Autophagy is required for performance adaptive response to resistance training and exercise‐induced adult neurogenesis

• Published in: Scandinavian journal of medicine & science in sports Vol. 30; no. 2; pp. 238 - 253
• Main Authors: Codina‐Martínez, Helena, Fernández‐García, Benjamín, Díez‐Planelles, Carlos, Fernández, Álvaro F., Higarza, Sara G., Fernández‐Sanjurjo, Manuel, Díez‐Robles, Sergio, Iglesias‐Gutiérrez, Eduardo, Tomás‐Zapico, Cristina
• Format: Journal Article
• Language: English
• Published: Denmark Blackwell Publishing Ltd 01.02.2020
• Subjects: Adaptation, Physiological; Animals; Atg4b; Autophagy; autophagy impairment; brain; Cerebral Cortex - physiology; endurance training; Exercise; Hippocampus - physiology; Male; Mice; Mice, 129 Strain; Mice, Inbred C57BL; Mice, Knockout; Microtubule-Associated Proteins - metabolism; Neurogenesis; physical activity; Physical Conditioning, Animal - methods; Sequestosome-1 Protein - metabolism; Strength training; Atg4b; brain; autophagy impairment; endurance training; physical activity
• ISSN: 0905-7188; 1600-0838
• DOI: 10.1111/sms.13586

Endurance training promotes exercise‐induced adaptations in brain, like hippocampal adult neurogenesis and autophagy induction. However, resistance training effect on the autophagy response in the brain has not been much explored. Questions such as whether partial systemic autophagy or the length of training intervention affect this response deserve further attention. Therefore, 8‐week‐old male wild‐type (Wt; n = 36) and systemic autophagy‐deficient (atg4b−/−, KO; n = 36) mice were randomly distributed in three training groups, resistance (R), endurance (E), and control (non‐trained), and in two training periods, 2 or 14 weeks. R and E maximal tests were evaluated before and after the training period. Forty‐eight hours after the end of training program, cerebral cortex, striatum, hippocampus, and cerebellum were extracted for the analysis of autophagy proteins (LC3B‐I, LC3B‐II, and p62). Additionally, hippocampal adult neurogenesis was determined by doublecortin‐positive cells count (DCX+) in brain sections. Our results show that, in contrast to Wt, KO were unable to improve R after both trainings. Autophagy levels in brain areas may be modified by E training only in cerebral cortex of Wt trained for 14 weeks, and in KO trained for 2 weeks. DCX + in Wt increased in R and E after both periods of training, with R for 14 weeks more effective than E. Interestingly, no changes in DCX + were observed in KO after 2 weeks, being even undetectable after 14 weeks of intervention. Thus, autophagy is crucial for R performance and for exercise‐induced adult neurogenesis.