ABSTRACT
Cardiovascular disease (CVD) places a heavy burden on older patients and the global healthcare system. A large body of evidence suggests that exercise training is essential in preventing and treating cardiovascular disease, but the underlying mechanisms are not well understood. Here, we used the Drosophila melanogaster animal model to study the effects of early-life exercise training (Exercise) on the aging heart and lifespan. We found in flies that age-induced arrhythmias are conserved across different genetic backgrounds. The fat body is the primary source of circulating lipoproteins in flies. Inhibition of fat body apoLpp (Drosophila apoB homolog) demonstrated that low expression of apoLpp reduced the development of arrhythmias in aged flies but did not affect average lifespan. At the same time, exercise can also reduce the expression of apoLpp mRNA in aged flies and have a protective effect on the heart, which is similar to the inhibition of apoLpp mRNA. Although treatment of UAS-apoLppRNAi and exercise alone had no significant effect on lifespan, the combination of UAS-apoLppRNAi and exercise extended the average lifespan of flies. Therefore, we conclude that UAS-apoLppRNAi and exercise are sufficient to resist age-induced arrhythmias, which may be related to the decreased expression of apoLpp mRNA, and that UAS-apoLppRNAi and exercise have a combined effect on prolonging the average lifespan.
