In:
Medicine & Science in Sports & Exercise, Ovid Technologies (Wolters Kluwer Health), Vol. 50, No. 12 ( 2018-12), p. 2409-2417
Abstract:
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 3 CI + 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 3 CII ) 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 (3 CI ) 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 3 CII 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.
Type of Medium:
Online Resource
ISSN:
1530-0315
,
0195-9131
DOI:
10.1249/MSS.0000000000001735
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
2018
detail.hit.zdb_id:
2031167-9
SSG:
31
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