“…These regional blood flow responses to acute hypoxia are similar to those previously reported from studies employing the typical method of doubling unilateral measurements (Lewis et al., 2014; Morris et al., 2017; Willie et al., 2012). There are as many studies reporting that the increase in blood flow to hypoxia is mediated by vasodilatation in both ICAs and VAs to extreme (<80% ) poikilocapnic hypoxia (Lewis et al., 2014; Morris et al., 2017) or isocapnic hypoxia (Fernandes et al., 2018; Hoiland et al., 2017) as there are reporting no vasodilatation (Lafave et al., 2019; Ogoh et al., 2013; Willie et al., 2012; Willie, Smith, et al., 2014), with others suggesting regionally specific vasodilatation (Kellawan et al., 2017; Subudhi et al., 2014). Notwithstanding the methodological differences of inducing hypoxia that is known to affect the cerebrovascular response, such as the clamping of carbon dioxide (Kellawan et al., 2017; Ogoh et al., 2013; Willie et al., 2012), exposure to high‐altitude hypobaric hypoxia (Hoiland et al., 2017; Lafave et al., 2019; Subudhi et al., 2014; Willie, Smith, et al., 2014) and length of exposure (Lewis et al., 2014), the aforementioned studies are often limited by their sample size and therefore sensitivity to detect small differences where high inter‐individual variability with exposure to acute severe hypoxia is notable (Willie, Smith, et al., 2014).…”