Evidence of Exercise-Induced O2 Arterial Desaturation in Non-Elite Sportsmen and Sportswomen Following High-Intensity Interval-Training

• Published in: International journal of sports medicine 2004, Vol.25 (1), p.6-13
• Main Authors: Mucci, P., Blondel, N., Fabre, C., Nourry, C., Berthoin, S.
• Format: Article
• Language: English
• Subjects: Adolescent; Analysis of Variance; Anthropometry; Exercise - physiology; Female; Humans; Hypoxia - physiopathology; Linear Models; Male; Oximetry; Oxygen - blood; Oxygen Consumption - physiology; Physical Education and Training; Physiology & Biochemistry; Pulmonary Gas Exchange - physiology; Respiratory Function Tests
• ISSN: 0172-4622; 1439-3964
• DOI: 10.1055/s-2003-45225

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. SaO 2 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·O 2 max for eight weeks. The training running speeds were set at ∼140 % V·O 2 max running speed up to 100 % 20-m maximal running speed. Pre- and post-training pulmonary gas exchanges and SaO 2 were measured during an incremental running field-test. After the training period, men and women increased their V·O 2 max (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·O 2 max 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 O 2 (V·E/V·O 2 , 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 SaO 2 at maximal workload and the matched V·E/V·O 2 (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 SaO 2 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.