Respiratory sinus arrhythmia (RSA) is an acceleration of heart rate during inspiration and deceleration with expiration. We asked whether or not in humans some of the volume-related information necessary for RSA originated from the chest wall. Men and women, 19–20 years old, were breathing supine. Rib cage and abdomen displacement provided an index of tidal volume (VT) and RSA was computed breath-by-breath from the peak and trough of instantaneous heart rate. First, measurements were taken during breathing at rest (protocol a, 129 male and 164 female). Then, in subgroups of the original subject population, measurements were collected for the first five breaths immediately following a brief breath-hold period (protocol b), predominantly with the rib cage or predominantly with the abdomen (protocol c), above functional residual capacity or below it (protocol d). As long as VT was constant, severe chest wall distortion (protocol c) did not modify RSA. A drop in absolute lung volume (protocol d) or an increase in VT (protocol b) respectively decreased and increased RSA. The results, globally taken, are compatible with the notion that in humans changes in lung volume are detected by lung mechanoreceptors, whereas chest wall reflexes play no role in RSA. No difference in RSA emerged between genders during resting breathing or modest breath-hold hyperventilation.

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