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·min). 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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