Duration-dependent oxidative stress responses in rat brain following long-term treadmill exercise: coenzyme Q10-associated attenuation of redox disturbance

Exercise-induced oxidative stress in the brain may depend on exercise workload, while Coenzyme Q10 (CoQ10) may attenuate redox disturbances through its mitochondrial and antioxidant functions. This study investigated brain oxidative stress responses to 13 weeks of treadmill running performed for 15, 30, or 60 min and examined CoQ10-associated changes across these exercise conditions in male Wistar rats. Brain tissue was analyzed for superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Bayesian analyses provided extreme evidence for between-group differences across all redox outcomes. The Run-60 condition showed the most pronounced redox disturbance, characterized by markedly higher MDA and 8-OHdG concentrations and lower SOD, CAT, and GSH levels compared with Control, Run-15, and Run-30. In contrast, shorter exercise durations were associated with comparatively preserved redox homeostasis. Under the 60-min exercise condition, CoQ10-supplemented animals exhibited lower MDA and 8-OHdG concentrations and greater preservation of antioxidant defenses than non-supplemented Run-60 animals. However, redox markers were not fully restored to control levels. Prolonged treadmill exercise produced the greatest disruption of brain redox homeostasis, whereas shorter exercise durations were associated with substantially smaller alterations. CoQ10 supplementation was associated with partial attenuation of the oxidative disturbance observed under the 60-min exercise condition. Because a sedentary CoQ10-only group was not included, these findings should be interpreted as CoQ10-associated effects within the exercise context rather than evidence of an independent neuroprotective effect of CoQ10. Not applicable.