Methodological aspects of a causal black-box model of heart period/arterial pressure interaction, arterial pressure closed-loop regulation and respiration effects on both heart period and arterial pressure are revisited in the "time" (more exactly heart beat count) domain. Parameters are estimated from experimental data (model identification) by means of multiple linear regressions of actual samples over the past ones. The elements composing either heart period or systolic arterial pressure variability are visualised as beat-by-beat series. Indexes describing the signal interactions, the loop properties and the spectral components of the variability series are consequently summarised. In 17 normal young volunteers, the analysis was carried out during active standing, rest, mild clinostatic pedalling exercise at 10%, 20%, and 30% of the maximum effort, and recovery. A negative effect of heart period changes on systolic arterial pressure of - 13.3 mm Hg/s was found at rest. This effect, though augmented by exercise, appeared insignificant in explaining arterial pressure variability. Arterial baroreflex was assessed by alphaart index which had a value of 5.18 mm Hg/ms at rest, 3.78 mm Hg/ms during active standing, and decreased progressively with exercise down to 0.55 mmHg/ms. The pressure regulation loop displayed a tendency to amplify disturbances at low frequency (around 0.1 Hz) 5.94 times at rest, augmented to 8.88 times during standing, 7.55 at 30% exercise. The first parameter of the pressure auto-regression was slightly higher than 1 at rest and even more augmented during standing, thus, indicating a tendency of arterial pressure perturbations to persist from one beat to the next. These mechanisms appear important in the genesis of low-frequency pressure waves. Nonetheless, the trace of different sources was evident in the regression residuals. Noticeably, during exercise it explained 10.16% of total heart period variability compared to 12.49% related to the low-frequency oscillations of closed-loops. The origin of high-frequency waves synchronous with respiration appeared miscellaneous as well. Arterial pressure appeared negligibly affected by heart period changes. Conversely, a limited effect of arterial pressure waves was found on heart period superimposed to a large effect of cardiopulmonary reflexes directly modulating the sinus node. In conclusion, both high-frequency and low-frequency waves are composite phenomena and a multi-channel analysis comparing heart period and arterial pressure variability yields a variety of figures assessing cardiovascular regulation and cardiorespiratory coupling.