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Acute High-Intensity Exercise Impairs Skeletal Muscle Respiratory Capacity

LAYEC, GWENAEL1,2,3; BLAIN, GREGORY M.4; ROSSMAN, MATTHEW J.2; PARK, SONG Y.2; HART, COREY R.2; TRINITY, JOEL D.1,2,3; GIFFORD, JAYSON R.1,2,3; SIDHU, SIMRANJIT K.1,5; WEAVIL, JOSHUA C.1; HUREAU, THOMAS J.1,3,6; AMANN, MARKUS1,2,3; RICHARDSON, RUSSELL S.1,2,3

Medicine & Science in Sports & Exercise: December 2018 - Volume 50 - Issue 12 - p 2409–2417
doi: 10.1249/MSS.0000000000001735
BASIC SCIENCES

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−1·s−1; post, 17 ± 2 ρm·mg−1·s−1; 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−1·s−1; post, 9 ± 2 ρm·mg−1·s−1; P < 0.05). Although complex I–driven state 3 (3CI) respiration was also lower (pre, 20 ± 2 ρm·mg−1·s−1; post, 14 ± 4 ρm·mg−1·s−1), 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.

1Department of Medicine, University of Utah, Salt Lake City, UT;

2Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT;

3Geriatric Research, Education, and Clinical Center, George E. Whalen VA Medical Center, Salt Lake City, UT;

4Université Côte d’Azur, LAMHESS, Nice, FRANCE;

5Discipline of Physiology, Adelaide Medical School, The University of Adelaide, Adelaide, AUSTRALIA; and

6Mitochondria, Oxidative Stress and Muscular Protection Laboratory, EA 3072, University of Strasbourg, Strasbourg, FRANCE

Address for correspondence: Gwenael Layec, Ph.D., VA Medical Center, Bldg 2, 500 Foothill Dr, Salt Lake City, UT 84148; E-mail: gwenael.layec@utah.edu.

Submitted for publication October 2017.

Accepted for publication July 2018.

© 2018 American College of Sports Medicine