During a maximal incremental ergocycle test, the power output associated with Respiratory Exchange Ratio equal to 1.00 (RER = 1.00) predicts maximal lactate steady state (MLSS). We hypothesised that these results are transferable for runners on the field. Fourteen runners performed a maximal progressive test, to assess the speed associated with RER = 1.00, and several 30 minutes constant velocity tests to determine the speed at MLSS. We observed that the speeds at RER = 1.00, at the second ventilatory threshold (VT2) and at MLSS did not differ (15.7 ± 1.1 km · h⁻¹, 16.2 ± 1.4 km · h⁻¹, 15.5 ± 1.1 km · h⁻¹ respectively). The speed associated with RER = 1.00 was better correlated with that at MLSS (r = 0.79; p = 0.0008) than that at VT2 (r = 0.73; p = 0.002). Neither the concentration of blood lactate nor the heart rate differed between the speed at RER = 1.00 and that at MLSS from the 10th and the 30th minute of the constant velocity test. Bland and Altman analysis showed a fair agreement between the speed at MLSS and that at RER (0.2 ± 1.4 km · h⁻¹). This study demonstrated that the speed associated with RER = 1.00 determined during maximal progressive track running allows a fair estimation of the speed associated with MLSS, markedly decreasing the burden of numerous invasive tests required to assess it.

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This study aimed to investigate the effects of sustained hypoxic exposure on cerebral and muscle oxygenation and cardiorespiratory function at rest. Eleven healthy subjects inhaled a normobaric hypoxic (FiO2=0.12) or normoxic (FiO2=0.21) gas mixture for 4 h at rest, on two separated blinded sessions. Arterial oxygen saturation (SpO2), heart rate variability (HRV), end-tidal CO2 (EtCO2), and oxygenation of quadriceps muscle, prefrontal and motor cortices assessed by near-infrared spectroscopy (NIRS) were measured continuously during each session. Acute mountain sickness symptoms were evaluated at the end of each session. During a hypoxic session, SpO2 reduction (∼13%) plateaued after 20 min, while deoxygenation pattern took 30 to 40 min at the cerebral sites to plateau (+5.3±1.6  μMol of deoxygenated-hemoglobin). Deoxygenation was more pronounced in the cerebral cortex compared to the muscle (+2.1±2.3  μMol of deoxygenated-hemoglobin), and NIRS-derived tissue perfusion index showed distinct profiles between the muscle (hypoperfusion) and the brain (hyperperfusion) with prolonged hypoxia. Changes in tissue oxygenation were not associated with cardiorespiratory responses (e.g., HRV, EtCO2) and altitude sickness symptom appearance during hypoxic sessions. These data demonstrate that sustained hypoxia elicits time delay in changes between arterial and tissue (especially cerebral) oxygenation, as well as a tissue-specific sensitivity.

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