## 1 Introduction  
Pulse rate variability (PRV) describes the changes in pulse rate through time, when it is measured from pulse wave signals such as the photoplethysmogram (PPG) [1,2]. PRV has been used as a surrogate of heart rate variability (HRV) and applied for the diagnosis and monitoring of several diseases [2], including the assessment of cardiovascular variables, such as blood pressure [3]. However, previous studies have shown that, although HRV and PRV show similar trends, they should not be considered to be the same, since the former tends to overestimate some of these indices, especially under haemodynamic changes, which have an effect on these differences [4, 5, 6]. It has been even suggested that PRV shows differences according to the site of measurement, implying that different processes affect this information in a more local way [7]. In an attempt to understand the differences between HRV and PRV, [PERSON] et al. evaluated how PRV changed in children with pacemakers set to a fixed heart rate [8]. They observed that PRV was present even in the absence of HRV and concluded that the differences between PRV and HRV arise from respiratory patterns and Pulse Transit Time (PTT). In 2014, [PERSON] et al. aimed to understand the relationship between PRV and HRV in rabbits during ventricular pacing to drive HRV to zero, and cardiac autonomic blockade, using atropine (cardiovagal blockade), metoprolol (sympathetic blockade) and both drugs (dual blockade) to understand the autonomic substrates of HRV and PRV [9]. Their results showed that: (a) PRV remained non-negligible even during ventricular pacing when HRV was almost completely eliminated, and HRV and PRV behaviour was not related in this scenario; (b) time-domain indices showed strong correlations between HRV and PRV during cardiac autonomic blockade; (c) LF and HF indices showed a relatively good agreement between HRV and PRV during the cardiac autonomic blockade, but with a consistent overestimation of HF and TP values, while normalised indices and LF/HF showed very poor accuracy and precision, especially during atropine and dual blockade and most likely because of the intrinsic PRV when HRV is decreased; and (d) non-linear measures, especially those based on entropy analysis, showed poor agreement and low correlation between HRV and PRV during any of the conditions of the autonomic blockade. Although they did not obtain PRV from human PPG signals, but from an invasive arterial pressure sensor placed into the abdominal aorta of rabbits, their results showed that PRV contains different information that may explain its differences from HRV, and they hypothesised that these differences must come from changes in pre-ejection time (PET), i.e., the time after ventricular depolarisation and before the opening of the aortic valve and which is a function of contractility, preload and afterload, or in PTT, which changes due to pulse pressure and arterial elasticity. Since both HRV and PRV relate to the changes in the duration of cardiac cycles but are measured using signals with different origins [1], there is an intrinsic difficulty in isolating PRV to understand how it is affected by physiological changes and explain the origin of the differences between HRV and PRV using data obtained from in-vivo studies. In recent years, the use of in-vitro models for the simulation of the circulatory system has gained attention, especially since it allows for the investigation of a specific process in the absence of many uncontrolled and confounding variables that are simultaneously occurring in the living human body [10]. Hence, in this study, the development of an in-vitro setup for the simulation of the upper-body circulatory system was proposed, from which PPG signals can be acquired while blood pressure and flow are modified by changing the stroke rate of a commercial pump that replicates the activity of the heart, but without the effects of autonomic modulation, i.e., in the absence of HRV.