O2 arterial desaturation in endurance athletes increases muscle deoxygenation

The aim of this study was to compare the muscle deoxygenation measured by near infrared spectroscopy in endurance athletes who presented or not with exercise-induced hypoxemia (EIH) during a maximal incremental test in normoxic conditions.

Nineteen male endurance sportsmen performed an incremental test on a cycle ergometer to determine maximal oxygen consumption (VO2max) and the corresponding power output (P(max)). Arterial O2 saturation (SaO2) was measured noninvasively with a pulse oxymeter at the earlobe to detect EIH, which was defined as a drop in SaO2 > 4% between rest and the end of the exercise. Muscle deoxygenation of the right vastus lateralis was monitored by near infrared spectroscopy and was expressed in percentage according to the ischemia-hyperemia scale.

Ten athletes exhibited arterial hypoxemia (EIH group) and the nine others were nonhypoxemic (NEIH group). Training volume, competition level, VO2max, Pmax, and lactate concentration were similar in the two groups. Nevertheless, muscle deoxygenation at the end of the exercise was significantly greater in the EIH group (P < 0.05).

Greater muscle deoxygenation at maximal exercise in hypoxemic athletes seems to be due, at least in part, to reduced oxygen delivery--that is, exercise-induced hypoxemia--to working muscle added to the metabolic demand. In addition, our finding is also consistent with the hypothesis of greater muscle oxygen extraction in order to counteract reduced O2 availability.