However, these changes were physiologically negligible. In addition, end‐tidal carbon dioxide partial pressure increased marginally (+1.1 ± 1.5 mmHg) during normocapnic hyperventilation, likely due to suboptimal tidal volume regulation, possibly because participants were required to focus simultaneously on both the eye movement task and voluntary breathing control. Given that this elevation is very small, we believe its influence such as on ventilatory drive would be negligible; however, this remains unclear in our study. Despite the slightly elevated end‐tidal carbon dioxide partial pressure observed during normocapnic hyperventilation, middle cerebral artery mean blood velocity paradoxically decreased (−8.5 ± 8.4 cm/s; Fig. 2B and  C ). [...] Despite the slightly elevated end‐tidal carbon dioxide partial pressure observed during normocapnic hyperventilation, middle cerebral artery mean blood velocity paradoxically decreased (−8.5 ± 8.4 cm/s; Fig. 2B and  C ). Since mean arterial pressure, cardiac responses and percutaneous oxygen saturation, all of which can influence cerebral blood flow, remained unchanged during normocapnic hyperventilation compared to pre‐hyperventilation levels, the reason for the observed reduction in middle cerebral artery mean blood velocity remains unclear. In addition, whether, and to what extent, the slight reduction in middle cerebral artery mean blood velocity influenced the latency of anti‐saccades remains uncertain. Nonetheless, it is important to note that the other oculomotor variables remained unaffected by normocapnic hyperventilation, indicating that this modest decrease in middle cerebral artery mean blood velocity likely had minimal impact on the overall results.