Abstract
BackgroundOxidative stress results in lipid, protein, and DNA oxidation, resulting in telomere erosion, chromosomal damage, and accelerated cellular aging. Training promotes healthy metabolic and oxidative profiles whereas the effects of multi-day, prolonged, and continuous exercise are unknown. This study investigated the effects of multi-day prolonged exercise on metabolic and oxidative stress as well as telomere integrity in healthy adults.MethodsFifteen participants performed a 14-day, 260-km, wilderness canoeing expedition (12 males) (EXP) (24 ± 7 years, 72 ± 6 kg, 178 ± 8.0 cm, 18.4 ± 8.4% BF, 47.5 ± 9.3 mlO2 kg–1 min–1), requiring 6–9 h of low- to moderate-intensity exercise daily. Ten controls participated locally (seven males) (CON) (31 ± 11 years, 72 ± 15 kg, 174 ± 10 cm, 22.8 ± 10.0% BF, 47.1 ± 9.0 mlO2 kg–1 min–1). Blood plasma, serum, and mononuclear cells were sampled before and after the expedition to assess hormonal, metabolic, and oxidative changes.ResultsSerum cholesterol, high- and low-density lipoprotein, testosterone, insulin, sodium, potassium, urea, and chloride concentrations were not different between groups, whereas triglycerides, glucose, and creatinine levels were lower following the expedition (p < 0.001). Malondialdehyde and relative telomere length (TL) were unaffected (EXP: 4.2 ± 1.3 vs. CON: 4.1 ± 0.7 μM; p > 0.05; EXP: 1.00 ± 0.48 vs. CON: 0.89 ± 0.28 TS ratio; p = 0.77, respectively); however, superoxidase dismutase activity was greater in the expedition group (3.1 ± 0.4 vs. 0.8 ± 0.5 U ml–1; p < 0.001).ConclusionThese results indicate a modest improvement in metabolic and oxidative profiles with increased superoxidase dismutase levels, suggesting an antioxidative response to counteract the exercise-associated production of free radicals and reactive oxygen species during prolonged exercise, mimicking the effects from long-term training. Although improved antioxidant activity may lead to increased TL, the present exercise stimulus was insufficient to promote a positive cellular aging profile with concordant chromosomal changes in our healthy and young participants.
Highlights
IntroductionOxidative stress is the result of an imbalance between the production of free radicals (reactive oxygen species and nitrogen oxygen species), and a defense system of enzymatic and non-enzymatic antioxidants
Oxidative stress is the result of an imbalance between the production of free radicals, and a defense system of enzymatic and non-enzymatic antioxidants
The production of free radicals is known to originate from multiple organs such as the heart, lungs, and even blood (Powers and Jackson, 2008; Nikolaidis and Jamurtas, 2009), an increase in skeletal muscle activity, and its corresponding response to radical production, has led to many studies and reviews examining the effects of exercise on oxidative stress and health and performance (Vollaard et al, 2005; Finaud et al, 2006; Powers et al, 2011, 2016)
Summary
Oxidative stress is the result of an imbalance between the production of free radicals (reactive oxygen species and nitrogen oxygen species), and a defense system of enzymatic and non-enzymatic antioxidants. A 12-week training study by Miyazaki et al (2001) further showed that antioxidative responses were influenced by training via higher levels of SOD and glutathione peroxidase (GXP), but oxidative stress was reduced as neutrophilic superoxide anion and thiobarbituric acid reactive substances (TBARS) were lower post training. This was substantiated by Vincent et al (2006) in older adults following a 6-month training program where lower levels of TBARS and PEROX as biomarkers of lipid peroxidation were shown. This study investigated the effects of multi-day prolonged exercise on metabolic and oxidative stress as well as telomere integrity in healthy adults
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