Effect of Intermittent Hypoxia on Ischemic‐Reperfusion Injury in Healthy Individuals

Brief periods of ischemia preceding an ischemic‐reperfusion injury attenuate the reduction in brachial artery endothelial function. It has remained unknown whether brief bouts of systemic hypoxemia would similarly mitigate the blunted vasodilatory response induced by an ischemic‐reperfusion injury. Therefore, the purpose of this study was to determine whether intermittent hypoxia protects against an ischemic‐reperfusion injury in young healthy adults. Ten healthy individuals, 7 men and 3 women (age: 24 ± 2 years, height: 176 ± 9 cm, weight: 77.1 ± 13.9 kg), participated in the study. Brachial artery endothelial function was assessed by flow‐mediated dilation before and after an ischemic‐reperfusion injury induced by a 20‐minute blood flow occlusion. The ischemic‐reperfusion injury was preceded by either intermittent hypoxia (Hyp) or intermittent normoxia (Norm). Both visits were separated by a period of seven days, whereas women who had regular menstrual cycles were scheduled in the early follicular phase. Intermittent hypoxia was created by titrating nitrogen into a breathing system to achieve an arterial oxygen saturation of 90%. Intermittent hypoxia consisted of three 4‐minute hypoxic cycles separated by 4‐minute normoxic cycles. As expected, intermittent hypoxia resulted in a lower arterial oxygen saturation (Hyp: 88 ± 4 vs. Norm: 98 ± 2%, p < 0.01), which was equivalent to a lower fraction of inspired oxygen (Hyp: 0.13 ± 0.04, Norm: 0.21 ± 0.03, p < 0.01). The reduction in flow‐mediated dilation resulting from the ischemic‐reperfusion injury was attenuated by intermittent hypoxia (Hyp: 5.9 ± 0.7 to 4.5 ± 0.7%, Norm: 6.0 ± 0.7 to 3.6 ± 0.7%, p = 0.07). Exposure to intermittent hypoxia did not affect mean arterial blood pressure (Hyp: 97 ± 7 to 99 ± 8 mmHg, Norm: 94 ± 8 to 95 ± 10 mmHg, p = 0.52) but significantly increased heart rate (Hyp: 63 ± 6 to 70 ± 7 bpm, Norm: 61 ± 7 to 61 ± 6 bpm, p < 0.01). Thus, intermittent hypoxia seems to prevent the reduction in flow‐mediated dilation induced by an ischemic‐reperfusion injury in young healthy individuals.