Document Detail


Mitochondrial function and antioxidative defence in human muscle: effects of endurance training and oxidative stress.
MedLine Citation:
PMID:  11034627     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The influence of endurance training on oxidative phosphorylation and the susceptibility of mitochondrial oxidative function to reactive oxygen species (ROS) was investigated in skeletal muscle of four men and four women. Mitochondria were isolated from muscle biopsies taken before and after 6 weeks of endurance training. Mitochondrial respiration was measured before and after exposure of mitochondria to exogenous ROS (H2O2 + FeCl2). Endurance training increased peak pulmonary O2 uptake (VO2,peak) by 24 % and maximal ADP-stimulated mitochondrial oxygen consumption (state 3) by 40% (P<0.05). Respiration in the absence of ADP (state 4), the respiratory control ratio (RCR = state 3/state 4) and the ratio between added ADP and consumed oxygen (P/O) remained unchanged by the training programme. Exposure to ROS reduced state 3 respiration but the effect was not significantly different between pre- and post-training samples. State 4 oxygen consumption increased after exposure to ROS both before (+189 %, P< 0.05) and after training (+243 %, P<0.05) and the effect was significantly higher after training (P<0.05, pre- vs. post-training). The augmented state 4 respiration could in part be attenuated by atractyloside, which indicates that ADP/ATP translocase was affected by ROS. The P/O ratio in ROS-treated mitochondria was significantly lower (P<0.05) compared to control conditions, both before (-18.6+/-2.2 %) and after training (-18.5+/-1.1%). Muscle activities of superoxide dismutase (mitochondrial and cytosolic), glutathione peroxidase and muscle glutathione status were unaffected by training. There was a positive correlation between muscle superoxide dismutase activity and age (r = 0.75; P<0.05; range of age 20-37 years), which may reflect an adaptation to increased generation of ROS in senescent muscle. The muscle glutathione pool was more reduced in subjects with high activity of glutathione peroxidase (r = 0.81; P<0.05). The influence of short-term training on mitochondrial oxygen consumption has for the first time been investigated in human skeletal muscle. The results showed that maximal mitochondrial oxidative power is increased after endurance training but that the efficiency of energy transfer (P/O ratio) remained unchanged. Antioxidative defence was unchanged after training when expressed relative to muscle weight. Although this corresponds to a reduced antioxidant protection per individual mitochondrion, the sensitivity of aerobic energy transfer to ROS was unchanged. However, the augmented ROS-induced non-coupled respiration after training indicates an increased susceptibility of mitochondrial membrane proton conductance to oxidative stress.
Authors:
M Tonkonogi; B Walsh; M Svensson; K Sahlin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of physiology     Volume:  528 Pt 2     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2000 Oct 
Date Detail:
Created Date:  2000-12-19     Completed Date:  2000-12-19     Revised Date:  2013-06-11    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  379-88     Citation Subset:  IM    
Affiliation:
Department of Physiology and Pharmacology, Karolinska Institutet and Department of Sport and Health Sciences, Stockholm University College of Physical Education and Sports, S-11486 Stockholm, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Adult
Antioxidants / metabolism*
Female
Glutathione / metabolism
Glutathione Peroxidase / metabolism
Humans
Male
Mitochondria, Muscle / metabolism*
Muscle, Skeletal / metabolism*
Oxidative Stress*
Oxygen Consumption
Physical Endurance / physiology*
Reactive Oxygen Species / metabolism
Superoxide Dismutase / metabolism
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Reactive Oxygen Species; 70-18-8/Glutathione; EC 1.11.1.9/Glutathione Peroxidase; EC 1.15.1.1/Superoxide Dismutase
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