Changes in Respiratory Sinus Arrhythmia (RSA) may result from changes in Tonic Vagal modulation of heart rate (VT), central respiratory drive, respiratory depth or respiratory frequency. The differential contribution of these parameters to RSA during different stressors is not clear, hampering the interpretation of reduced RSA found in high risk or patient groups. Using the VU-AMS device, this study tested the contributions of these determinants of RSA in a within-subject design.

Twenty-two healthy participants were submitted to mental stress, relaxation and mild physical exercise during three different breathing conditions: normal breathing, breathing compressed room air, and breathing compressed 5% CO2-enriched air. The CO2-enriched air was used to manipulate central respiratory drive, which was estimated with the end-tidal partial pressure of CO2 (PetCO2). RSA was estimated as High Frequency (HF) heart period variability power. Respiratory depth and frequency were derived from the thoracic impedance signal. The Pre-Ejection Period (PEP) was measured to obtain an indication of changes in the Tonic Sympathetic modulation of heart rate (ST), and used in combination with changes in heart rate to estimate changes in VT.

Path-analysis demonstrated that changes in VT, PetCO2, respiratory depth and respiratory frequency each had an independent contribution to changes in HF power. Reductions in HF power were enhanced by increases in respiratory frequency and reduced by increases in PetCO2 and respiratory depth. The relative contributions of these determinants were different under conditions of mental stress and physical exercise. To index within-subject changes in VT, changes in RSA should be corrected for changes in central respiratory drive, respiratory depth and respiratory frequency.

Paper presented at Measuring Behavior 2002 , 4^th International Conference on Methods and Techniques in Behavioral Research, 27-30 August 2002, Amsterdam, The Netherlands

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