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A theoretical study of the physiological significance of respiratory sinus arrhythmia
Author(s) -
Ben-Tal Alona,
Shamailov Sophie S.,
Paton Julian F.R.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.702.5
Subject(s) - expiration , vagal tone , carbon dioxide , heart rate , breathing , respiratory system , cardiology , respiration , anesthesia , medicine , diaphragmatic breathing , blood pressure , chemistry , heart rate variability , anatomy , pathology , alternative medicine , organic chemistry
Respiratory sinus arrhythmia (RSA) is a phenomenon whereby the heart rate increases during inspiration and decreases during expiration. We used mathematical models to test two hypotheses for the physiological function of RSA: 1) a previously suggested hypothesis that RSA improves gas exchange efficiency and 2) a new hypothesis that RSA minimizes the work done by the heart while maintaining physiological levels of arterial carbon dioxide. The study was performed in two parts. First, the optimal heart rate (HR) was calculated using techniques from optimal control theory. Second, the HR function was prescribed and the cardiac work, as well as the volumes of oxygen and carbon dioxide taken up or removed by the blood respectively were calculated. We found that although gas exchange efficiency improved with slow and deep breathing and with increased mean heart rate, this was unrelated to RSA. When we tested the second, new hypothesis by direct calculation of the HR we found that the calculated HR was remarkably similar to RSA and that this became more profound under slow and deep breathing. When the HR was prescribed, we found that cardiac work was minimized for RSA‐like HR functions when the blood partial pressure of carbon dioxide was controlled, most profoundly under slow and deep breathing. These findings provide new insights into potential benefits of RSA under physiological conditions. Supported by NIH grant R01 NS069220.