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The overall risk to heart health gets better

TABLE 1 Summary of results and characteristics of the studies which investigated the effects of bFGF in tendon healing

N-acetylcysteine (NAC) pretreatment abolished PPVII-mediated cytotoxicity, autophagic flux, and AKT/mTORC1 suppression, establishing ROS overproduction as the central mechanistic driver of these phenomena

Future research should investigate how genetic polymorphisms in DNA repair genes or exercise-responsive signaling pathways, as well as individual epigenetic landscapes, modulate the capacity for exercise-induced DNA repair and subsequent muscle adaptation