## 4 Discussion  
This preliminary investigation aimed to examine the effect of 3 mg/kg of caffeine ingested before an evening (i.e., 7:00 PM) judo training session on a variety of actigraphy-derived and self-rated sleep measures during the night following the trial and a subjective recovery-stress state analysis carried out the following morning. The main findings of the study are as follows: (i) there were no significant differences in actigraphy-derived sleep measures between caffeine and placebo conditions; (ii) caffeine supplementation led to a significant decrease in self-reported sleep quality compared with the placebo condition; (iii) no significant differences between conditions were observed in the reports of recovery-stress state. Our results revealed that caffeine consumed before an evening training session caused no significant disruption to various actigraphy-derived sleep measures. The results of our study are contrary to previous findings concerning caffeine supplementation in athletes in which objective methods were used for sleep monitoring [30; 31]. In these investigations, significant disruptions in sleep onset latency [30], sleep duration [30], sleep efficiency [30; 31], number of awakenings [31], and REM sleep duration [30] were observed when caffeine was ingested before late-afternoon (i.e., 5:00 PM) [30] and evening (i.e., 8:00 PM) [31] exercise. The differences between the results of these studies [30; 31] and the results of the present study may be related to the caffeine doses (3 mg/kg vs. 6 mg/kg). Although evening caffeine intake might disturb sleep through a reduction in 6-sulfatoxylin melatonin (the main metabolite of melatonin) [49], and via adrenaline and noradrenaline stimulation in the adrenal medulla [50; 51], the magnitude of sleep interruptions might be dose-dependent [19; 52; 53]. Moreover, a large inter-individual variability in caffeine pharmacokinetics has been observed [1], with a half-life ranging from 2 to 10 h [54]. It is worth noting that the CYP1A2 gene impacts the speed of caffeine metabolism. Individuals with the AA genotype are considered \"fast metabolizers\" of caffeine, while those with the AC or CC genotype tend to have a slower caffeine metabolism [55]. Because only one participant reported side effects (mainly observed in \"slow metabolizers\"), it is possible that the sample consisted mainly of those with the fast-metabolizing genotype. Additionally, in the study by [PERSON] et al. [56], a decrease in caffeine half-life to 2.3 h in athletes after a single 250 mg dose of caffeine was observed, suggesting faster caffeine elimination during exercise. In summary, it is possible that the caffeine doses in the current study being half the size of those administered in the previous studies [29; 30; 32] resulted in caffeine plasma levels that \begin{table}
\begin{tabular}{l c c c c c} \hline \hline  & **Placebo** & **Caffeine** & **Z** & **\(p\)** & **ES (95\% CI)** \\ \hline Muscular Stress & 2.4 \(\pm\) 0.9 & 2.6 \(\pm\) 1.0 & 0.25 & 0.79 & \(-\)0.21 (\(-\)1.13, 0.73) \\ \hline Lack of Activation & 2.8 \(\pm\) 1.5 & 2.4 \(\pm\) 1.2 & 0.52 & 0.60 & \(-\)0.29 (\(-\)1.21, 0.65) \\ \hline Negative Emotional State & 1.6 \(\pm\) 0.7 & 2.2 \(\pm\) 1.6 & 0.91 & 0.36 & 0.49 (\(-\)0.47, 1.40) \\ \hline Overall Stress & 2.7 \(\pm\) 1.2 & 2.9 \(\pm\) 1.2 & 0.54 & 0.58 & 0.17 (\(-\)0.77, 1.08) \\ \hline Physical Performance Capability & 3.4 \(\pm\) 0.7 & 3.4 \(\pm\) 1.1 & 0.17 & 0.86 & 0.00 (\(-\)0.92, 0.92) \\ \hline Mental Performance Capability & 3.9 \(\pm\) 1.1 & 3.4 \(\pm\) 1.1 & 0.77 & 0.44 & \(-\)0.45 (\(-\)1.37, 0.50) \\ \hline Emotional Balance & 4.1 \(\pm\) 1.1 & 4.0 \(\pm\) 1.1 & 0.40 & 0.69 & \(-\)0.09 (\(-\)1.01, 0.84) \\ \hline Overall Recovery & 3.6 \(\pm\) 1.0 & 3.1 \(\pm\) 1.2 & 0.77 & 0.44 & \(-\)0.45 (\(-\)1.37, 0.50) \\ \hline \end{tabular} Data reported as mean \(\pm\) standard deviation. _Z_: Wilcoxon pairwise order test result.  
\end{table} 
Table 3: Results of short recovery and stress scale for caffeine and placebo conditions.