## 4 Discussion
\begin{table}
\begin{tabular}{c c c c} \hline \multicolumn{4}{c}{**Hybrid (Cycle Ergometer + WB-ENMS)**} \\ \hline - & **Baseline** & **Just after Exercise** & **20 min after Exercise** \\ (_n = 15_) & **(_n = 15_)** & **(_n = 15_)** \\ \hline
**Variables** & **Mean \(\pm\) SD** & **Mean \(\pm\) SD** & **Mean \(\pm\) SD** \\ \hline Diacon-reactive oxygen metabolites (U. CARR) & 303.8 \(\pm\) 73.3 & 328.8 \(\pm\) 66.5 & 319.5 \(\pm\) 68.7 \\ Biological antioxidant potential (\(\mathrm{\mu mol/L}\)) & 2407.9 \(\pm\) 332.9 & 2771.0 \(\pm\) 481.8 \({}^{\star}\) & 2707.5 \(\pm\) 494.4 \\ Total vessel density of & 10.9 \(\pm\) 1.8 & 12.3 \(\pm\) 1.9 & 12.1 \(\pm\) 2.5 \\ small vessels (mm/mm\({}^{2}\)) & 7.8 \(\pm\) 2.3 & 8.7 \(\pm\) 2.5 & 8.1 \(\pm\) 3.6 \\ Percentage of perfused small vessels (\%) & 73.6 \(\pm\) 1 & 73.4 \(\pm\) 19.0 & 62.3 \(\pm\) 19.8 \\ \hline \end{tabular} \({}^{\star}\)_p_ \(<\) 0.05 vs. baseline, \({}^{\star}\)_p_ \(<\) 0.01 vs. baseline, \({}^{\star}\)_p_ \(<\) 0.05 vs. just after exercise, \({}^{\star}\)_n_ \(p\) \(<\) 0.01 vs. just after exercise.  
\end{table} 
Table 4: \(Cont.\)prolonged whole blood passage time. During exercise, blood is redistributed to active muscles, and blood volume to the digestive system decreases; even in healthy adults, visceral perfusion decreases immediately after exercise [22]. Decreased visceral blood flow may be reflected in the sublingual blood flow [23]; additionally, it has been reported that high dehydration levels and prolonged exercise may reduce functional capillary density [24]. We predicted that the sublingual and nailfold microcirculatory flow would decrease due to the decrease in visceral blood flow caused by dehydration and blood flow distribution to the motor muscles. Nevertheless, no changes in the sublingual microvascular flow index or nailfold microvascular flow were observed in vivo. Exercise causes shear stress in the vascular endothelium, resulting in vasodilation due to nitric oxide (NO) synthase activity and NO utilization. This may be the reason for the difference between the blood fluidity observed ex vivo, and blood flow observed in vivo. NMES can increase skin perfusion via vasodilation [25]. NMES has been reported to enhance hypoxia-inducible factor (HIF) 1\(\alpha\) and vascular endothelial growth factor, which may have accelerated wound healing of diabetic foot ulcers. [26]. HIF-1\(\alpha\) is highly expressed in fast-twitch muscle (type II), which has a high glycolytic capacity. Therefore, sustained contraction of fast-twitch muscle by WB-NMES may have elevated HIF-1\(\alpha\) and lactate production. Vasodilation due to lactate accumulation in addition to NO-induced vasodilation may have offset the deterioration of sublingual and nailfold microcirculation due to exercise-induced activation of the sympathetic nervous system. During acute exercise, active oxygen is produced in the body by reperfusion after muscle damage or organ ischemia, causing oxidative stress damage, such as tissue damage and inflammation. Conversely, after acute exercise, antioxidant enzymes increase and suppress the increase in oxidative stress. Creatine kinase and the induction of muscle damage have been reported as side effects of WB-NMES [27]; however, there was no significant increase in oxidative stress due to WB-NMES observed in this study, which was proven to be safe and effective.