DNA damage in mononuclear cells following maximal exercise in sedentary and physically active lean and obese men

Abstract

We evaluated the impact of maximal exercise on oxidative stress and DNA damage in peripheral blood mononuclear cells (PBMC) from sedentary and exercised lean and obese men. PBMC were collected before, immediately and 1-h after exercise and exposed to hydrogen peroxide (H 2 O 2 ; 25 and 50 μM, 4 h). A leukocytosis was induced by maximal exercise immediately and 1-h after exercise in all groups. However, a lymphopenia was observed 1-h after exercise in the Sedentary obese group. In the control condition, low DNA damage index concomitant to increases in intracellular glutathione content (GSH) was identified immediately after exercise in all groups. However, higher DNA damage index and lipid peroxidation occurred 1-h after the bout in Sedentary and Exercised Obese groups. PBMC exposed to both H 2 O 2 25 and 50 μM experienced higher DNA damage and lipid peroxidation index immediately after exercise in all groups. Both lipid peroxidation and DNA damage index remained higher in PBMC of Sedentary Lean, Sedentary Obese, and Exercised obese groups obtained 1-h after exercise in both H 2 O 2 25 and 50 μM, with the highest values identified in PBMC from Sedentary Obese group. However, increases in GSH content were identified in treated PBMC from sedentary and exercised lean groups as well as exercised obese group 1-h after exercise. Habitual exercise confers increased resistance of PBMC to DNA damage induced by oxidative stress, reducing the detrimental effects of obesity.

The Interplay between Oxidative Stress, Exercise, and Pain in Health and Disease: Potential Role of Autonomic Regulation and Epigenetic Mechanisms

“…The person's basal training level also influences oxidative stress. Physically active individuals (more than 150 min of exercise per week) are less prone to DNA damage caused by exercise-induced oxidative stress than sedentary individuals [64]. This sort of decreased vulnerability to oxidative damage is probably the result of coping mechanisms taking place in response to oxidative stress during the recovery phase, including the activation of antioxidant and oxidative damage repair systems mediated via the increased ROS production.…”

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“…The response of monocytes, lymphocytes, or peripheral blood mononuclear cells (PBMCs) in obese patients has been evaluated predominantly by aerobic exercise sessions, performed in different schemes and intensities, such as continuous and moderate-intensity [33], continuous and high volume (marathons) [34], high-intensity intermittent exercise (HIIE) [21,35,36] and higher efforts (to exhaustion) [37][38][39]. Slusher et al [33] applied a 30-minute session of continuous aerobic exercise at 75 % of peak oxygen consumption (V ̇ O 2peak ) in obese and eutrophic individuals.…”

Type and Intensity as Key Variable of Exercise in Metainflammation Diseases: A Review

“…The response of monocytes, lymphocytes, or peripheral blood mononuclear cells (PBMCs) in obese patients has been evaluated predominantly by aerobic exercise sessions, performed in different schemes and intensities, such as continuous and moderate-intensity [33], continuous and high volume (marathons) [34], high-intensity intermittent exercise (HIIE) [21,35,36] and higher efforts (to exhaustion) [37][38][39]. Slusher et al [33] applied a 30-minute session of continuous aerobic exercise at 75 % of peak oxygen consumption (V ̇ O 2peak ) in obese and eutrophic individuals.…”

“…On the other hand, after maximum test on the treadmill, there was a reduction in DNA damage and increase in the content of intracellular total glutathione (GSH) in unstimulated PBMCs from trained and sedentary obese individuals and only lean sedentary individuals. However, after 1-h there was an increase of DNA damage and thiobarbituric acid reactive species (TBARS) production only in obese individuals [39]. Additionally, the PBMCs of sedentary obese individuals stimulated with hydrogen peroxide (H 2 O 2 ) showed greater DNA damage and less total GSH compared with sedentary eutrophic subjects and trained obese subjects after the maximum exercise session [39].…”

“…However, after 1-h there was an increase of DNA damage and thiobarbituric acid reactive species (TBARS) production only in obese individuals [39]. Additionally, the PBMCs of sedentary obese individuals stimulated with hydrogen peroxide (H 2 O 2 ) showed greater DNA damage and less total GSH compared with sedentary eutrophic subjects and trained obese subjects after the maximum exercise session [39]. The exhaustive exercise also increased the inflammatory monocytes percentage, histone H4 acetylation and reduced the histone deacetylase 2 activity in obese individuals [37].…”