Respiratory sinus arrhythmia and pulmonary gas exchange efficiency: time for a reappraisal

Abstract

In many cases parents still rely on the belief that ‘playing basketball makes you taller’ or better still ‘gymnastics will lead to shortness’ when orienting their child’s sports participation. Although these convictions naively dismiss strong selection bias, they demonstrate that opinions based upon faulty logic can have a long duration, unless being meticulously challenged. The main physiological role of respiratory sinus arrhythmia (RSA), which refers to the shortening and lengthening of beat-tobeat cardiac cycle intervals throughout the respiratory cycle, was first proposed 15 years ago (Hayano et al. 1996). Hayano’s initial work (Hayano et al. 1996) set a progressive acceptance that RSA could be regarded as an intrinsic function of the cardiopulmonary system, with the clustering and scattering of heartbeats during inspiration and expiration, respectively, suggested to improve pulmonary gas exchange efficiency via efficient ventilation–perfusion matching and to save unnecessary heartbeats during the ebb of perfusion that may result in wasted pulmonary blood flow. This ‘theory’ has important clinical applications, and may partly account for the association between low RSA and a variety of cardiovascular/cardiopulmonary risk factors and disease processes (see references in the article by Sin et al. 2010). Nevertheless, while the pioneering demonstrations in dogs (Hayano et al. 1996) and humans (Giardino et al. 2003) were appealing, recent findings by Tzeng, Galletly, Larsen and co-workers came, with time, to question Hayano’s views (e.g. Tzeng et al. 2007, 2009). After having exemplified the lack or inconsistencies of heartbeats clustering during inspiration in a series of wellconducted experiments in humans (e.g. Tzeng et al. 2007, 2009), the same group of authors provide, in this issue of Experimental Physiology, additional evidence for the lack of causal links between RSA and pulmonary gas exchange efficiency (Sin et al. 2010). In this very simple but intelligent study design, Peter Y. W. Sin et al. (2010) compared the response of ventilatory equivalents (VE/VO2 and VE/VCO2 ) to fast and slow breathing in control subjects and in patients with fixedrate cardiac pacemakers. While the slowing of breathing frequency was associated, as expected (Giardino et al. 2003), with increased RSA amplitude and improved pulmonary exchange efficiency in healthy control subjects (i.e. decreased ventilatory equivalents), similar improvements in pulmonary function were also observed in patients, despite unchanged RSA. Additionally, in healthy control subjects, Sin et al. (2010) could not find any correlation between the changes in RSA and ventilatory equivalents. These interesting findings are in line with the authors’ previous provocative conclusions (Tzeng et al. 2009), and clearly confirm that it may be too simplistic to assume that temporal variation in heart rate necessarily accounts for putative improvements in ventilation– perfusion matching and, conversely, that redistribution of heartbeats throughout the respiratory cycle is compulsory for improved pulmonary gas exchange efficiency. In addition, the findings of Sin et al. (2010) have important and immediate clinical implications, since they give support, irrespective of the mechanisms involved, to respiratory training at slow frequencies to improve pulmonary gas exchange efficiency in cardiovascular and pulmonary diseases (see references in the article by Sin et al. 2010). As discussed by the authors (Tzeng et al. 2009; Sin et al. 2010), other mechanisms might be responsible (and possibly effective enough) for the improved pulmonary exchange efficiency with slower breathing rates in cardiac patients lacking RSA, such as improved cardiac efficiency (via facilitation of venous return as a consequence of changes in intrathoracic pressure) and/or changes in the ratio of alveolar to dead-space ventilation. Future studies investigating (both in healthy individuals and patients) the influence of changes in intrathoracic pressure, central blood volume, cardiac function and pulmonary blood flow/O2 partial pressure on both RSA and pulmonary gas exchange efficiency might facilitate the understanding of their improbable associations. To conclude, and this is the beauty of research, this study (Sin et al. 2010) shows once again that the common beliefs of today do not always become the certitudes of tomorrow.