10-min exposure to a 2.5% hypercapnic environment increases cerebral blood blow but does not impact executive function.

Space travel and exploration are associated with increased ambient CO2 (i.e., a hypercapnic environment). Some work reported that the physiological changes (e.g., increased cerebral blood flow [CBF]) associated with a chronic hypercapnic environment contributes to a "space fog" that adversely impacts cognition and psychomotor performance, whereas other work reported no change or a positive change. Here, we employed the antisaccade task to evaluate whether transient exposure to a hypercapnic environment influences top-down executive function (EF). Antisaccades require a goal-directed eye movement mirror-symmetrical to a target and are an ideal tool for identifying subtle EF changes. Healthy young adults (aged 19-25 years) performed blocks of antisaccade trials prior to (i.e., pre-intervention), during (i.e., concurrent) and after (i.e., post-intervention) 10-min of breathing factional inspired CO2 (FiCO2) of 2.5% (i.e., hypercapnic condition) and during a normocapnic (i.e., control) condition. In both conditions, CBF, ventilatory and cardiorespiratory responses were measured. Results showed that the hypercapnic condition increased CBF, ventilation and end-tidal CO2 and thus demonstrated an expected physiological adaptation to increased FiCO2. Notably, however, null hypothesis and equivalence tests indicated that concurrent and post-intervention antisaccade reaction times were refractory to the hypercapnic environment; that is, transient exposure to a FiCO2 of 2.5% did not produce a real-time or lingering influence on an oculomotor-based measure of EF. Accordingly, results provide a framework that - in part - establishes the FiCO2 percentage and timeline by which high-level EF can be maintained. Future work will explore CBF and EF dynamics during chronic hypercapnic exposure as more direct proxy for the challenges of space flight and exploration.

Acute stress imparts a transient benefit to task-switching that is not modulated following a single bout of exercise.

Introduction: Cognitive flexibility represents a core component of executive function that promotes the ability to efficiently alternate-or "switch"-between different tasks. Literature suggests that acute stress negatively impacts cognitive flexibility, whereas a single bout of aerobic exercise supports a postexercise improvement in cognitive flexibility. Here, we examined whether a single bout of aerobic exercise attenuates a stress-induced decrement in task-switching. Materials and Methods: Forty participants (age range = 19-30) completed the Trier Social Stress Test (TSST) and were randomized into separate Exercise or Rest groups entailing 20-min sessions of heavy intensity exercise (80% of heart rate maximum via cycle ergometer) or rest, respectively. Stress induction was confirmed via state anxiety and heart rate. Task-switching was assessed prior to the TSST (i.e., pre-TSST), following the TSST (i.e., post-TSST), and following Exercise and Rest interventions (i.e., post-intervention) via pro- (i.e., saccade to veridical target location) and antisaccades (i.e., saccade mirror-symmetrical to target location) arranged in an AABB task-switching paradigm. The underlying principle of the AABB paradigm suggests that when prosaccades are preceded by antisaccades (i.e., task-switch trials), the reaction times are longer compared to their task-repeat counterparts (i.e., unidirectional prosaccade switch-cost). Results: As expected, the pre-TSST assessment yielded a prosaccade switch cost. Notably, post-TSST physiological measures indicated a reliable stress response and at this assessment a null prosaccade switch-cost was observed. In turn, post-intervention assessments revealed a switch-cost independent of Exercise and Rest groups. Conclusion: Accordingly, the immediate effects of acute stress supported improved task-switching in young adults; however, these benefits were not modulated by a single bout of aerobic exercise.

Passive exercise increases cerebral blood flow velocity and supports a postexercise executive function benefit.

Executive function entails high-level cognitive control supporting activities of daily living. Literature has shown that a single-bout of exercise involving volitional muscle activation (i.e., active exercise) improves executive function and that an increase in cerebral blood flow (CBF) may contribute to this benefit. It is, however, unknown whether non-volitional exercise (i.e., passive exercise) wherein an individual's limbs are moved via an external force elicits a similar executive function benefit. This is a salient question given that proprioceptive and feedforward drive from passive exercise increases CBF independent of the metabolic demands of active exercise. Here, in a procedural validation participants (n = 2) used a cycle ergometer to complete separate 20-min active and passive (via mechanically driven flywheel) exercise conditions and a non-exercise control condition. Electromyography showed that passive exercise did not increase agonist muscle activation or increase ventilation or gas exchange variables (i.e., V̇O2 and V̇CO2 ). In a main experiment participants (n = 28) completed the same exercise and control conditions and transcranial Doppler ultrasound showed that active and passive exercise (but not the control condition) increased CBF through the middle cerebral artery (ps <.001); albeit the magnitude was less during passive exercise. Notably, antisaccade reaction times prior to and immediately after each condition showed that active (p < .001) and passive (p = .034) exercise improved an oculomotor-based measure of executive function, whereas no benefit was observed in the control condition (p = .85). Accordingly, results evince that passive exercise 'boosts' an oculomotor-based measure of executive function and supports convergent evidence that increased CBF mediates this benefit.

'Delaying' a saccade: Preparatory phase cortical hemodynamics evince the neural cost of response inhibition.

Minimally delayed (MD) saccades require inhibition of a prepotent response until a target is extinguished, and unlike the more extensively studied antisaccade task, do not require the additional cognitive component of vector inversion (i.e., 180° target spatial transposition). Here, participants completed separate blocks of MD and prepotent stimulus-driven saccades (i.e., respond at target onset) while cortical hemodynamics were measured via functional transcranial Doppler ultrasound. MD saccades produced longer and more variable reaction times (RT). In turn, MD and stimulus-driven saccade preparatory phase cortical hemodynamics increased and decreased, respectively, relative to baseline and the two conditions differed from one another throughout the preparatory phase. The longer RTs and increased cortical hemodynamics of MD saccades is taken to evince response complexity and the increased neural activity to accommodate response inhibition. To our knowledge, such findings provide the first work to examine the neural foundations of MD saccades.

Exercise intensity-specific changes to cerebral blood velocity do not modulate a postexercise executive function benefit.

Executive function is transiently improved (i.e., <60-min) following a single bout of aerobic exercise. A candidate mechanism for this improvement is an exercise-mediated increase in cerebral blood flow (CBF). Further, it has been proposed that an increase in CBF across the continuum of increasing exercise intensities improves the magnitude of a postexercise executive function benefit (i.e., drive theory); however, this proposal has not been empirically tested. Here, participants completed four experimental sessions: a V̇O2peak test to determine cardiorespiratory fitness and estimated lactate threshold (LT), followed by separate 10-min sessions of light- (i.e., 25 W), moderate- (i.e., 80% estimated LT), and heavy-intensity (i.e., 15% of the difference between LT and V̇O2peak) aerobic exercise. An estimate of CBF during exercise was achieved via transcranial Doppler ultrasound and near-infrared spectroscopy to quantify blood velocity (BV) through the middle cerebral artery and deoxygenated hemoglobin (HHb), respectively. Executive function was assessed before and after each session via the executive-mediated antisaccade task (i.e., saccade mirror-symmetrical to a target). Results demonstrated that BV increased in relation to increasing exercise intensity, whereas HHb decreased by a comparable magnitude independent of intensity. In terms of executive function, null hypothesis and equivalence tests indicated a comparable magnitude postexercise reduction in antisaccade reaction time across exercise intensities. Accordingly, the magnitude of CBF change during exercise does not impact the magnitude of a postexercise executive function benefit.