Document Detail

Ultraendurance exercise increases the production of reactive oxygen species in isolated mitochondria from human skeletal muscle.
MedLine Citation:
PMID:  20110545     Owner:  NLM     Status:  MEDLINE    
Exercise-induced oxidative stress is important for the muscular adaptation to training but may also cause muscle damage. We hypothesized that prolonged exercise would increase mitochondrial production of reactive oxygen species (ROS) measured in vitro and that this correlates with oxidative damage. Eight male athletes (24-32 yr) performed ultraendurance exercise (kayaking/running/cycling) with an average work intensity of 55% V(O(2peak)) for 24 h. Muscle biopsies were taken from vastus lateralis before exercise, immediately after exercise, and after 28 h of recovery. The production of H(2)O(2) was measured fluorometrically in isolated mitochondria with the Amplex red and peroxidase system. Succinate-supported mitochondrial H(2)O(2) production was significantly increased after exercise (73% higher, P = 0.025) but restored to the initial level at recovery. Plasma level of free fatty acids (FFA) increased fourfold and exceeded 1.2 mmol/l during the last 6 h of exercise. Plasma FFA at the end of exercise was significantly correlated to mitochondrial ROS production (r = 0.74, P < 0.05). Mitochondrial content of 4-hydroxy-nonenal-adducts (a marker of oxidative damage) was increased only after recovery and was not correlated with mitochondrial ROS production. Total thiol group level and glutathione peroxidase activity were elevated after recovery. In conclusion, ultraendurance exercise increases ROS production in isolated mitochondria, but this is reversed after 28 h recovery. Mitochondrial ROS production was not correlated with oxidative damage of mitochondrial proteins, which was increased at recovery but not immediately after exercise.
Kent Sahlin; Irina G Shabalina; C Mikael Mattsson; Linda Bakkman; Maria Fernström; Zinaida Rozhdestvenskaya; Jonas K Enqvist; Jan Nedergaard; Björn Ekblom; Michail Tonkonogi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-28
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  108     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-08-17     Completed Date:  2010-11-16     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  780-7     Citation Subset:  IM    
The Swedish School of Sport and Health Sciences (GIH), Astrand Laboratory of Work Physiology, Stockholm, Sweden.
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MeSH Terms
Creatine Kinase / metabolism
Exercise Tolerance / physiology*
Hydrogen Peroxide / metabolism*
Mitochondria, Muscle / metabolism*
Mitochondrial Proteins / metabolism
Oxidative Stress / physiology
Quadriceps Muscle / metabolism*
Reactive Oxygen Species / metabolism*
Young Adult
Reg. No./Substance:
0/Mitochondrial Proteins; 0/Reactive Oxygen Species; 7722-84-1/Hydrogen Peroxide; EC Kinase

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