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Indexed/Abstracted in: Chemical Abstracts, CINAHL, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,111
Online ISSN 1827-1928
PHYSIOLOGY AND BIOMECHANICS
Prieur F. 1, 2, Dupont G. 3, 4, Blondel N. 3, 4, Mucci P. 3, 5
1 Laboratoire AMAPP, EA 4248, Université d’Orléans, Orléans, France;
2 Laboratoire CIAMS, Equipe RIME, Université Paris XI, Paris, France;
3 Univ Lille Nord de France, Lille, France;
4 UArtois, Liévin, France;
5 UDSL, Lille, France
AIM: The aim of this study was to determine whether an increase in O2 availability induces an alteration of the balance between O2 consumption (ׁVO2) and O2 delivery (ׁQO2) at the muscle level. For that, we examined the effect of moderate hyperoxia on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise.
METHODS: Eight young male adults performed step transitions from 35 W to heavy-intensity exercise corresponding to a power output half-way between the first ventilatory threshold and ׁVO2max in normoxia and in hyperoxia (FIO2=0.30). Muscle deoxygenation (HHb) and total hemoglobin (Hbtot) were monitored continuously by near-infrared spectroscopy. HHb data were fit with a mono-exponential model from the onset of exercise up to 90 seconds.
RESULTS: Hyperoxia neither altered the delay before the increase in HHb (normoxia: 10.7±1.8 s vs. hyperoxia: 9.5±1.9 s; NS) nor the HHb mean response time (normoxia: 20.6±2.8 s vs. hyperoxia: 19.6±2.3 s; NS). Likewise, Hbtot was not different between normoxia and hyperoxia.
CONCLUSION: These results indicate that moderate hyperoxia has no effect on muscle deoxygenation kinetics at the onset of heavy exercise. It suggests that muscle ׁVO2 increases at the same rate than O2 delivery when O2 availability is enhanced.