Xanthine oxidase inhibition attenuates skeletal muscle signaling following acute exercise but does not impair mitochondrial adaptations to endurance training.

Wadley, Glenn D., Nicolas, Marc, Hiam, Danielle and McConell, Glenn K. 2013, Xanthine oxidase inhibition attenuates skeletal muscle signaling following acute exercise but does not impair mitochondrial adaptations to endurance training., American journal of physiology - endocrinology and metabolism, vol. 304, no. 8, pp. E853-E862.

Attached Files
Name Description MIMEType Size Downloads

Title Xanthine oxidase inhibition attenuates skeletal muscle signaling following acute exercise but does not impair mitochondrial adaptations to endurance training.
Author(s) Wadley, Glenn D.
Nicolas, Marc
Hiam, Danielle
McConell, Glenn K.
Journal name American journal of physiology - endocrinology and metabolism
Volume number 304
Issue number 8
Start page E853
End page E862
Total pages 10
Publisher American Physiological Society
Place of publication Bethesda, Maryland
Publication date 2013-04
ISSN 0193-1849
1522-1555
Keyword(s) contraction
reactive oxygen species
allopurinol
PGC-1a
MAPK
Summary The aim of this research was to examine the impact of the xanthine oxidase (XO) inhibitor allopurinol on the skeletal muscle activation of cell signaling kinases' and adaptations to mitochondrial proteins and antioxidant enzymes following acute endurance exercise and endurance training. Male Sprague-Dawley rats performed either acute exercise (60 min of treadmill running, 27 m/min, 5% incline) or 6 wk of endurance training (5 days/wk) while receiving allopurinol or vehicle. Allopurinol treatment reduced XO activity to 5% of the basal levels (P < 0.05), with skeletal muscle uric acid levels being almost undetectable. Following acute exercise, skeletal muscle oxidized glutathione (GSSG) significantly increased in allopurinol- and vehicle-treated groups despite XO activity and uric acid levels being unaltered by acute exercise (P < 0.05). This suggests that the source of ROS was not from XO. Surprisingly, muscle GSSG levels were significantly increased following allopurinol treatment. Following acute exercise, allopurinol treatment prevented the increase in p38 MAPK and ERK phosphorylation and attenuated the increase in mitochondrial transcription factor A (mtTFA) mRNA (P < 0.05) but had no effect on the increase in peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), nuclear respiratory factor-2, GLUT4, or superoxide dismutase mRNA. Allopurinol also had no impact on the endurance training-induced increases in PGC-1α, mtTFA, and mitochondrial proteins including cytochrome c, citrate synthase, and β-hydroxyacyl-CoA dehydrogenase. In conclusion, although allopurinol inhibits cell signaling pathways in response to acute exercise, the inhibitory effects of allopurinol appear unrelated to exercise-induced ROS production by XO. Allopurinol also has little effect on increases in mitochondrial proteins following endurance training.
Language eng
Field of Research 110602 Exercise Physiology
Socio Economic Objective 920104 Diabetes
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2013, American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30057123

Document type: Journal Article
Collection: School of Exercise and Nutrition Sciences
Connect to link resolver
 
Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved.

Versions
Version Filter Type
Citation counts: Scopus Citation Count Cited 4 times in Scopus
Google Scholar Search Google Scholar
Access Statistics: 22 Abstract Views, 3 File Downloads  -  Detailed Statistics
Created: Wed, 23 Oct 2013, 08:31:17 EST by Glenn Wadley

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.