Suprasystolic limb occlusion (SLO) is a common challenge for assessing endothelial activity and cardiovascular risk. It is commonly carried out by inflating a pneumatic pressure cuff above systolic pressure for a certain period of time, during which perfusion in distal territories decreases significantly. Upon cuff release perfusion increases producing a well-known reactive hyperemia. Although it remains underexplored, the contralateral limb also responds to SLO. Previous results from our group suggest that this contralateral response is a sympathetically-driven perfusion decrease. This study aims to further expand the knowledge on the physiological response to SLO by exploring the physiological mechanisms underlying the contralateral vascular response. Ten healthy male subjects (mean 20.2 ± 2.3 y.o.) participated in this study after giving informed written consent. After acclimatization, subjects performed a standard SLO protocol on a random upper limb while sitting upright, as follows: 10 min resting with both arms at heart level (phase I), 5 min random arm occlusion (200 mmHg, phase II) and 10 min recovery in the initial position (phase III). Photoplethysmography (PPG) signals were acquired from the second finger of the occluded (test) and non-occluded (control) arms and then decomposed into their main frequency components (cardiac, respiratory, myogenic, sympathetic, endothelial) with the wavelet transform (WT). The electrodermal activity (EDA) was also acquired from the third and fourth fingers of both hands. Nonparametric statistics were used for comparing the activity of each frequency between phases and arms (p<0.05). As previously reported, occlusion caused a significant decrease in cardiac, respiratory, myogenic and sympathetic activities together with a significant increase in NO-dependent and NO-independent endothelial activities in the test arm. The contralateral arm responded to occlusion with a significant decrease in perfusion, however no significant changes in the signal components. Nevertheless, the cardiac activity decreased, whereas the myogenic, sympathetic and endothelial NO-dependent increased. In contrast, the respiratory and endothelial NO-independent activities remained unchanged. Therefore, the perfusion decrease of the contralateral limb should be explained by the decrease of the cardiac and by the increase of the sympathetic activities. EDA increased significantly in both limbs during occlusion. These results show an overall agreement between EDA and the PPG sympathetic activity, reinforcing the usefulness of WT for assessing the mechanisms underlying perfusion regulation. They also highlight that only the non-occluded arm can be used for measuring the sympathetic nervous activity during SLO with decomposed PPG signals.