Surfboard riders are at risk of low energy availability - A pilot study.

BACKGROUND: Surfing is a rapidly growing sport and recreational activity. The previously reported, intermittent high-intensity energetics of surfing place athletes and recreational participants at risk of low energy availability (LEA). AIM: As such, this pioneering study aims to be the first to investigate LEA risk and the second to investigate dietary intake in surfers. METHODS: Twenty-one intermediate and advanced surfers (female - 5, male - 16) were recruited to complete an online self-administered questionnaire and 4 consecutive 24-hour food logs to establish LEA risk and asses dietary intake. The Low Energy Availability in Female Questionnaire and Eating Disorder Examination Questionnaire were used to identify at-risk individuals in females and males, respectively, with respective cut-off's of ≥8 and ≥2.3. RESULTS: Fifty-seven percent were classed as at-risk of LEA (50% and 80% in males and females, respectively). No significant relationship of competitive status, surfing ability and body mass index on risk classification was found. However, a non-significant medium effect of age was observed (p = 0.338, R = 0.549). And 77% of the 70 total analysed food records showed inadequate carbohydrate (CHO) consumption. CONCLUSION: In summary, an alarmingly high portion of surfers are at risk of LEA and dietary inadequacy. Future studies should confirm whether surfing organisations need to intervene, by addressing limitations of the present study including a small sample, which was heavily biased away from female and high-level competitors.

Targeted Antioxidants in Exercise-Induced Mitochondrial Oxidative Stress: Emphasis on DNA Damage.

Exercise simultaneously incites beneficial (e.g., signal) and harming (e.g., damage to macromolecules) effects, likely through the generation of reactive oxygen and nitrogen species (RONS) and downstream changes to redox homeostasis. Given the link between nuclear DNA damage and human longevity/pathology, research attempting to modulate DNA damage and restore redox homeostasis through non-selective pleiotropic antioxidants has yielded mixed results. Furthermore, until recently the role of oxidative modifications to mitochondrial DNA (mtDNA) in the context of exercising humans has largely been ignored. The development of antioxidant compounds which specifically target the mitochondria has unveiled a number of exciting avenues of exploration which allow for more precise discernment of the pathways involved with the generation of RONS and mitochondrial oxidative stress. Thus, the primary function of this review, and indeed its novel feature, is to highlight the potential roles of mitochondria-targeted antioxidants on perturbations to mitochondrial oxidative stress and the implications for exercise, with special focus on mtDNA damage. A brief synopsis of the current literature addressing the sources of mitochondrial superoxide and hydrogen peroxide, and available mitochondria-targeted antioxidants is also discussed.

The mitochondria-targeted antioxidant MitoQ, attenuates exercise-induced mitochondrial DNA damage.

High-intensity exercise damages mitochondrial DNA (mtDNA) in skeletal muscle. Whether MitoQ - a redox active mitochondrial targeted quinone - can reduce exercise-induced mtDNA damage is unknown. In a double-blind, randomized, placebo-controlled design, twenty-four healthy male participants consisting of two groups (placebo; n = 12, MitoQ; n = 12) performed an exercise trial of 4 x 4-min bouts at 90-95% of heart rate max. Participants completed an acute (20 mg MitoQ or placebo 1-h pre-exercise) and chronic (21 days of supplementation) phase. Blood and skeletal muscle were sampled immediately pre- and post-exercise and analysed for nuclear and mtDNA damage, lipid hydroperoxides, lipid soluble antioxidants, and the ascorbyl free radical. Exercise significantly increased nuclear and mtDNA damage across lymphocytes and muscle (P < 0.05), which was accompanied with changes in lipid hydroperoxides, ascorbyl free radical, and α-tocopherol (P < 0.05). Acute MitoQ treatment failed to impact any biomarker likely due to insufficient initial bioavailability. However, chronic MitoQ treatment attenuated nuclear (P < 0.05) and mtDNA damage in lymphocytes and muscle tissue (P < 0.05). Our work is the first to show a protective effect of chronic MitoQ supplementation on the mitochondrial and nuclear genomes in lymphocytes and human muscle tissue following exercise, which is important for genome stability.

