## 4 Discussion  
In this study, the effects of caffeine intake on BP, HR, SpO\({}_{2}\), blood vessel diameter, and cognitive function were analyzed. The BP change was not significant when 100 mg was ingested in a short duration, but BP increased significantly after 200 mg of intake. HR tended to decrease at both doses, and SpO\({}_{2}\) increased further when 200 mg was ingested. In the cognitive function evaluation, the accuracy improved until 30 min after 100 mg of intake but decreased thereafter, and the accuracy continuously decreased when 200 mg was ingested. On the other hand, the reaction time was shortened under all conditions, suggesting the possibility that caffeine may have a positive effect on rapid cognitive response. SBP demonstrated a general upward trend over time across all levels of caffeine intake, with a significant increase observed only at 200 mg. This increase could be attributed to the stimulation of the sympathetic nervous system, leading to catecholamine release, which induces vasoconstriction and subsequent BP elevation [8; 10; 13; 20]. The most pronounced increase occurred approximately 45 min post-intake, aligning with the peak absorption of caffeine [29; 30]. DBP showed a modest increase for up to 30 min following 100 mg of intake, followed by a decrease at 60 min. Conversely, a 200 mg intake resulted in a gradual increase in DBP up to 60 min. These observations are consistent with the mechanisms underlying \begin{table}
\begin{tabular}{c c c c c c c} \hline \hline
**Variation** & **Caffeine Dose** & **0 min** & **\(\Delta\)** & **30 min** & **\(\Delta\)** & **60 min** \\ \hline \multirow{2}{*}{VAS} & 100 mg & \(3.13\pm 2.19\) & \(-0.06\) & \(3.07\pm 2.03\) & \(-0.27\) & \(2.8\pm 2.04\) \\  & 200 mg & \(2.87\pm 2.16\) & \(-0.03\) & \(2.83\pm 2.09\) & \(-0.26\) & \(2.57\pm 2.05\) \\ \hline \multirow{2}{*}{KSS} & 100 mg & \(4.87\pm 1.59\) & \(-0.46\) & \(4.00\pm 1.46\) & \(-0.28\) & \(4.13\pm 1.41\) \\  & 200 mg & \(5.00\pm 1.55\) & \(-1.13\) & \(3.87\pm 1.22\) & \(0.00\) & \(3.87\pm 1.28\) \\ \hline \multirow{2}{*}{CFS} & 100 mg & \(16.30\pm 5.53\) & \(-1.90\) & \(14.40\pm 5.62\) & \(2.10\) & \(16.00\pm 5.64\) \\  & 200 mg & \(14.80\pm 5.58\) & \(-1.60\) & \(13.20\pm 5.64\) & \(-0.40\) & \(12.80\pm 5.31\) \\ \hline \hline \end{tabular} Abbreviations: CFS, Chalder Fatigue Scale; KSS, Karolinska Sleepiness Scale; VAS, visual analog scale.  
\end{table} 
Table 8: Results of subjective evaluation. SBP changes, indicating that the limited increase in DBP after 30 min of consuming 200 mg of caffein may reflect a physiological threshold influenced by blood flow. The changes in SBP and DBP were more pronounced with 200 mg than with 100 mg, with significant differences observed only at 60 min, indicating that higher caffeine doses exert greater effects on BP. The MaxD and MinD increased at 30 min compared to the baseline with a 100 mg intake but decreased by 60 min. Following an intake of 200 mg, MaxD slightly increased at 30 min and subsequently slightly decreased at 60 min, while MinD progressively declined. These findings suggest that high doses of caffeine have a strong effect on vasoconstriction. Changes in MaxD and MinDs were more pronounced at 100 mg than at 200 mg, with significant differences observed only at 30 min, indicating a shorter recovery period for vessel diameter compared to BP [9, 13]. PWV remained relatively stable at 30 min for all doses. At 100 mg, it increased slightly at 60 min, likely due to the smooth muscle contraction triggered by elevated intracellular calcium levels, resulting in vascular stiffening and increased wave propagation speed [31, 32]. In contrast, the PWV at 200 mg remained constant for up to 60 min. Neither time nor dosage resulted in significant differences in the PWV. Previous studies have reported either the maintenance of or an increase in PWV following acute caffeine intake [32, 33]. Differences in measurement methods, such as foot-to-foot versus the one-point approach, may account for these discrepancies.