Prolonged depletion of antioxidant capacity after ultraendurance exercise

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.

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.

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).

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.