A combined γ-H2AX and 53BP1 approach to determine the DNA damage-repair response to exercise in hypoxia.

This study examines the interplay between exercise and hypoxia in relation to the DNA damage-repair response; with specific interest to DNA double strand damage. Following two V̇O2max tests, 14 healthy, male participants completed two exercise trials (hypoxia; 12% FiO2, normoxia; 20.9% FiO2) consisting of cycling for 30-min at 80-85% of V̇O2max relative to the environmental condition. Blood was sampled pre-, immediately post-, 2-, and 4-h post-exercise with additional blood cultured in vitro for 24-, 48-, and 72-h following the experimental trial. Samples were analysed for single- and double-strand DNA damage, FPG-sensitive sites, lipid hydroperoxides, lipid soluble antioxidants, and the ascorbyl free radical quantified by EPR. Exercise increased single strand breaks and FPG-sensitive sites (P < 0.05) which was exacerbated following hypoxia (P = 0.02) and a similar increase in DNA double strand breaks occurred as a result of hypoxia per se (P < 0.000). With respect to the DNA damage-repair response, single strand breaks, FPG-sensitive sites, and double strand lesions were fully repaired by the 4- (in vivo), 24-, and 48-h (in vitro) time-points respectively. Changes in lipid hydroperoxides (P = 0.001), the ascorbyl free radical (P = 0.02), and lipid soluble antioxidants (P > 0.05), were also observed following exercise in hypoxia. These findings highlight significant single- and double strand DNA damage and oxidative stress as a function of high-intensity exercise, which is substantially exacerbated in hypoxia and may be attributed to multiple mechanisms of ROS generation. In addition, full repair of DNA damage (SSB, DSB, and FPG-sensitive sites) was observed within 24- and 48-h of normoxic and hypoxic exercise, respectively.

Exogenous Plant-Based Nutraceutical Supplementation and Peripheral Cell Mononuclear DNA Damage Following High Intensity Exercise.

Plant-based nutraceuticals are categorised as nutritional supplements which contain a high concentration of antioxidants with the intention of minimising the deleterious effect of an oxidative insult. The primary aim of this novel study was to determine the effect of exogenous barley-wheat grass juice (BWJ) on indices of exercise-induced oxidative stress. Ten (n = 10) apparently healthy, recreationally trained (V̇O2max 55.9 ± 6 mL·kg−1·min−1), males (age 22 ± 2 years, height 181 ± 6 cm, weight 87 ± 8 kg, body mass index (BMI) 27 ± 1) volunteered to participant in the study. In a randomised, double-blinded, placebo-controlled crossover design, participants consumed either a placebo, a low dose (70 mL per day) of BWJ, or a high dose (140 mL per day) of BWJ for 7-days. Experimental exercise consisted of a standard maximal oxygen uptake test until volitional fatigue. DNA damage, as assessed by the single cell gel electrophoresis comet assay, increased following high intensity exercise across all groups (time × group; p < 0.05, Effect Size (ES) = 0.7), although there was no selective difference for intervention (p > 0.05). There was a main effect for time in lipid hydroperoxide concentration (pooled-group data, pre- vs. post-exercise, p < 0.05, ES = 0.2) demonstrating that exercise increased lipid peroxidation. Superoxide dismutase activity (SOD) increased by 44.7% following BWJ supplementation (pooled group data, pre- vs. post). The ascorbyl free radical (p < 0.05, ES = 0.26), α-tocopherol (p = 0.007, ES = 0.2), and xanthophyll (p = 0.000, ES = 0.5), increased between the pre- and post-exercise time points indicating a main effect of time. This study illustrates that a 7-day supplementation period of a novel plant-derived nutraceutical product is insufficient at attenuating exercise-induced oxidative damage. It is possible that with a larger sample size, and longer supplementation period, this novel plant-based nutraceutical could potentially offer effective prophylaxis against exercise-induced oxidative stress; as such, this justifies the need for further research.