Interaction between hypoxia and training on NIRS signal during exercise: Contribution of a mathematical model

Abstract Acute exposure to hypoxia provokes a decrease in peak oxygen consumption ( V ˙ O 2 , peak ). At and above 4000 m, the decrease in V ˙ O 2 , peak is greater than expected from the decrease in arterial oxygen content ( C a O 2 ) suggesting the participation of other factors. We hypothesized that O 2 transfer within the active muscle may play a role. Therefore we used Near Infra Red Spectroscopy (NIRS) to assess oxy (O 2 Hb) and deoxyhemoglobin (HHb) concentration in the vastus lateralis of trained athletes (TA) and untrained subjects (US) exercising at various inspired oxygen pressure ( P I O 2 = 149.4 , 131.4, 107.3 and 87.0 mmHg). A mathematical model has been developed to compute: (i) the pulmonary ( K p ) and muscular ( K tm ) O 2 diffusion coefficients and (ii) the proportion of arteriolar:capillary:venous blood participating in the NIRS signal at every exercise intensity from rest to peak exercise in the normoxic and various hypoxic conditions. In TA, O 2 Hb decreased near maximal exercise at 2500 and 4000 m, while in US, altitude had no effect. In normoxia O 2 Hb was higher in TA than in US, the difference disappearing in hypoxia. K tm increased linearly with workload and altitude and was higher in TA than US while K p plateaued near maximal exercise, which was consistent with athletes’ greater decrease in C a O 2 . The greater participation of arterial blood in the NIRS signal in TA at altitudes account for their higher O 2 Hb values as well as the greater decrease they underwent in hypoxia. At 4000 m, athletes loose their advantages of adaptation to training due to a reduced arterial content, and both from NIRS variables and model output, characteristics of O 2 transfer of TA converge toward those of US.