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Lifelong endurance training attenuates age-related genotoxic stress in human skeletal muscle

James N Cobley1, George K Sakellariou2, Scott Murray3, Sarah Waldron4, Warren Gregson1, Jatin G Burniston1, James P Morton1, Lesley A Iwanejko2 and Graeme L Close1*

Author Affiliations

1 Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, L3 3AF, UK

2 Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L69 3GA, UK

3 Cardiology Department, Liverpool Heart and Chest Hospital, Liverpool, L14 3PE, UK

4 Stepping Hill Hospital, Stockport, SK2 7JE, UK

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Longevity & Healthspan 2013, 2:11  doi:10.1186/2046-2395-2-11

Published: 12 July 2013



The aim of the present study was to determine the influence of age and habitual activity level, at rest and following a single bout of high-intensity exercise, on the levels of three proteins poly(ADP-ribose) polymerase-1 (PARP-1), cleaved-PARP-1 and poly(ADP-ribose) glycohydrolase (PARG), involved in the DNA repair and cell death responses to stress and genotoxic insults. Muscle biopsies were obtained from the vastus lateralis of young trained (22 ± 3 years, n = 6), young untrained (24 ± 4 years, n = 6), old trained (64 ± 3 years, n = 6) and old untrained (65 ± 6 years, n = 6) healthy males before, immediately after and three days following a high-intensity interval exercise bout.


PARP-1, which catalyzes poly(ADP-ribosyl)ation of proteins and DNA in response to a range of intrinsic and extrinsic stresses, was increased at baseline in old trained and old untrained compared with young trained and young untrained participants (P ≤ 0.05). Following exercise, PARP-1 levels remained unchanged in young trained participants, in contrast to old trained and old untrained where levels decreased and young untrained where levels increased (P ≤ 0.05). Interestingly, baseline levels of the cleaved PARP-1, a marker of apoptosis, and PARG, responsible for polymer degradation, were both significantly elevated in old untrained compared with old trained, young trained and young untrained (P ≤ 0.05). Despite this baseline difference in PARG, there was no change in any group following exercise. There was a non-significant statistical trend (P = 0.072) towards increased cleaved-PARP-1 expression post-exercise in younger but not old persons, regardless of training status.


Collectively, these results show that exercise slows the progression towards a chronically stressed state but has no impact on the age-related attenuated response to acute exercise. Our findings provide valuable insight into how habitual exercise training could protect skeletal muscle from chronic damage to macromolecules and may reduce sarcopenia in older people.

PARP-1; Cleaved PARP-1; PARG; Apoptosis; DNA repair; Exercise; Training; Ageing