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We compared the effects of hypobaric and normobaric hypoxia on select cardio-respiratory responses, oxidative stress and acute mountain sickness (AMS) severity in prematurely born individuals, known to exhibit blunted hypoxic ventilatory response. Sixteen prematurely born but otherwise healthy males underwent two 8-h hypoxic exposures under: (1) hypobaric hypoxic [HH; terrestrial altitude 3840 m; PiO2:90.2 (0.5) mmHg; BP: 478 (2) mmHg] and (2) normobaric hypoxic [NH; PiO2:90.6 (0.9) mmHg; FiO2:0.142 (0.001)] condition. Resting values of capillary oxyhemoglobin saturation (SpO2), heart rate (HR) and blood pressure were measured before and every 2 h during the exposures. Ventilatory responses and middle cerebral artery blood flow velocity (MCAv) were assessed at rest and during submaximal cycling before and at 4 and 8 h. Plasmatic levels of selected oxidative stress and antioxidant markers and AMS symptoms were also determined at these time points. HH resulted in significantly lower resting (P = 0.010) and exercise (P = 0.004) SpO2 as compared to NH with no significant differences in the ventilatory parameters, HR or blood pressure. No significant differences between conditions were found in resting or exercising MCAv and measured oxidative stress markers. Significantly lower values of ferric-reducing antioxidant power (P = 0.037) were observed during HH as opposed to NH. AMS severity was higher at 8 h compared to baseline (P = 0.002) with no significant differences between conditions. These data suggest that, in prematurely born adults, 8-h exposure to hypobaric, as opposed to normobaric hypoxia, provokes greater reductions in systemic oxygenation and antioxidant capacity. Further studies investigating prolonged hypobaric exposures in this population are warranted. NCT02780908 (ClinicalTrials.gov).

We compared the effects of hypobaric and normobaric hypoxia on select cardio-respiratory responses, oxidative stress and acute mountain sickness (AMS) severity in prematurely born individuals, known to exhibit blunted hypoxic ventilatory response.Sixteen prematurely born but otherwise healthy males underwent two 8-h hypoxic exposures under: (1) hypobaric hypoxic [HH; terrestrial altitude 3840 m; PHH resulted in significantly lower resting (P = 0.010) and exercise (P = 0.004) SpOThese data suggest that, in prematurely born adults, 8-h exposure to hypobaric, as opposed to normobaric hypoxia, provokes greater reductions in systemic oxygenation and antioxidant capacity. Further studies investigating prolonged hypobaric exposures in this population are warranted.NCT02780908 (ClinicalTrials.gov).

The aim of this study was to determine the response of blood markers to acute hypoxia in high-level endurance athletes before training based on "living high-training low" model. Thirty endurance athletes performed a hypoxic cycling test and spent 3 h at rest in a simulated altitude of 3,000 m. At the end of the hypoxic cycling test, the quantity of the natural antisense transcript of HIF-1alpha mRNA (aHIF) transcript increased significantly (+37%, P = 0.024). After 3-h exposure, at a simulated altitude of 3,000 m, the amount of HIF-1alpha mRNA increased significantly (+57%, P = 0.012). Moreover, a large inter-subject range was observed in response to the hypoxic cycling test and to the prolonged hypoxic exposure: -133%/+79% and -82%/+653% for HIF-1alpha mRNA, 69%/+324% and -76%/+229% for aHIF. This study shows a large inter-variability of blood markers in elite athletes in response to acute hypoxic exposure corroborating previous observations made in other populations.

The “living high–training low” model (Hi–Lo) may improve aerobic performance in athletes, and the main mechanism of this improvement is thought to be augmented erythropoiesis. A positive effect of Hi–Lo has been demonstrated previously by using altitudes of 2,000–3,000 m. Since the rate of erythropoiesis is altitude-dependent, we tested whether a higher altitude (3,500 m) during Hi–Lo increases erythropoiesis and maximal aerobic performance. Nordic skiers trained for 18 days at 1,200 m, while sleeping at 1,200 m in ambient air (control group, n = 5) or in hypoxic rooms (Hi–Lo, n = 6; 3 × 6 days at simulated altitudes of 2,500, 3,000 and finally 3,500 m, 11 h day−1). Measurements were done before, during (blood samples only) and 2 weeks after the intervention (POST). Maximal aerobic performance was examined from $$\dot{V}\hbox{O}_{2}\hbox{max}$$ and time to exhaustion (T exh) at $$v\dot{V}\hbox{O}_{2}\hbox{max}$$ (minimum speed associated with $$\dot{V}\hbox{O}_{2}\hbox{max}$$ ), respectively. Erythropoietin and soluble transferrin receptor responses were higher during Hi–Lo, whereas reticulocytes did not change. In POST (vs. before): hematological parameters were similar to basal levels, as well as red blood cell volume, being 2.68 ± 0.83 l (vs. 2.64±0.54 l) in Hi–Lo and 2.62±0.57 l (vs. 2.87 ± 0.59 l) in controls. At that time, neither $$\dot{V}\hbox{O}_{2}\hbox{max}$$ nor T exh were improved by Hi–Lo, $$\dot{V}\hbox{O}_{2}\hbox{max}$$ being non-significantly decreased by 2.0% (controls) and 3.7% (Hi–Lo). The present results suggest that increasing the altitude up to 3,500 m during Hi–Lo stimulates erythropoiesis but does not confer any advantage for maximal O2 transport.