Document Detail


Endurance training and detraining in mitochondrial myopathies due to single large-scale mtDNA deletions.
MedLine Citation:
PMID:  17085458     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
At present there are limited therapeutic interventions for patients with mitochondrial myopathies. Exercise training has been suggested as an approach to improve physical capacity and quality of life but it is uncertain whether it offers a safe and effective treatment for patients with heteroplasmic mitochondrial DNA (mtDNA) mutations. The objectives of this study were to assess the effects of exercise training and detraining in eight patients with single, large-scale mtDNA deletions to determine: (i) the efficacy and safety of endurance training (14 weeks) in this patient population; (ii) to determine the effect of more prolonged (total of 28 weeks) exercise training upon muscle and cardiovascular function and (iii) to evaluate the effect of discontinued training (14 weeks) upon muscle and cardiovascular function. Our results show that: (i) 14 weeks of exercise training significantly improved tolerance of submaximal exercise and peak capacity for work, oxygen utilization and skeletal muscle oxygen extraction with no change in the level of deleted mtDNA; (ii) continued training for an additional 14 weeks maintained these beneficial adaptations; (iii) the cessation of training (detraining) resulted in loss of physiological adaptation to baseline capacity with no overall change in mutation load. Patients' self assessment of quality of life as measured by the SF-36 questionnaire improved with training and declined with detraining. Whilst our findings of beneficial effects of training on physiological outcome and quality of life without increases in the percentage of deleted mtDNA are encouraging, we did not observe changes in mtDNA copy number. Therefore there remains a need for longer term studies to confirm that endurance exercise is a safe and effective treatment for patients with mitochondrial myopathies. The effects of detraining clearly implicate physical inactivity as an important mechanism in reducing exercise capacity and quality of life in patients with mitochondrial myopathy.
Authors:
Tanja Taivassalo; Julie L Gardner; Robert W Taylor; Andrew M Schaefer; Jane Newman; Martin J Barron; Ronald G Haller; Douglass M Turnbull
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-11-03
Journal Detail:
Title:  Brain : a journal of neurology     Volume:  129     ISSN:  1460-2156     ISO Abbreviation:  Brain     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-11-29     Completed Date:  2006-12-18     Revised Date:  2011-01-05    
Medline Journal Info:
Nlm Unique ID:  0372537     Medline TA:  Brain     Country:  England    
Other Details:
Languages:  eng     Pagination:  3391-401     Citation Subset:  AIM; IM    
Affiliation:
Department of Kinesiology, McGill University, Montreal, Quebec, Canada.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / physiology
Adult
DNA, Mitochondrial / genetics*
Electron Transport Complex IV / metabolism
Exercise Test / methods
Exercise Therapy / methods*
Female
Gene Deletion*
Heart Rate / physiology
Humans
Lactates / blood
Male
Middle Aged
Mitochondrial Myopathies / genetics,  physiopathology,  therapy*
Muscle Fibers, Skeletal / enzymology
Muscle, Skeletal / metabolism
Oxygen / physiology
Patient Compliance
Physical Endurance / physiology
Physical Exertion / physiology
Polymerase Chain Reaction / methods
Quality of Life
Treatment Outcome
Grant Support
ID/Acronym/Agency:
074454//Wellcome Trust; //Wellcome Trust
Chemical
Reg. No./Substance:
0/DNA, Mitochondrial; 0/Lactates; 7782-44-7/Oxygen; EC 1.9.3.1/Electron Transport Complex IV

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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