The impact of hypoxia on aerobic exercise capacity

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Acute hypoxia impairs aerobic exercise by reducing the capacity for maximal O2 uptake (VO2max). This is mainly the consequence of a lower arterial O2 content (caO2) and, in severe hypoxia, cardiac output during maximal exercise as the combination of these two factors attenuates convective O2 supply to the exercising muscle cells. Nevertheless, the incapacitating effect of hypoxia is partially restored during prolonged exposure as an increased renal erythropoietin release induces polycythemia that normalizes caO2. Since this mechanism may benefit performance not only in hypoxia but also in normoxia different forms of altitude training were developed all aiming to enhance athletic performance at sea level. The purpose of the present project was to enhance our understanding regarding the interaction between both, acute and chronic hypoxia and aerobic exercise. In acute hypoxia the contribution of the intrinsic responses of the pulmonary and the cerebral circulation to the reduction in VO2max was investigated. Specifically, we hypothesized that the hypoxiainduced rise in pulmonary artery pressure induces exercise limitations by increasing right ventricular afterload and/ or promoting pulmonary ventilation-perfusion mismatch. Furthermore, we suggested that the cerebral hypoxia that develops during exercise at altitude would limit VO2max by accelerating the development of supraspinal fatigue. Regarding chronic hypoxia we tested the efficacy and underlying mechanisms of the contemporary altitude training strategy, i.e. the Live High – Train Low approach, on elite endurance athletes in a double-blinded and placebo-controlled study design. The results collected in three independent studies revealed the following: 1) At 4,559 m altitude pulmonary vasodilation induced by the glucocorticoid Dexamethasone elevates VO2max of individuals present with an excessive vasoconstrictive response to hypoxia without affecting arterial O2 saturation (SaO2). A direct comparison to normal individuals further suggested a larger hypoxia-induced exercise impairment in these individuals but also no differences in SaO2 during maximal exercise. We thus conclude that hypoxic pulmonary vasoconstriction may contribute to the reduced VO2max in acute hypoxia potentially by increasing right ventricular afterload and thereby attenuating cardiac output. 2) Although administration of CO2 during exercise at 3,454 m altitude elevated cerebral blood flow and, as a consequence, cerebral oxygenation, VO2max remained unaffected. This indicates that the contribution of the reduced cerebral oxygenation on the limitation of VO2max in hypoxia is neglectable. Nevertheless, as a VO2max test induces progressive demand for muscular O2 supply, the capacity of the O2 transport system might have been exhausted before supraspinal fatigue occurred, and thus we cannot exclude that the decline in cerebral oxygenation may play a role during submaximal exercise in hypoxia. 3) Four weeks of discontinuous (16 hours per day) exposure to normobaric hypoxia corresponding to 3,000 m combined with daily training in normoxia failed to benefit the performance of elite endurance athletes. This was explained by the absence of an effect of hypoxia on total red cell volume. These findings suggest a potential role of a placeboeffect in earlier studies and indicate that four weeks of discontinuous hypoxic exposure may be insufficient to induce physiological adaptations. Athletes should take this into consideration before shouldering the inconveniences associated with Live High – Train Low altitude training. In brief, the present results support a limiting role of pulmonary vasoconstriction but not of attenuated cerebral oxygenation on VO2max in hypoxia. They further indicate that altitude training following the Live High – Train Low strategy may not be superior to conventional endurance training.