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Abstract Details

Abstract Title

Autophagy as a Regulator for Exercise Adaptation and Performance

Abstract Theme

Elite performance

Type Presentation

Poster

Abstract Authors

Presenter Ning Chen - Wuhan Sports University (Hubei Exercise Training and Monitoring Key Laboratory, Hubei Provincial Collaborative Innovation Center for Exercise and Health Promotion, College of Health Science) - CN
Jingjing Fan - Wuhan Sports University (Hubei Exercise Training and Monitoring Key Laboratory, Hubei Provincial Collaborative Innovation Center for Exercise and Health Promotion, College of Health Science) - CN
Shaohui Jia - Wuhan Sports University (Hubei Exercise Training and Monitoring Key Laboratory, Hubei Provincial Collaborative Innovation Center for Exercise and Health Promotion, College of Health Science) - CN
Xianjuan Kou - Wuhan Sports University (Hubei Exercise Training and Monitoring Key Laboratory, Hubei Provincial Collaborative Innovation Center for Exercise and Health Promotion, College of Health Science) - CN
Yi Yang - Wuhan Sports University (Hubei Exercise Training and Monitoring Key Laboratory, Hubei Provincial Collaborative Innovation Center for Exercise and Health Promotion, College of Health Science) - CN
Ying Zhang - Wuhan Sports University (Graduate School) - CN
Ziyang Shu - Wuhan Sports University (Graduate School) - CN
Xu Zhang - Wuhan Sports University (Graduate School) - CN

Presentation Details

Poster Exhibition Site (Local): White - 12        Date: 2 September        Time: 8am to 7pm        Presenter: Ning Chen

Abstract Resume

Background: Autophagy is an evolutionarily conserved catabolic process whereby cytoplasmic proteins, protein aggregates and organelles are captured by the formation of autophagsome
vesicles that are delivered to the lysosomal compartment for degradation. Under the environment of cellular stress, autophagy is activated to promote cell survival through preventing the accumulation
of damaged proteins and organelles from oxidative stress. Therefore, it is highly necessary for exploring whether exercise adaptation and performance improvement resulted from high-altitude training
is correlated with autophagy activation, which will be benefit for the monitoring of exercise training and exercise fatigue, and the genetic screening of athletic talents.

Methods: The mice were subjected to the rearing in hypoxia environment as a mimic high altitude environment and swimming training at normal environment for 6 weeks. The mice reared at
normal conditions with and without swimming training were used as the controls. The autophagy activation, corresponding autophagy-related protein expression or antioxidant signal pathway were
investigated by Western blot and RT-PCR analysis, and transmitted electronic microscopic evaluation.

Results: In our study, the mice subjected to mimic high-altitude training revealed a significantly improved exercise performance when compared with the mice without exercise training
or without high altitude training, which may be correlated with reduced body weights, extended exhaustive swimming time, reduced generation of ROS and inflammatory factors, increased NRF2 expression
and enhanced mitochondrial quality control from mitophagy in hypoxia environment. On the other hand, the mice subjected to genetic or transient pharmacological autophagy inhibition could not result in
the improved exhaustive swimming time and mitochondrial quality of the mice even in the presence of hypoxia training.

Conclusions: The functional status of autophagy is the determinant for exercise performance improvement of mice subjected to high altitude training. High-altitude training-induced
autophagy activation can delay the occurrence of fatigue. Moreover, the functional status of autophagy has the potential as the monitor of exercise training and exercise fatigue as well as genetic
talent screening in the future.

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