## 4 Discussion
### Tissue Oxygen in Dynamic Arm Movement  
Previously, it was assumed that exoskeleton-assisted arm movement could compensate for a negative effect on tissue oxygen saturation by regular loading and unloading at the interface, activating the cardiovascular system as well as the musculovenous pump. The metabolic effects on the TSI response were estimated to be negligible because the shoulder muscles performed the main work of the dynamic task and the upper arm muscles had to perform only minor stabilization functions.  
When visually inspecting the TSI trajectories under motion and closed pHMIs (Figure 7), TSI first overshoots, drops rapidly after ~15 s in a wave-like manner, and settles at a level slightly above baseline value after ~1.5 min. After reopening the pHMIs, the signal increases rapidly and overshoots significantly higher than in resting exoskeleton or venous conditions but returns to baseline faster than in arterial occlusion in resting posture. This signal behavior, especially the TSI recovery rate and overshoot after occlusion, is usually not observed in studies with light exercise; compare [49; 57; 58]. It may have occurred as a motion artifact when subjects inadvertently tried to assist the examiner in closing the pHMI and slightly tightened the upper arm muscles.  
The results of the dynamic TSI measurements are not yet fully understood. Contrary to hypothesis (ii), the study showed that exercise does not neutralize oxygen saturation in the tissue as long as the pHMI is closed. TSI\({}_{\text{Slopel}}\) dropped significantly steeper in the occlusion period with movement compared to the resting conditions and TSI\({}_{\text{Slope2}}\) showing significantly higher growths as well as higher TSI\({}_{\text{Overshoot}}\) values with movements (compare Tables 3 and 5). On the other hand, hypothesis (ii) is supported by the fact that the TSI values settle at a balanced level after some time of occlusion during the light activity. The reason for this will be functional vasodilation of the anterior arteries and arterioles due to motion [56].  
The steeper downslope during occlusion with exercise, compared to rest, could be explained by enhanced metabolic activity as well as persistent stasis due to pHMI pressure. It seems unlikely that the increase in blood pressure in the capillary bed (due to vasodilation) rises to an extent that the external restrictive occlusion of pHMI is exceeded. Accordingly, the pHMI does not allow the removal of venous blood and the metabolites. This is also supported by the upslope and overshoot behavior of TSI.  
TSI\({}_{\text{Slope2}}\) and TSI\({}_{\text{Overshoot}}\), as expressions of a hyperemic response, show significant results only for the factor movement, but are not determined by the factor pHMI design or the interaction between both; compare Table 5. Therefore, the steeper increase in TSI\({}_{\text{Slope2}}\) and the higher percentage of TSI\({}_{\text{Overshoot}}\) when performed with exercise probably reflect a combination of functional and reactive hyperemia, caused by blood stasis, metabolite accumulation, and cardiovascular activity. However, the influence of movement on TSI\({}_{\text{Slope2}}\) and TSI\({}_{\text{Overshoot}}\) cannot be quantified, since in this first pilot no testing was run with motion only. The faster decline to baseline can probably be explained by the increased cardiovascular activity due to exercise.