The practice of sleeping in hypoxia while training in normoxia (ie, live high/train low) has gained great popularity as a legal alternative to the dangerous and illegal practice of blood doping. Several studies58,59 have been conducted, unfortunately, none as yet with true placebo control subjects, showing small but positive effects on sea-level performance in many athletes, but certainly not in all. Maladaptive responses to acute and chronic hypoxia (both constant and intermittent hypoxia) include pulmonary vasoconstriction, greatly augmented sympathetic vasoconstrictor activity, impaired endothelial function, and remodeled vascular smooth muscle.60 These potential long-term effects, which also persist following the cessation of the hypoxic exposure, have not yet been studied for the live high/train low paradigm. We would not predict these problems to occur in otherwise healthy subjects when the intermittent hypoxic exposures are in the range of 2,500 m altitude (resting SaO2, > 90%); however, this practice could potentially present serious problems in those athletes who choose to further enhance their RBC production by exposure to altitudes over 3,000 m, at which resting SaO2 (< 90%) resides on the steep, volatile portion of the hemoglobin-O2 disassociation curve. Periodic breathing is also common during sleep at these altitudes and, when present, will greatly exacerbate the degree of arterial hypoxemia at any given altitude.61 Given the recent tendency for athletes to sleep at these higher altitudes for their live high/train low regimen, further careful study of the long-term cardiovascular effects of intermittent hypoxia in healthy subjects is warranted.