Cited by 49Exercise and Physiological ResponsesAntioxidant Activity and Oxidative StressCardiovascular and exercise physiology

Prolonged Depletion of Antioxidant Capacity after Ultraendurance Exercise

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TURNER, JAMES E., HODGES, NIKOLAS J., BOSCH, JOS A., ALDRED, SARAH·2011·Medicine & Science in Sports & Exercise

Abstract

PURPOSE: The purpose of this study was to examine the short- and long-term (up to 1 month) effects of an ultraendurance running event on redox homeostasis. METHODS: Markers of oxidative stress and antioxidant capacity in peripheral blood were assessed after a single-stage 233-km (143 miles) running event. Samples were collected from nine men (mean±SD: age=46.1±5.3 yr, body mass index=24.9±2.3 kg·m⁻², maximal oxygen uptake=56.3±3.3 mL·kg⁻¹·min⁻¹). Peripheral blood mononuclear cells were assayed for nonspecific DNA damage (frank strand breaks) and damage to DNA caused specifically by oxidative stress (formamidopyrimidine DNA glycosylase-dependent damage). Protein carbonylation and lipid peroxidation were assessed in plasma. Reduced glutathione (GSH) was measured in whole blood. RESULTS: Peripheral blood mononuclear cell frank strand breaks were elevated above baseline at 24 h after the race (P<0.001). Formamidopyrimidine DNA glycosylase-dependent oxidative DNA damage was increased immediately after the race (P<0.05). Protein carbonylation remained elevated for 7 d after the race (P<0.04), whereas lipid peroxidation was increased for 24 h (P<0.05) and fell below baseline 28 d later (P<0.05). GSH, a measure of antioxidant capacity, also showed a biphasic response, increasing by one-third after the race (P<0.01) and falling to two-thirds of baseline levels 24 h later (P<0.001). GSH remained depleted to approximately one-third of prerace values 28 d after the race (P<0.01). CONCLUSIONS: Ultraendurance exercise causes oxidative stress, which persists for one calendar month depending on the specific biomarker examined. These results suggest that ultraendurance events are associated with a prolonged period of reduced protection against oxidative stress.

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Crossref · 10.1249/mss.0b013e31821240bb

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Authors
TURNER, J. E., HODGES, N. J., BOSCH, J. A., & ALDRED, S.
Affiliations
  • University of Birmingham (GB)
  • Heidelberg University (DE)
Venue
Medicine & Science in Sports & Exercise
Published
2011-09
Volume
43
Issue
9
Pages
1770-1776
ISSN
0195-9131 (ISSN-L)
OpenAlex
W2055548700
Cited by
49
References
37
Citations by year
2026: 3 · 2025: 1 · 2024: 4 · 2023: 4 · 2022: 3 · 2021: 7 · 2020: 2 · 2019: 4 · 2018: 1 · 2017: 4 · 2016: 4 · 2015: 1 · 2014: 7 · 2013: 3 · 2012: 1
FWCI
3.57
Type
journal article
Language
en
Open access
Licence
other-oa
Locations
  • Medicine & Science in Sports & Exercise (publishedVersion)
  • PubMed (publishedVersion)
  • Pure Amsterdam UMC (publishedVersion, other-oa)
  • Pure (University of Bath) (publishedVersion, other-oa)
  • The University of Bath Online Publications Store (The University of Bath) (acceptedVersion)
  • University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
Topics
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
Keywords
oxidative stress, antioxidant capacity, redox homeostasis, DNA damage, protein carbonylation, lipid peroxidation, reduced glutathione, peripheral blood mononuclear cells, long-term training effects
MeSH terms
Antioxidants, DNA Damage, Glutathione, Humans, Leukocytes, Mononuclear, Male, Oxidation-Reduction, Physical Endurance, Running, Lipid Peroxidation, Exercise, Oxidative Stress, DNA-Formamidopyrimidine Glycosylase, Protein Carbonylation

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