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

Clinicians and experimentalists routinely estimate vagal-cardiac nerve traf fic from respiratory sinus arrhythmia. However, evidence suggests that symp athetic mechanisms may also modulate respiratory sinus arrhythmia. Our stud y examined modulation of respiratory sinus arrhythmia by sympathetic outflo w. We measured R-R interval spectral power in 10 volunteers that breathed s equentially at 13 frequencies, from 15 to 3 breaths/min, before and after b eta -adrenergic blockade. We fitted changes of respiratory frequency R-R in terval spectral power with a damped oscillator model: frequency-dependent o scillations with a resonant frequency, generated by driving forces and modi fied by damping influences. beta -Adrenergic blockade enhanced respiratory sinus arrhythmia at all frequencies (at some, fourfold). The damped oscilla tor model fit experimental data well (39 of 40 ramps; r = 0.86 +/- 0.02). b eta -Adrenergic blockade increased respiratory sinus arrhythmia by amplifyi ng respiration-related driving forces (P < 0.05), without altering resonant frequency or damping influences. Both spectral power data and the damped o scillator model indicate that cardiac sympathetic outflow markedly reduces heart period oscillations at all frequencies. This challenges the notion th at respiratory sinus arrhythmia is mediated simply by vagal-cardiac nerve a ctivity. These results have important implications for clinical and experim ental estimation of human vagal cardiac tone.