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Impairments of cognitive function during alterations in arterial blood gases (e.g., high‐altitude hypoxia) may result from the disruption of neurovascular coupling; however, the link between changes in arterial blood gases, cognition, and cerebral blood flow (CBF) is poorly understood. To interrogate this link, we developed a multimodal empirical strategy capable of monitoring neural correlates of cognition and CBF simultaneously. Human participants performed a sustained attention task during hypoxia, hypercapnia, hypocapnia, and normoxia while electroencephalographic (EEG) activity and CBF (middle and posterior cerebral arteries; transcranial Doppler ultrasound) were simultaneously measured. The protocol alternated between rest and engaging in a visual target detection task that required participants to monitor a sequence of brief‐duration colored circles and detect infrequent, longer duration circles (targets). The target detection task was overlaid on a large, circular checkerboard that provided robust visual stimulation. Spectral decomposition and event‐related potential (ERP) analyses were applied to the EEG data to investigate spontaneous and task‐specific fluctuations in neural activity. There were three main sets of findings: (1) spontaneous alpha oscillatory activity was modulated as a function of arterial CO2 (hypocapnia and hypercapnia), (2) task‐related neurovascular coupling was disrupted by all arterial blood gas manipulations, and (3) changes in task‐related alpha and theta band activity and attenuation of the P3 ERP component amplitude were observed during hypocapnia. Since alpha and theta are linked with suppression of visual processing and executive control and P3 amplitude with task difficulty, these data suggest that transient arterial blood gas changes can modulate multiple stages of cognitive information processing., Changes in arterial blood gases (e.g., from high‐altitude exposure) are associated with impairments of a variety of cognitive functions, potentially via disruption of how blood flow responds to brain activity. We used a novel multimodal approach to simultaneously measure human brain electrical activity using electroencephalography and blood flow using transcranial Doppler ultrasound, while participants performed a demanding sustained attention task at varying levels of arterial oxygen and carbon dioxide (CO2). We observed changes in both spontaneous and task‐related brain activity as a function of changes in arterial CO2 as well as disruptions in neurovascular coupling, suggesting that transient changes in arterial CO2 can affect multiple stages of cognitive processing.

Aging and physical inactivity are associated with an increased risk of developing metabolic syndrome (MetS). With the rising prevalence of MetS, it is important to determine the extent to which it affects cerebrovascular health. The primary purpose of this report is to examine the impact of MetS on cerebrovascular health (resting cerebral blood flow (CBF) peak velocity (![Formula][1] ), cerebrovascular conductance (CVC), and CBF responses to hypercapnia) in healthy older adults with normal cognition. A secondary goal was to examine the influence of apolipoprotein E ( APOE ) e 4 expression on these indices. In a sample of 258 healthy men and women older than 53 years, 29.1% met criteria for MetS. MetS, sex, and age were found to be significant predictors of CVC, and ![Formula][2] , MetS, and APOE status were significant predictors of ![Formula][3] ‐reactivity, and CVC‐reactivity was best predicted by MetS status. After controlling for these factors, participants with MetS demonstrated lower cerebrovascular measures (CVC, ![Formula][4] , CVC‐reactivity, and ![Formula][5] ‐reactivity) compared to participants without MetS. APOE e 4 carriers had higher ![Formula][6] ‐reactivity than noncarriers. These results provide evidence that cardiometabolic and vascular risk factors clustered together as the MetS predict measures of cerebrovascular health indices in older adults. Higher ![Formula][7] ‐reactivity in APOE e 4 carriers suggests vascular compensation for deleterious effects of this known risk allele for Alzheimer's disease and stroke. [1]: /embed/mml-math-1.gif [2]: /embed/mml-math-2.gif [3]: /embed/mml-math-3.gif [4]: /embed/mml-math-4.gif [5]: /embed/mml-math-5.gif [6]: /embed/mml-math-6.gif [7]: /embed/mml-math-7.gif