To determine whether extreme endurance exercise induces lipid peroxidation, we studied 14 athletes (5 females: 9 males) during a 50 km ultramarathon (trial 1) and during a sedentary protocol (trial 2) one month later. At dinner the evening before the race (or sedentary trial), subjects consumed vitamin E labeled with stable isotopes (75 mg each d₃-RRR and d₆-all rac-α-tocopheryl acetates). Blood samples were taken at baseline, 30 minutes pre-race, mid-race, post-race, 1 h post-race, 24 h post-race, and at corresponding times for each individual during trial 2. During the sedentary day of trial 2, subjects consumed the same amounts of race day foods, including ergogenic aids, that they had consumed in trial 1; vitamin E intakes were 77 ± 40 mg, and vitamin C 406 ± 169 mg. All 14 subjects completed the race; average time to completion was 390 ± 67 minutes. Plasma F₂-isoprostanes (F₂-I), labeled and unlabeled α-tocopherol, and ascorbic acid (AA) were measured. F₂-I increased from 76 ± 24 pg/ml pg/ml at pre-race to 117.4 ± 38.0 pg/ml (p<0.0008) at mid-race to 130 ± 54 pg/ml (p<0.0001) at post-race, then returned to baseline at 24 hours post-race; F₂-I were unchanged during trial 2. Deuterated d₃ α-tocopheryl (d₃ α-Toc) disappearance rates were faster (2.8x10⁻⁴ ± 0.5x10⁻⁴) during the race compared to the sedentary trial (2.3x10⁻⁴ ± 0.6x10⁻⁴; p < 0.03). Plasma AA increased from 75.2 ± 11.2 μM at pre-race to 157.7 ± 36.2 μM at race end (p<0.0001) and decreased to below baseline concentrations at 24 h post-race (40.4 ± 5.2 μM p<0.0001). AA levels also increased during trial 2. Despite increased plasma AA, F2-I increased during exercise, but not during the sedentary period. Additionally, vitamin E disappeared faster during the run compared to the sedentary protocol. Thus, extreme endurance exercise results in the generation of lipid peroxidation and increased vitamin E utilization. / Graduation date: 2001