Spendiff 2014 Abstract MiP2014

From Bioblast
Lessons from the master athlete: mitochondrial contributions to aging.


Spendiff S

Mitochondr Physiol Network 19.13 - MiP2014

Spendiff S, Purves-Smith FM, Filion ME, Giouspillou G, Wright K, Vuda M, Morais J, Hepple RT, Taivassalo T (2014)

Event: MiP2014

Age related loss of independence and mobility and an ill health are largely associated with sarcopenia, for which a prominent explanation is mitochondrial damage. Increases in mitochondrial DNA (mtDNA) mutations and mitochondrial dysfunction have been reported in aging skeletal muscle [1,2]. Master athletes (MAs) continue training and competing well into old age and represent an prominent model of healthy muscle aging [3]. The cellular mechanisms facilitating this achievement are currently unknown. Given their remarkable aging trajectory, it is reasonable to hypothesize that MAs have superior mitochondrial function and indices of mtDNA integrity.

15 world class elite MAs and 14 age-sex matched none-athlete controls (NAC), all over the age of 75, underwent muscle MRI scans to assess muscle mass and a biopsy of the vastus lateralis. mtDNA integrity was assessed using the duel cytochrome c oxidase/succinate dehydrogenase stain to ascertain the number of fibres with a respiratory system defect (RSD) and QPCR to provide an indication of mtDNA deletions and copy number. Three aspects of mitochondrial function were assessed in permeabilized myofibres: ROS production, respiration and calcium retention capacity.

MAs had significantly more muscle mass than their sedentary counterparts, fewer myofibres with a RSD and an increased mtDNA copy number. However, there were very few differences in any of the three aspects of mitochondrial function examined. Therefore, while MAs have less RSD than NACs at the individual fibre level, this is not sufficient to result in an improvement in mitochondrial function, when studied at the whole muscle level. Thus a superior mitochondrial profile probably does not explain MAs’ remarkable muscle aging trajectory. However, in the presence of age related comorbidities the increased RSD may result in an exacerbation of these conditions in NACs.

This data raises questions regarding the impact of age related mitochondrial changes on the muscle, as MAs, with the same level of mitochondrial function as controls, still displayed remarkable strength.

β€’ O2k-Network Lab: CA Montreal Hepple RT, US FL Gainesville Hepple RT

Labels: MiParea: Respiration, mtDNA;mt-genetics, Exercise physiology;nutrition;life style  Pathology: Aging;senescence  Stress:Oxidative stress;RONS  Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Regulation: Calcium 

HRR: Oxygraph-2k  Event: A3, Oral  MiP2014 


1-Dep Kinesiology, McGill Univ; 2-McGill Univ Health Centre; 3-DΓ©p Kinanthropologie, Univ QuΓ©bec MontrΓ©al; MontrΓ©al Canada. - [email protected]


  1. Bua E, Johnson J, Herbst A, Delong B, McKenzie D, Salamat S, Aiken JM (2006) Mitochondrial DNA-deletion mutations accumulate intracellularly to detrimental levels in aged human skeletal muscle fibers. Am J Hum Genet 79: 469-80.
  2. Gouspillou G, Sgarioto N, Kapchinsky S, Purves-Smith F, Norris B, Pion CH, Barbat-Artigas S, Lemieux F, Taivassalo T, Morais JA, Aubertin-Leheudre M, Hepple RT (2014) Increased sensitivity to mitochondrial permeability transition and myonuclear translocation of endonuclease G in atrophied muscle of physically active older humans. FASEB J 28: 1621-33.
  3. McCrory JL, Salacinski AJ, Hunt SE, Greenspan SL (2009) Thigh muscle strength in senior athletes and healthy controls. J Strength Conditioning Res 23: 2430-6.
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