Endurance exercise protects aging from high-salt diet (HSD)-induced climbing capacity decline and lifespan decrease by enhancing antioxidant capacity.

A high-salt diet (HSD) is a major cause of many chronic and age-related defects such as myocardial hypertrophy, locomotor impairment and mortality. Exercise training can efficiently prevent and treat many chronic and age-related diseases. However, it remains unclear whether endurance exercise can resist HSD-induced impairment of climbing capacity and longevity in aging individuals. In our study, flies were given exercise training and fed a HSD from 1-week old to 5-weeks old. Overexpression or knockdown of and were built by UAS/Gal4 system. The results showed that a HSD, gene overexpression and knockdown significantly reduced climbing endurance, climbing index, survival, expression and SOD activity level, and increased malondialdehyde level in aging flies. Inversely, in a HSD aging flies, endurance exercise and overexpression significantly increased their climbing ability, lifespan and antioxidant capacity, but they did not significantly change the gene expression. Overall, current results indicated that a HSD accelerated the age-related decline of climbing capacity and mortality via upregulating expression and inhibiting the /SOD pathway. Increased /SOD pathway activity played a key role in mediating endurance exercise resistance to the low salt tolerance-induced impairment of climbing capacity and longevity in aging This article has an associated First Person interview with the first author of the paper.