Fig. 6

Mitophagic LC3II flux following acute exercise, training, and combined treatments in WT and KO animals. Representative Western blots of mitochondrial LC3II localization of WT (a) and Parkin KO (b) mice injected with water (Veh) or 0.4 mg/kg colchicine (Col). Quantification of mitochondrial LC3II flux (c) is shown (n = 6). Mitophagic LC3II flux was assessed under basal conditions, and immediately following acute exercise, in untrained and trained groups of WT and KO animals. The fold change in LC3II flux (D) was calculated with acute exercise-induced values over basal values (n = 6). Values are means ± SEM. ¶P < 0.05, vs untrained WT; #P < 0.05, main effect of exercise; §P < 0.05, main effect of genotype; *P < 0.05, vs all other experimental conditions; †P < 0.05, interaction effect of genotype and training. Voltage-dependent anion channel (VDAC) was used as a mitochondrial loading control. WT, wild type; KO, Parkin knockout; UT, untrained; T, trained; LC3II, lipidated microtubule-associated protein 1A/1B-light chain 3; A.U., arbitrary units