Sympathovagal balance: a reappraisal.

Editor must not exceed 400 words in length and may be subject to editing or abridgment. Letters must be limited to three authors and five references. They should not have tables or figures and should relate solely to an article published in Circulation within the preceding 12 weeks. Only some letters will be published. Authors of those selected for publication will receive prepublication proofs, and authors of the article cited in the letter will be invited to reply. Replies must be signed by all authors listed in the original publication. A letter is inadequate to rebut fully Eckberg's destructive and selectively referenced polemic against sympathovagal balance, 1 which ignored many prior contributions constructively addressing the same points now raised. Because RR low frequency (LF) is much reduced by atropine, its relation to sympathetic outflow was questioned. De Boer et al 2 explained the origin of LF oscillations as the interaction of fast vagal and slow sympathetic responses, validated by the LF oscillations that follow a single stimulus to the human carotid sinus. 3 Eckberg states that there is no evidence that LF power is related to sympathetic nerve traffic. We 4 showed that sympathetic reinnervation in transplanted hearts was associated with nonrespiratory LF. Exact quantitative correlations between different sympathetic measures would be surprising. It was stated by Eckberg that respiratory RR interval variability (high frequency, or HF) " reflects primarily respiratory gating of vagal-cardiac motor neurone responses, " whereas there is much evidence that in conscious humans it represents baroreceptor-driven responses to respiratory blood pressure swings. 5,6 During increasing exercise, and also with denervation, nonneural mechanisms, such as sinus node stretch from increasing respiratory fluctuation in venous return, become important contributors to RR HF. 7 Fluctuations in nerve traffic were not thought important compared with absolute levels; the widely reported ATRAMI 8 and UK HEART 9 studies contradict this view. The concept of reciprocal changes in sympathetic and vagus output was questioned by citing the diving reflex, in contrast to more physiological states such as standing, arousal, or emotion, in which there is clear reciprocity. Both HF and LF RR variability are greatly influenced by the gain of the baroreflex. 2,5 It is not surprising that LF is paradoxically reduced in exercise and heart failure (despite increased sympathetic drive), because baroreflex sensitivity gain for heart rate control is markedly reduced in these conditions. 5 Eckberg's own study showed a " …