Exercise‐induced lipid peroxidation: Implications for deoxyribonucleic acid damage and systemic free radical generation

Abstract

Exercise-induced deoxyribonucleic acid (DNA) damage is often associated with an increase in free radicals; however, there is a lack of evidence examining the two in parallel. This study tested the hypothesis that high-intensity exercise has the ability to produce free radicals that may be capable of causing DNA damage. Twelve apparently healthy male subjects (age: 23 ± 4 years; stature: 181 ± 8 cm; body mass: 80 ± 9 kg; and VO(2max) : 49 ± 5 ml/kg/min) performed three 5 min consecutive and incremental stages (40, 70, and 100% of VO(2max) ) of aerobic exercise with a 15-min period separating each stage. Blood was drawn after each bout of exercise for the determination of ex vivo free radicals, DNA damage, protein carbonyls, lipid hydroperoxide (LOOH) concentration, and a range of lipid-soluble antioxidants. Lipid-derived oxygen-centered free radicals (hyperfine coupling constants a(Nitrogen) = 13.7 Gauss (G) and aβ(Hydrogen) = 1.8 G) increased as a result of acute moderate and high-intensity exercise (P < 0.05), while DNA damage was also increased (P < 0.05). Systemic changes were observed in LOOH and for lipid-soluble antioxidants throughout exercise (P < 0.05); however, there was no observed change in protein carbonyl concentration (P > 0.05). These findings identify lipid-derived free radical species as possible contributors to peripheral mononuclear cell DNA damage in the human exercising model. This damage occurs in the presence of lipid oxidation but in the absence of any change to protein carbonyl concentration. The significance of these findings may have relevance in terms of immune function, the aging process, and the pathology of carcinogenesis.

A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep and exercise

“…There is mounting evidence to suggest that exercise is accompanied by an increased generation of free radicals, resulting in measurable elevations in oxidative stress biomarkers after both acute aerobic (Benitez-Sillero et al, 2011, Bloomer, 2008, Fogarty et al, 2011 and anaerobic exercise (Bloomer and Goldfarb, 2004, Pittaluga et al, 2006, Vollaard et al, 2005. Given the substantial evidence for the protective effects of exercise on oxidative stress-associated diseases, this seems paradoxical.…”

Effects of endurance training on exhaustive exercise-induced oxidative stress markers

“…Nevertheless, no agreement was reached about whether lipid peroxidation was affected by exercise or not. Fogarty et al (2011) determined that LOOH level, which is an indicator of lipid peroxidation, increased during 3x5 min exercise with 40, 70 and 100% VO 2max . Similarly, Ajmani et al (2003) stated that maximal running exercise increased LOOH level significantly.…”

Low Dose Radiation Adaptive Protection to Control Neurodegenerative Diseases

“…In view of the observed evidence for the beneficial effects of exercise, we would be justified in ignoring the concerns raised in the article by Fogarty et al (2011) regarding the increased DNA damage from exercise. The beneficial health effects of exercise were nullified when antioxidant supplements were taken, indicating the key role played by the small amount of oxidative damage caused by exercise in upregulating the adaptive protection (Ristow et al, 2009).…”

“…Concerns have also been expressed about the observed increase in DNA damage from even five minutes of strenuous exercise in an article (Fogarty et al, 2011) entitled "Exercise-induced lipid peroxidation: Implications for deoxyribonucleic acid damage and systemic free radical generation". Another cause of DNA damage that has traditionally been a concern since the 1950s is low dose radiation (LDR) (UNSCEAR, 1958) and it continues to be a concern (NRC, 2006).…”