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Exercise and DNA damage and repair in middle aged men / Matthew Andrew Aikman

Regular physical activity (PA) leads to an increased quality of life by means of certain
physiological adaptations. Regular PA is beneficial to the human body and its functionality,
including the physiological, biochemical and even psychological modalities. During PA an
increased burden is placed on all physiological mechanisms due to the increased energy demand,
resulting in an adaptation of the physiological systems. Currently the biochemical mechanisms
by which these adaptations occur are not well understood or defined.

During the flow of electrons through the electron transport chain in the mitochondria free
radicals and reactive oxygen species (ROS) are produced. PA results in increased ROS
production. The relationship of different exercise intensities and ROS production with resulting
DNA damage is unclear. These free radicals and ROS disturb the pro-oxidant anti-oxidant
balance resulting in oxidative stress. When this balance is disturbed oxidative stress could lead to
potential oxidative damage, Oxidative damage occurs in lipid, protein and nucleic acid
macromolecules. ROS can attack DNA bases or deoxyribose residues to produce damaged bases
and/or single and double strand breaks. When the DNA is regarded and the damages are
replicated it could cause mutations or apoptosis, affecting the cell function and physiology.

The purpose of this study was to investigate the influence of different aerobic intensities on
oxidative DNA damage and repair in middle aged men by means of the Comet assay. Five PA
males and five physically inactive males were assigned to an experimental and control group
respectively. The subjects did not differ significantly at baseline. The VO2-max of each subject
was determined at baseline. Subjects were then randomly assigned to 60, 70, 80 and 90% of
individual baseline VO2-max intensities for an acute exercise intervention of 30 minutes on a
bicycle ergometer. Blood sampling was done at baseline, post-exercise and 24 hours post-exercise
for oxygen radical absorbance capacity (ORAC) and hydroperoxide analysis (dROM).
Peripheral blood was obtained for DNA damage testing by means of Comet analysis at baseline,
post-exercise, 5, 15, 30 minutes, and also 6, 12, 24, 48 and 72 hours after exercise. The results
obtained indicated that subjects who regularly participate in PA had an increased baseline
reading of ORAC and dROM values. ORAC levels after each acute exercise session increased,
with the highest increase in the control group, with a decrease in the direction of baseline
readings 24 hours post exercise. A biphasic damage-repair cycle over the 72 hour period was
observed with the Comet analysis. The most damaged cells occur directly after acute exercise.
The highest incidence of DNA damage over a 72 hour period was observed at 70% VO2-max,
with the least amount of damage after 90% VO2-max.
In conclusion the study indicates stress proteins or other kinds of physiological reaction to
minimize the damaging effect of oxidative stress, is in place to restore the cell's homeostasis.
Thus PA results in the development of oxidative DNA damage. To minimize DNA damage the
optimal intensity for acute physical exercise is between 70-80% VO2-max. At higher intensities
the release of stress proteins are initiated to buffer the damaging effect of oxidative stress and to
restore homeostasis. / Thesis (M.Sc. (Human Movement Science))--North-West University, Potchefstroom Campus, 2007.

Identiferoai:union.ndltd.org:netd.ac.za/oai:union.ndltd.org:nwu/oai:dspace.nwu.ac.za:10394/1490
Date January 2007
CreatorsAikman, Matthew Andrew
PublisherNorth-West University
Source SetsSouth African National ETD Portal
Detected LanguageEnglish
TypeThesis

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