…”

Respiratory modulation of cardiovagal baroreflex sensitivity

“…We believe that this act of artificially amalgamating the two rhythms is likely to bring about a great deal of complexity that precludes any simple interpretation of the data. For example, there is evidence that a significant degree of respiratory-related R-R interval fluctuations persists during slow breathing (ϳ120 ms) after vagalsympathetic blockade, indicating that in addition to neural processes, myocardial stretch mechanisms, which cannot be easily accounted for, also significantly contribute to R-R interval fluctuations during slow breathing (28).…”