Intermittent hypoxia reduces endothelial function

Obstructive sleep apnea contributes to endothelial dysfunction. We tested the hypothesis that short bouts of repetitive hypoxic apneas (intermittent hypoxia, IH) will induce endothelial dysfunction. Six sedentary young men (age=26.2 ± 6.0 yrs, ht=68.2 ± 4.7 in, wt=171.2 ± 20.3 lbs) free of cardiovascular and pulmonary disease were enrolled in the study. Each was exposed to one hour of room air (RA) and IH on separate days with the order randomly assigned. Ultrasound of the right brachial artery and antioxidant enzyme activity (n=4) was recorded immediately pre‐ and post‐exposure on both days. Flow mediated dilation (FMD) calculated as a percentage change in brachial artery diameter in response to the forearm hyperemic response was used as a measure of endothelial function. Brachial artery percent dilation decreased following IH (6.02 ± 1.8% (SD) to 3.88 ± 1.5%. p=0.030, pre vs. post‐ respectively) and did not change following RA (6.16 ± 2.6% to 6.18 ± 2.9%, p=0.988, pre vs. post‐ respectively). Superoxide dismutase (Δ RA=−0.03 U/g Hgb; ΔIH=−0.07), glutathione peroxidase (Δ RA=23.3 IU/L; ΔIH=4.3), glutathione reductase (ΔRA=−2.4 IU/L; ΔIH=2.8), and paraoxonase 1 (ΔRA=2.6 IU/L; ΔIH=−0.34) were not significantly different post‐exposure. The short time exposure might not be adequate to capture the change in inflammatory markers. In summary, these data indicate short term exposure to IH alters endothelial function.