Key points: Cognitive performance is impaired by hypoxia despite global cerebral oxygen delivery and metabolism being maintained. Using arterial spin labelled (ASL) magnetic resonance imaging, this is the first study to show regional reductions in cerebral blood flow (CBF) in response to decreased oxygen supply (hypoxia) at 2 h that increased in area and became more pronounced at 10 h. Reductions in CBF were seen in brain regions typically associated with the ‘default mode’ or ‘task negative’ network. Regional reductions in CBF, and associated vasoconstriction, within the default mode network in hypoxia is supported by increased vasodilatation in these regions to a subsequent hypercapnic (5% CO₂) challenge. These results suggest an anatomical mechanism through which hypoxia may cause previously reported deficits in cognitive performance. Hypoxia causes an increase in global cerebral blood flow, which maintains global cerebral oxygen delivery and metabolism. However, neurological deficits are abundant under hypoxic conditions. We investigated regional cerebral microvascular responses to acute (2 h) and prolonged (10 h) poikilocapnic normobaric hypoxia. We found that 2 h of hypoxia caused an expected increase in frontal cortical grey matter perfusion but unexpected perfusion decreases in regions of the brain normally associated with the ‘default mode’ or ‘task negative’ network. After 10 h in hypoxia, decreased blood flow to the major nodes of the default mode network became more pronounced and widespread. The use of a hypercapnic challenge (5% CO₂) confirmed that these reductions in cerebral blood flow from hypoxia were related to vasoconstriction. Our findings demonstrate steady‐state deactivation of the default network under acute hypoxia, which become more pronounced over time. Moreover, these data provide a unique insight into the nuanced localized cerebrovascular response to hypoxia that is not attainable through traditional methods. The observation of reduced perfusion in the posterior cingulate and cuneal cortex, which are regions assumed to play a role in declarative and procedural memory, provides an anatomical mechanism through which hypoxia may cause deficits in working memory.

The effectiveness of a nap as a recovery strategy for endurance exercise is unknown and therefore the present study investigated the effect of napping on endurance exercise performance. Eleven trained male runners completed this randomised crossover study. On two occasions, runners completed treadmill running for 30 min at 75% ⩒O_2max in the morning, returning that evening to run for 20 min at 60% ⩒O_2max, and then to exhaustion at 90% ⩒O_2max. On one trial, runners had an afternoon nap approximately 90 min before the evening exercise (NAP) whilst on the other, runners did not (CON). All runners napped (20 ± 10 min), but time to exhaustion (TTE) was not improved in all runners (NAP 596 ± 148 s vs. CON 589 ± 216 s, P = .83). Runners that improved TTE after the nap slept less at night than those that did not improve TTE (night‐time sleep 6.4 ± 0.7 h vs. 7.5 ± 0.4 h, P < .01). Furthermore, night‐time sleep predicted change in TTE, indicating that runners sleeping least at night improved TTE the most after the nap compared to CON (r² = −0.76, P = .001). In runners that improved TTE, ratings of perceived exertion (RPE) were lower during the TTE on NAP than CON compared to runners that did not improve (−0.4 ± 0.6 vs. 0 ± 0, P = .05). Reduced exercising sense of effort (RPE) may account for the improved TTE after the nap. In conclusion, a short afternoon nap improves endurance performance in runners that obtain less than 7 h night‐time sleep.