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Endurance training and detraining in mitochondrial myopathies due to single large-scale mtDNA deletions

Lookup NU author(s): Dr Julie Murphy, Professor Robert Taylor, Dr Andrew Schaefer, Dr Joseph Newman, Dr Martin Barron, Professor Doug Turnbull

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Abstract

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. © 2006 The Author(s).


Publication metadata

Author(s): Taivassalo T, Gardner JL, Taylor RW, Schaefer AM, Newman J, Barron MJ, Haller RG, Turnbull DM

Publication type: Article

Publication status: Published

Journal: Brain

Year: 2006

Volume: 129

Issue: 12

Pages: 3391-3401

Print publication date: 01/12/2006

ISSN (print): 0006-8950

ISSN (electronic): 1460-2156

Publisher: Oxford University Press

URL: http://dx.doi.org/10.1093/brain/awl282

DOI: 10.1093/brain/awl282

PubMed id: 17085458


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