To mitigate these potential risks, voluntary regulation of breathing to prevent hypocapnia appears to be an immediate and effective intervention. Alternatively, inhalation of carbon dioxide‐enriched air during episodes of hyperventilation may attenuate hypocapnia, thus reducing the above‐mentioned risks. Future studies are warranted to directly investigate these possibilities. Considerations End‐tidal carbon dioxide partial pressure and middle cerebral artery mean blood velocity decreased (−0.3 ± 0.4 mmHg and −1.7 ± 2.1 cm/s, respectively) over time in the spontaneous breathing condition (i.e., before versus during the breathing intervention), indicative of a time‐dependent modulation (Fig. 2B and  C ). [...] It might be that oxygen level in arterialized capillary blood samples from fingertip was influenced by hypocapnia‐related factors such as reduction in finger blood flow (Umeda et al.,). We did not directly measure brain activity, brain temperature and reginal differences in brain blood flow. Future studies incorporating neuroimaging techniques (e.g., fMRI, MRS and EEG) would elucidate the underlying neural and physiological mechanisms of hypocapnia‐induced alterations in oculomotor behaviour. Conclusion We show that hyperventilation‐induced hypocapnia impairs oculomotor function in healthy young adults as evidenced by reduced fixation and saccade frequency, prolonged fixation duration, and shortened scanpath length during free viewing. Additionally, both hypocapnia and hyperventilation per se prolong saccadic latency in the anti‐saccade task.