Objective Exercise has been approved as an effective anti-aging approach. However, how exercise affects the organelle-specific redox status of the endoplasmic reticulum (ER) and whether it contributes to ER function and healthy aging are still unknown.Methods We constructed an ER-specific reductive stress C. elegans model that overexpresses ctl-1, a homolog of the mammalian catalase gene, to research the effect of ER reductive stress on aging at the organismal level. We then used the Hyperion_ER probe which responds well to hydrogen peroxide to evaluate the redox status in the ER of body wall muscle during swimming and during aging.Results Our results show that H₂O₂ in the ER was markedly reduced during aging and the number of body bending, the life span and the stress response ability in Pnfya-1::ctl-1_ER::mCherry C. elegans was markedly decreased compared with that in Pnfya-1::ctl-1-M_ER::mCherry, indicating that ER reductive stress occurs during the aging process and ER reductive stress promotes aging at the organismal level. Both short-term and long-term exercise can increase the oxidative power of the ER in C. elegans, and exercise alleviates the age-related ER reductive stress and promotes healthy aging.Conclusion Our results demonstrate the effect of exercise on ER redox status at the organelle level for the first time and uncover a new mechanism for exercise in delaying aging at the organismal level from the redox point of view, suggesting that maintaining the oxidation power of the ER may be a valuable geroprotective strategy.