The purpose of this study is to evaluate the multiple effects of respiration on cardiovascular variability in different postures, by analyzing respiratory sinus arrhythmia (RSA) and respiratory-related blood pressure (BP) variations for systolic BP (SBP), diastolic BP (DBP), and pulse pressure (PP) in the respiratory-phase domain. The measurements were conducted for 420 s on healthy humans in the sitting and standing positions, while the subjects were continuously monitored for heart rate and BP variability and instantaneous lung volume. The waveforms of RSA and respiratory-related BP variations were extracted as a function of the respiratory phase. In the standing position, the waveforms of the BP variations for SBP, DBP, and PP show their maxima at around the end of expiration ( rad) and the minima at around the end of inspiration (2 rad), while the waveform of RSA is delayed by ϳ0.35 rad compared with the BP waveforms. On the other hand, in the sitting position, the phase of the DBP waveform (1.69 rad) greatly and significantly (P Ͻ 0.01) differs from that in the standing position (1.20 rad). Also, the phase of PP is delayed and that of RSA is advanced in the sitting position (P Ͻ 0.01). In particular, the phase shift of the DBP waveform is sufficiently large to alter whole hemodynamic fluctuations, affecting the amplitudes of SBP and PP variations. We conclude that the postural change associated with an altered autonomic balance affects not only the amplitude of RSA, but also the phases of RSA and BP variations in a complicated manner, and the respiratory-phase domain analysis used in this study is useful for elucidating the dynamic mechanisms of RSA.heart rate variability; Hilbert transform; respiratory phase; blood pressure variability RESPIRATION HAS STRONG AND multiple effects on the cardiovascular system. The best known effect of respiration is respiratory sinus arrhythmia (RSA) (12, 13, 26), i.e., fluctuations in heart rate (HR), depending on the phases of inspiration and expiration. RSA mainly reflects the modulation of the central autonomic outflow caused by respiration-related factors, such as spontaneous oscillations of respiratory centers and pulmonary stretch receptor afferents (8), and hemodynamic factors through the baroreflex and the Bainbridge reflex (30), which interact with each other in a complicated manner (4).Blood pressure (BP) is also affected by multiple interactions of these factors. To describe quantitatively the effects of respiration on HR and BP, Saul et al. (21) constructed a model in which HR is determined by the sum of central vagal and sympathetic activity, low-pass filtered and time delayed due to peripheral neurotransmitter kinetics. Arterial BP, determining the baroreceptor activity, is influenced by HR with some (mechanical) time delays. Then they incorporated the respiratory effects on HR and BP in two ways. First, instantaneous lung volume (ILV) has a (respiration-related) inhibitory effect on the central nervous system, which is known to be the inhibitory effect of in...