Key findings
Following eccentric leg contractions designed to produce systemic oxidative stress, erythrocytes showed a consistent pattern of oxidative damage: F2‑isoprostanes increased by 22%, protein carbonylation rose by 28%, and reduced glutathione levels fell by ~20% compared with control. These changes indicate both lipid and protein oxidative modifications and a depletion of a primary intracellular antioxidant buffer. The observed declines in glutathione are biologically meaningful in erythrocytes, which rely on glutathione/NADPH to cope with oxidants in the plasma and within the cell.
Under oxidative stress alone (before arm exercise), erythrocyte glycolytic flux increased by approximately 53% relative to the control resting state. When participants performed isolated arm exercise, glycolytic flux rose in both experimental conditions, but with different magnitudes: in control it increased by ~200%, whereas after prior eccentric‑induced oxidative stress the increase was ~86%. The authors interpret this pattern as evidence that RBC metabolism reacts dynamically to systemic workload and oxidative challenge but that the capacity for further activation during acute exercise is attenuated after oxidative insult.
