Effectiveness of the experimental manipulation
Participants reported comparable levels of sleepiness/alertness at the beginning of both experimental sessions (t20 = 0.271, p = 0.789, d = 0.06). For the level of activation, there were significant differences for the substance (F1,20 = 40.51, p < 0.001, ƞp2 = 0.67), point of measure (F1,20 = 39.17, p < 0.001, ƞp2 = 0.66), and the interaction substance × point of measure (F1,20 = 26.36, p < 0.001, ƞp2 = 0.57). Consequently, we performed two separate paired samples t-tests for the subjective scores of activation in both experimental sessions (caffeine, placebo), considering the point of measure as the only within-participants factor. These analyses revealed that participants reported higher levels of activation after caffeine intake (t20 = 8.22, p < 0.001, d = 1.79), but not after ingesting the placebo capsule (t20 = 0.34, p = 0.741, d = 0.08) (Fig. 1).
Effects of caffeine intake on DVA
Table 1 shows descriptive values for the DVA parameters assessed in this study.
Table 1 Descriptive values (mean ± standard deviation) for the dynamic visual acuity parameters assessed at the different measurement moments in both experimental conditions For the horizontal RT, we found a statistically significant effect for the target velocity (F3,60 = 25.28, p < 0.001, ƞp2 = 0.56) and the interaction “substance × point of measure” (F1,20 = 4.37, p = 0.049, ƞp2 = 0.18). No differences were observed for the main effects of substance (F1,20 = 0.38, p = 0.546) and point of measure (F1,20 = 1.79, p = 0.197), as well as any other interactive effect (all Ps > 0.544). Complementarily, we performed two separate (2 [point of measure] × 4 [velocity]) ANOVAs for the caffeine and placebo conditions. For the caffeine condition, the horizontal RT was significantly shorter after caffeine intake (F1,20 = 7.64, p = 0.012, ƞp2 = 0.28), and faster target velocities caused shorter horizontal RTs (F3,60 = 24.09, p < 0.001, ƞp2 = 0.55). The interactive effect “point of measure × target velocity” did not reach statistical significance (F3,60 = 1.06, p = 0.373). For the placebo condition, faster target velocities were associated with shorter horizontal RTs (F3,60 = 9.86, p < 0.001, ƞp2 = 0.33), but no effects were observed for the point of measure (F1,20 = 0.04, p = 0.852) or the interaction “point of measure × target velocity” (F3,60 = 0.23, p = 0.877) (Fig. 2A).
The analysis of the random RT yielded a statistically significant effect for the target velocity (F3,60 = 58.49, p < 0.001, ƞp2 = 0.75), but no differences were obtained for the main effects of substance (F1,20 = 0.04, p = 0.846) and point of measure (F1,20 = 0.67, p = 0.424), as well as for any interaction (all Ps > 0.505) (Fig. 2B).
For the horizontal DVA, there were a statistically significant effect of the point of measure (F1,20 = 16.17, p < 0.001, ƞp2 = 0.45), target velocity (F3,60 = 117.37, p < 0.001, ƞp2 = 0.85), and the interaction “substance × point of measure” (F1,20 = 6.03, p = 0.023, ƞp2 = 0.23). Also, the interaction “point of measure × target velocity” (F3,60 = 2.70, p = 0.053, ƞp2 = 0.12) showed a marginal effect, whereas no statistically significant differences were obtained for main effect of substance (F1,20 = 0.08, p = 0.785), the interactions “substance × target velocity” (F3,60 = 0.21, p = 0.889), and “substance × point of measure × target velocity” (F3,60 = 0.50, p = 0.685). Thus, we carried out separate (2 [point of measure] × 4 [velocity]) ANOVAs for the caffeine and placebo conditions in order to clarify the differences observed for the interactions in the main analysis. In the caffeine condition, we obtained a statistically significant effect for the point of measure (F1,20 = 17.16, p < 0.001, ƞp2 = 0.46) and target velocity (F3,60 = 77.83, p < 0.001, ƞp2 = 0.80), showing a better DVA after caffeine intake and with lower velocities of target motion. No differences were observed for the interaction “point of measure × target velocity” (F3,60 = 1.78, p = 0.230). For the placebo condition, the main factor of target velocity reached statistical significance (F3,60 = 67.03, p < 0.001, ƞp2 = 0.77), with lower velocities being associated with better VA. However, no effects were obtained for the main effect of point of measure (F1,20 = 1.38, p = 0.255) or the interaction “point of measure × target velocity” (F3,60 = 1.37, p = 0.261) (Fig. 3A).
Lastly, we analyzed the changes in random DVA, observing a statistically significant effect for the point of measure (F1,20 = 9.05, p = 0.007, ƞp2 = 0.31), target velocity (F3,60 = 124.51, p < 0.001, ƞp2 = 0.86), and the interaction “substance × point of measure” (F1,20 = 6.17, p = 0.022, ƞp2 = 0.24). The main effect of substance (F1,20 = 0.75, p = 0.398) and the rest of interactions (all Ps > 0.704) did not reach statistical significance. Again, two separate (2 [point of measure] × 4 [velocity]) ANOVAs for the caffeine and placebo conditions were conducted. For the caffeine condition, there were statistically significant differences for the point of measure (F1,20 = 12.26, p = 0.002, ƞp2 = 0.3) and target velocity (F3,60 = 52.91, p < 0.001, ƞp2 = 0.73), but not for the interaction “point of measure × target velocity” (F3,60 = 0.19, p = 0.903). Overall, the ingestion of caffeine lead to better DVA, and faster velocities of target motion were associated with worse DVA. The analysis of the placebo condition exhibited a statistically significant effect of target velocity (F3,60 = 125.13, p < 0.001, ƞp2 = 0.86), indicating that faster velocities of target motion caused reduced DVAs. No differences were obtained for the point of measure (F1,20 = 0.23, p = 0.634) or the interaction “point of measure × target velocity” (F3,60 = 0.25, p = 0.862) (Fig. 3B).