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|Title:||Acute high-intensity exercise impairs skeletal muscle respiratory capacity|
|Citation:||Medicine and Science in Sports and Exercise, 2018; 50(12):2409-2417|
|Publisher:||Lippincott Williams & Wilkins|
|Gwenael Layec, Gregory M. Blain, Matthew J. Rossman, Song Y. Park, Corey R. Hart, Joel D. Trinity, Jayson R. Gifford, Simranjit K. Sidhu, Joshua C. Weavil, Thomas J. Hureau, Markus Amann And Russell S. Richardson|
|Abstract:||PURPOSE:The effect of an acute bout of exercise, especially high-intensity exercise, on the function of mitochondrial respiratory complexes is not well understood, with potential implications for both the healthy population and patients undergoing exercise-based rehabilitation. Therefore, this study sought to comprehensively examine respiratory flux through the different complexes of the electron transport chain in skeletal muscle mitochondria before and immediately after high-intensity aerobic exercise. METHODS:Muscle biopsies of the vastus lateralis were obtained at baseline and immediately after a 5-km time trial performed on a cycle ergometer. Mitochondrial respiratory flux through the complexes of the electron transport chain was measured in permeabilized skeletal muscle fibers by high-resolution respirometry. RESULTS:Complex I + II state 3 (state 3CI + CII) respiration, a measure of oxidative phosphorylation capacity, was diminished immediately after the exercise (pre, 27 ± 3 ρm·mg·s; post, 17 ± 2 ρm·mg·s; P < 0.05). This decreased oxidative phosphorylation capacity was predominantly the consequence of attenuated complex II-driven state 3 (state 3CII) respiration (pre, 17 ± 1 ρm·mg·s; post, 9 ± 2 ρm·mg·s; P < 0.05). Although complex I-driven state 3 (3CI) respiration was also lower (pre, 20 ± 2 ρm·mg·s; post, 14 ± 4 ρm·mg·s), this did not reach statistical significance (P = 0.27). In contrast, citrate synthase activity, proton leak (state 2 respiration), and complex IV capacity were not significantly altered immediately after the exercise. CONCLUSIONS:These findings reveal that acute high-intensity aerobic exercise significantly inhibits skeletal muscle state 3CII and oxidative phosphorylation capacity. This, likely transient, mitochondrial defect might amplify the exercise-induced development of fatigue and play an important role in initiating exercise-induced mitochondrial adaptations.|
|Keywords:||Oxidative phosphorylation capacity; electron transport chain; state 3 respiration; cycling time trial; mitohormesis|
|Rights:||© 2018 by the American College of Sports Medicine.|
|Appears in Collections:||Aurora harvest 8|
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