Evidence of Exercise-Induced O2Arterial Desaturation in Non-Elite Sportsmen and Sportswomen Following High-Intensity Interval-Training

Abstract

The aim of this study was to investigate the development of exercise-induced hypoxemia (EIH defined as an exercise decrease > 4 % in oxygen arterial saturation, i. e. SaO₂ measured with a portable pulse oximeter) in twelve sportsmen and ten sportswomen (18.5 ± 0.5 years) who were non-elite and not initially engaged in endurance sport or training. They followed a high-intensity interval-training program to improve V·O₂max for eight weeks. The training running speeds were set at ∼140 % V·O₂max running speed up to 100 % 20-m maximal running speed. Pre- and post-training pulmonary gas exchanges and SaO₂ were measured during an incremental running field-test. After the training period, men and women increased their V·O₂max (p < 0.001) by 10.0 % and 7.8 %, respectively. Nine subjects (seven men and two women) developed EIH. This phenomenon appeared even in sportsmen with low V·O₂max from 45 ml × min^-1 × kg^-1 and seemed to be associated with inadequate hyperventilation induced by training: because only this hypoxemic group showed 1) a decrease in maximal ventilatory equivalent in O₂ (V·E/V·O₂, p < 0.01) although maximal ventilation increased (p < 0.01) with training, i. e. in EIH-subjects the ventilatory response increased less than the metabolic demand after the training program; 2) a significant relationship between SaO₂ at maximal workload and the matched V·E/V·O₂ (p < 0.05, r = 0.67) which strengthened a relative hypoventilation implication in EIH. In conclusion, in this field investigation the significant decrease in the minimum SaO₂ inducing the development of EIH after high-intensity interval-training indicates that changes in training conditions could be accompanied in ∼40 % non-endurance sportive subjects by alterations in the degree of arterial oxyhemoglobin desaturation developing during exercise.