## 4 Discussion
The latter provides more localized measurements, thereby reducing variability. Overall, PSV exhibited a decreasing trend 30 min after intake across all doses. Recovery was observed after 60 min for 100 mg, whereas a slight decrease was observed for 200 mg. Although the reduction observed at 30 min was more substantial at a 100 mg caffein dose, both doses showed similar levels at 60 min, without significant differences. This aligns with the effects of caffeine on the carotid and peripheral arteries, where vasoconstriction impedes smooth blood flow owing to reduced adenosine activity [8, 34, 35]. HR decreased significantly over time for all doses, with greater reductions at 200 mg than at 100 mg at 30 min. After 60 min, both of the doses resulted in similar reductions. This trend is likely a baroreflex response to elevated BP, aimed at reflexively lowering HR [36, 37, 38]. SpO\({}_{2}\) increased across all doses up to 30 min, followed by a slight decline at 100 mg, and continued to increase at 200 mg up to 60 min. These results are consistent with previous findings indicating that a low dose of caffeine reduces tissue oxygen consumption, leading to increased SpO\({}_{2}\) levels [39, 40]. In cognitive function tests, comprising the 2_B test assessment, the accuracy rate increased at 30 min for 100 mg but returned to baseline by 60 min, whereas it showed a continuous decline until 60 min after a 200 mg dose. The transient improvement at 30 min with the lower dose reflected the peak absorption and immediate effects of caffeine [29, 30]. However, the subsequent decline highlights the short-lived nature of the cognitive effects of caffeine. Increased sympathetic activity due to higher caffeine doses likely contributed to the reduced accuracy. The participants' stationary posture during the experiment may have activated the default mode network, which is associated with reduced focus and concentration [41, 42, 43, 44, 45, 46]. The response time consistently improved over time for all doses, indicating enhanced cognitive arousal with caffeine intake, regardless of the dose. Subjective measures, such as the VAS, KSS, and CFS, demonstrated increased comfort and reduced sleepiness and fatigue at 30 and 60 min for both doses. VAS and KSS showed greater changes at 100 mg, whereas CFS showed greater changes at 200 mg. These findings indicate the arousal effects of caffeine, which are mediated by dopaminergic modulation in the prefrontal cortex, which enhances mood and relaxation [47, 48, 49]. The general expectation of the effects of caffeine may have influenced the subjective evaluations regardless of the actual dose [50]. Overall, our findings indicate that caffeine exerts both dose- and time-dependent effects on physiological and cognitive parameters. Moderate caffeine intake appears to be beneficial for maintaining vascular health and cognitive activation, while excessive intake may lead to adverse vascular changes and cognitive impairment. The limitations of this study include that the participants of the experiment were limited to their 20 s, so it was not possible to compare the results according to age, and the effect of caffeine on the patients with any disease could not be confirmed. In addition, the change after 60 min could not be confirmed because the measurement was made within a limited time up to 60 min after caffeine intake. The number of study participants is still small. Therefore, in a future study, it is necessary to supplement these limitations and increase the number of samples to conduct studies on various age groups and patients with diseases and additional studies on changes after 60 min. Unlike some previous studies that were conducted in the lying down position and/or with a single dose [32; 51], this study was conducted in a sitting position and with two different doses. In addition, this study examined the vascular physiology of caffeine, cognitive function, and subjective changes in comparison to the previous study [51].