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Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice
Published on: March 15, 2019
Exercise effects on erythrocyte deformability in exercise-induced arterial hypoxemia
R Alis1, F Sanchis-Gomar1, D Ferioli2
1Research Universitary Institute Dr. Viña Giner, Molecular and Mitochondrial Medicine, Catholic University of Valencia San Vicente Mártir, Valencia, Spain.
Exercise-induced arterial hypoxemia (EIAH) in trained athletes may improve red blood cell flexibility. This adaptation enhances oxygen transport, aiding high-intensity exercise performance despite lower arterial oxygen saturation.
Area of Science:
- Physiology
- Exercise Science
- Hematology
Background:
- Exercise-induced arterial hypoxemia (EIAH) is common in endurance athletes.
- The impact of erythrocyte deformability (ED) on EIAH is not well understood.
- Investigating erythrocyte properties offers insight into EIAH mechanisms.
Purpose of the Study:
- To examine the relationship between erythrocyte properties, lactate accumulation, and ED response in EIAH.
- To compare ED in sedentary, trained non-EIAH, and trained EIAH subjects.
- To elucidate the role of ED in exercise performance under hypoxemic conditions.
Main Methods:
- Erythrocyte deformability (ED) measured before, during, and after maximal incremental exercise tests.
- Analysis of mean corpuscular volume (MCV) and red blood cell lactate concentrations.
- Comparison of ED responses between sedentary, trained non-EIAH, and trained EIAH groups.
Main Results:
- EIAH observed in 6 of 16 trained subjects.
- Sedentary and non-EIAH subjects showed decreased ED post-exercise.
- EIAH subjects exhibited no change in ED, suggesting an adaptive response.
- Lactate and MCV increased similarly across all groups post-exercise.
Conclusions:
- Erythrocyte deformability is influenced by cell volume but also other factors in EIAH.
- Oxygen-regulated cellular mechanisms, potentially involving membrane-cytoskeleton interactions, affect ED.
- The improved ED response in EIAH may be an adaptive mechanism for enhanced perfusion and exercise capacity.
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