Sports Med. 2020 Jan;50(1):103-127. doi: 10.1007/s40279-019-01181-y.
DNA Damage Following Acute Aerobic Exercise: A Systematic Review and Meta-analysis.
Sports medicine (Auckland, N.Z.)
Despoina V Tryfidou, Conor McClean, Michalis G Nikolaidis, Gareth W Davison
Affiliations
Affiliations
- Sport and Exercise Sciences Research Institute, Ulster University, Shore Road, Newtownabbey, Northern Ireland, UK.
- Department of Physical Education and Sports Science at Serres, Aristotle University of Thessaloniki, Serres, Greece.
- Sport and Exercise Sciences Research Institute, Ulster University, Shore Road, Newtownabbey, Northern Ireland, UK. [email protected].
PMID: 31529301
PMCID: PMC6942015 DOI: 10.1007/s40279-019-01181-y
Abstract
BACKGROUND: Exercise is widely recognised for its health enhancing benefits. Despite this, an overproduction of reactive oxygen and nitrogen species (RONS), outstripping antioxidant defence mechanisms, can lead to a state of (chronic) oxidative stress. DNA is a vulnerable target of RONS attack and, if left unrepaired, DNA damage may cause genetic instability.
OBJECTIVE: This meta-analysis aimed to systematically investigate and assess the overall effect of studies reporting DNA damage following acute aerobic exercise.
METHODS: Web of Science, PubMed, MEDLINE, EMBASE, and Scopus were searched until April 2019. Outcomes included (1) multiple time-points (TPs) of measuring DNA damage post-exercise, (2) two different quantification methods (comet assay and 8-oxo-2'-deoxyguanosine; 8-OHdG), and (3) protocols of high intensity (≥ 75% of maximum rate of oxygen consumption; VO
RESULTS: Literature search identified 4316 non-duplicate records of which 35 studies were included in the meta-analysis. The evidence was strong, showcasing an increase in DNA damage immediately following acute aerobic exercise with a large-effect size at TP 0 (0 h) (SMD = 0.875; 95% CI 0.5, 1.25; p < 0.05). When comparing between comet assay and 8-OHdG at TP 0, a significant difference was observed only when using the comet assay. Finally, when isolating protocols of long-distance and high-intensity exercise, increased DNA damage was only observed in the latter. (SMD = 0.48; 95% CI - 0.16, 1.03; p = 0.15 and SMD = 1.18; 95% CI 0.71, 1.65; p < 0.05 respectively).
CONCLUSIONS: A substantial increase in DNA damage occurs immediately following acute aerobic exercise. This increase remains significant between 2 h and 1 day, but not within 5-28 days post-exercise. Such an increase was not observed in protocols of a long-distance. The relationship between exercise and DNA damage may be explained through the hormesis theory, which is somewhat one-dimensional, and thus limited. The hormesis theory describes how exercise modulates any advantageous or harmful effects mediated through RONS, by increasing DNA oxidation between the two end-points of the curve: physical inactivity and overtraining. We propose a more intricate approach to explain this relationship: a multi-dimensional model, to develop a better understanding of the complexity of the relationship between DNA integrity and exercise.
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