Mark Fogarty

Exercise-Induced Lipid Peroxidation: Implications for Deoxyribonucleic Acid Damage and Systemic Free Radical Generation

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 VO2max: 49 ± 5 ml/kg/min) performed three 5 min consecutive and incremental stages (40, 70, and 100% of VO2max) 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 aNitrogen = 13.7 Gauss (G) and aβHydrogen = 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. Environ. Mol. Mutagen. 52:35–42, 2011.

Exercise and postprandial lipaemia: effects on peripheral vascular function, oxidative stress and gastrointestinal transit

Postprandial lipaemia may lead to an increase in oxidative stress, inducing endothelial dysfunction. Exercise can slow gastric emptying rates, moderating postprandial lipaemia. The purpose of this study was to determine if moderate exercise, prior to fat ingestion, influences gastrointestinal transit, lipaemia, oxidative stress and arterial wall function. Eight apparently healthy males (age 23.6 ± 2.8 yrs; height 181.4 ± 8.1 cm; weight 83.4 ± 16.2 kg; all data mean ± SD) participated in the randomised, crossover design, where (i) subjects ingested a high-fat meal alone (control), and (ii) ingested a high-fat meal, preceded by 1 h of moderate exercise. Pulse Wave Velocity (PWV) was examined at baseline, post-exercise, and in the postprandial period. Gastric emptying was measured using the 13C-octanoic acid breath test. Measures of venous blood were obtained prior to and following exercise and at 2, 4 and 6 hours post-ingestion. PWV increased (6.5 ± 1.9 m/sec) at 2 (8.9 ± 1.7 m/sec) and 4 hrs (9.0 ± 1.6 m/sec) post-ingestion in the control group (time × group interaction, P < 0.05). PWV was increased at 2 hrs post-ingestion in the control compared to the exercise trial; 8.9 ± 1.7 vs. 6.2 ± 1.5 m/sec (time × group interaction, P < 0.05). Lipid hydroperoxides increased over time (pooled exercise and control data, P < 0.05). Serum triacylglycerols were elevated postprandially (pooled exercise and control data, P < 0.05). There were no changes in gastric emptying, cholesterol, or C-reactive protein levels. These data suggest that acute exercise prior to the consumption of a high-fat meal has the potential to reduce vascular impairments.

Acute and chronic watercress supplementation attenuates exercise-induced peripheral mononuclear cell DNA damage and lipid peroxidation

Pharmacological antioxidant vitamins have previously been investigated for a prophylactic effect against exercise-induced oxidative stress. However, large doses are often required and may lead to a state of pro-oxidation and oxidative damage. Watercress contains an array of nutritional compounds such as β-carotene and α-tocopherol which may increase protection against exercise-induced oxidative stress. The present randomised controlled investigation was designed to test the hypothesis that acute (consumption 2 h before exercise) and chronic (8 weeks consumption) watercress supplementation can attenuate exercise-induced oxidative stress. A total of ten apparently healthy male subjects (age 23 (SD 4) years, stature 179 (SD 10) cm and body mass 74 (SD 15) kg) were recruited to complete the 8-week chronic watercress intervention period (and then 8 weeks of control, with no ingestion) of the experiment before crossing over in order to compete the single-dose acute phase (with control, no ingestion). Blood samples were taken at baseline (pre-supplementation), at rest (pre-exercise) and following exercise. Each subject completed an incremental exercise test to volitional exhaustion following chronic and acute watercress supplementation or control. The main findings show an exercise-induced increase in DNA damage and lipid peroxidation over both acute and chronic control supplementation phases (P< 0.05 v. supplementation), while acute and chronic watercress attenuated DNA damage and lipid peroxidation and decreased H₂O₂ accumulation following exhaustive exercise (P< 0.05 v. control). A marked increase in the main lipid-soluble antioxidants (α-tocopherol, γ-tocopherol and xanthophyll) was observed following watercress supplementation (P< 0.05 v. control) in both experimental phases. These findings suggest that short- and long-term watercress ingestion has potential antioxidant effects against exercise-induced DNA damage and lipid peroxidation.

The Impact of Acute Moderate Intensity Exercise on Arterial Regional Stiffness, Lipid Peroxidation, and Antioxidant Status in Healthy Males

There is a paucity of research examining the influence of acute exercise on pulse wave velocity (PWV) and oxidative stress. The purpose of this study was to examine the effects of acute moderate aerobic exercise on PWV and oxidative stress in healthy males. Eight apparently healthy males (age 23.6 ± 2.8 yrs; stature 181.4 ± 8.1 cm; weight 83.4 ± 16.2 kg; all data mean ±SD) participated in a randomized crossover design consisting of (i) a one hour bout of moderate aerobic exercise and (ii) a control trial of one hour rest. Pre- and post-exercise blood samples were drawn for the determination of lipid hydroperoxides (LOOHs) and lipid-soluble antioxidants (lycopene, retinol, and β-carotene). Exercise had no effect on stiffness and LOOHs (P > 0.05). Retinol and lycopene were increased following exercise (P < 0.05). These findings suggest that acute moderate exercise has no effect on PWV and LOOHs, but it can increase systemic antioxidants, which may be of benefit to health.

Effects of α-lipoic acid on mtDNA damage after isolated muscle contractions.

INTRODUCTION Although pharmacological antioxidants have previously been investigated for a prophylactic effect against exercise oxidative stress, it is not known if α-lipoic acid supplementation can protect against DNA damage after high-intensity isolated quadriceps exercise. This randomized controlled investigation was designed to test the hypothesis that 14 d of α-lipoic acid supplementation can attenuate exercise-induced oxidative stress. METHODS Twelve (n = 12) apparently healthy male participants (age = 28 ± 10 yr, stature = 177 ± 12 cm and body mass = 81 ± 15 kg) were randomly assigned to receive either a daily supplement of 1000 mg of α-lipoic acid (2 × 500-mg tablets) for 14 d (n = 6) or receive no supplement (n = 6) in a double-blinded experimental approach. Blood and muscle biopsy tissue samples were taken at rest and after the completion of 100 isolated and continuous maximal knee extension (minimum force = 200 N, speed of contraction = 60° · s(-1)). RESULTS Exercise increased mitochondrial 8-hydroxy-2-deoxyguanosine (8-OHdG) concentration in both groups (P < 0.05 vs rest) with a concomitant decrease in total antioxidant capacity (P < 0.05 vs rest). There was a marked increase in blood total antioxidant capacity after oral α-lipoic acid supplementation (P < 0.05 vs nonsupplemented), whereas DNA damage (Comet assay and 8-OHdG), lipid peroxidation, and hydrogen peroxide increased after exercise in the nonsupplemented group only (P < 0.05 vs supplemented). Exercise increased protein oxidation in both groups (P < 0.05 vs rest). CONCLUSIONS These findings suggest that short-term α-lipoic acid supplementation can selectively protect DNA (but not in muscle mitochondria) and lipids against exercise-induced oxidative stress.