Abstract

We appreciate and welcome the comments from Drs Tharion and Subramani on our paper (Sin et al. 2010), which we summarize as follows: (1) ventilatory equivalents of carbon dioxide ( ) and oxygen ( ) are imperfect measures of pulmonary gas exchange efficiency; and therefore (2) our study does not allow conclusions to be drawn regarding the role of respiratory sinus arrhythmia (RSA) in pulmonary gas exchange optimization. At first glance it may seem that our measurement choice compromises our study conclusions. Closer examination of our stated hypothesis, however, shows that the conclusions are in fact well justified. To date, evidence in favour of Hayano's hypothesis that ‘RSA improves pulmonary gas exchange efficiency by matching alveolar ventilation and capillary perfusion throughout respiratory cycle…by suppressing unnecessary heartbeats during expiration and ineffective ventilation during waning phases of perfusion’ is largely based on animal experiments (Hayano & Yasuma, 2003). In an attempt to establish the relevance of this hypothesis in humans, Giardino et al. (2003) showed that and were significantly reduced during slow breathing and attributed this ‘pulmonary gas exchange’ improvement to the concomitant rise in RSA amplitude. We were sceptical of this interpretation given we had already shown that physiological levels of RSA do not give rise to significant heartbeat redistribution (Tzeng et al. 2009). Consequently, the study was conducted to test our hypothesis that a previously described association between RSA amplitude, and is unrelated to the presence of RSA itself; the study was not an attempt to re-examine Hayano's hypothesis, which we had already shown to be physiologically improbable (Tzeng et al. 2009). Although ventilatory equivalents have been previously applied as indices of pulmonary gas exchange efficiency (e.g. Giardino et al. 2003), we are in full agreement with Drs Tharion and Subramani that they are not gold standard and never alluded to this being the case. Nevertheless, as discussed in the Viewpoint article that accompanied our work, ‘opinions based upon faulty logic can have a long duration, unless being meticulously challenged’ (Buchheit, 2010). Knowing that the fundamental premise of Hayano's hypothesis is not met, we simply took one further step to demonstrate unequivocally the faulty logic that underpins current evidence. Thus, for the benefit of the general readership, we reiterate again that the use of ventilatory equivalents, whatever they reflect, does not compromise our position that the concurrent rise in RSA and reduction in and during slow breathing cannot be taken as evidence that RSA optimizes human pulmonary gas exchange efficiency. The commentary from Drs Tharion and Subramani further reinforces our core message that a teleological role of human RSA, if it has one, remains to be determined.

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