Cardiorespiratory Rhythmicities in Humans

Abstract

Although the basic determinants of cardiovascular and respiratory regulation are well described, the complex integration of these processes on a beat-to-beat, breath-to-breath basis is less widely appreciated. Cardiorespiratory interactions occurring on this small time scale manifest as two periodicities known as respiratory sinus arrhythmia (RSA), the respiratory modulation of heart rate (HR), and cardioventilatory coupling (CVC), the cardiac triggering of inspiratory activity. This thesis sought to further our global understanding of how these cardiorespiratory rhythmicities represent underlying autonomic control processes and their physiological significance to the human body.

In this thesis, pattern analysis of RSA demonstrated temporal changes in HR, reflected dynamic changes in parasympathetic activity, and was not subject to sympathetic modulation. Further examination demonstrated non-linearities in the temporal HR-to-blood pressure (BP) relationship, indicating RSA cannot be explained by afferent baroreceptor activity and thus indices of baroreflex function cannot be accurately derived from spontaneous cardiovascular oscillations. This thesis also found evidence that does not support the notion that impaired baroreflex function may be ameliorated with slow breathing exercises. These observations highlight the caution required when inferring information about autonomic function from spontaneous cardiovascular rhythms.

Investigations into the functional role of these cardiorespiratory rhythmicities showed RSA does not cause significant redistribution of heartbeats within the respiratory cycle despite mediating oscillations in HR, thus challenging the growing opinion that RSA improves gas exchange by preferential redistribution of heartbeats. It was also shown that previously observed associations between RSA amplitude, modified by stepwise paced breathing, with pulmonary gas exchange efficiency were independent of the presence of RSA itself. This provides further evidence that RSA does not improve pulmonary gas exchange efficiency. In addition, no association between artificial CVC and pulmonary gas exchange efficiency was found.

Overall, this thesis validated the utility of pattern analysis to more accurately assess the complex temporal relations of physiological rhythms. This methodology may therefore be applied to assess other rhythms within or beyond the scope of physiology. Findings from this thesis also do not support the clinical use of slow, yogic breathing in the amelioration of baroreflex dysfunction. Finally, the negative observations regarding the teleological function of RSA and CVC reiterate the need for further exploration into the physiological roles of cardiorespiratory rhythms.