Sprint and Strength Training Modulates Autophagy and Proteostasis in Aging Sprinters

Purpose Exercise and aging may modulate muscle protein homeostasis and autophagy, but few studies examine highly-trained middle-aged or older individuals. This study elucidated the effects of a new long-term training stimulus on markers of muscle autophagy and unfolded protein response (UPR) and on sprint running performance in masters sprinters. Methods Thirty-two male competitive sprinters (aged 40–76 years) were randomly divided into experimental (EX) and control (CTRL) groups. The EX training program was a combination of heavy and explosive strength and sprint exercises aimed at improving sprint performance. Fifteen and thirteen participants completed the 20-week intervention period in EX and CTRL, respectively. The latter were told to continue their routine exercises. Key protein markers were analyzed by western blotting from vastus lateralis (VL) muscle biopsies. Muscle thickness of VL was analyzed by ultrasonography and sprint performance by a 60-meter running test. Results EX induced improvement in 60-meter sprint performance when compared to controls (time x group, P = 0.003) without changes in VL muscle thickness. Content of lipidated microtubule-associated protein 1A/1B-light chain 3 (LC3-II) increased in EX (P = 0.022) suggesting increased autophagosome content. Additionally, an autophagosome clearance marker sequestosome 1 (p62) decreased in EX (P = 0.006). Markers of UPR selectively modulated with decreases (e.g. ATF4, P = 0.003) and increases (e.g. EIF2α, P = 0.019) observed in EX. Conclusions These findings suggest that a new intensive training stimulus that combines strength training with sprint training may increase muscle autophagosome content in a basal state without any evidence of impaired autophagosome clearance in masters sprinters. Simultaneously, the combined training may have a selective effect on the content of UPR signaling components.