Exercise and Mitochondrial Health

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (20 March 2023) | Viewed by 6259

Special Issue Editors


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Guest Editor
Key Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, Shanghai, China
Interests: skeletal muscle; mitochondria; oxidative stress; autophagy; skeletal muscle physiology

E-Mail Website
Guest Editor
Key Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, Shanghai, China
Interests: exercise and mitochondrial heterogeneity

E-Mail Website
Guest Editor
Key Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, Shanghai, China
Interests: exercise and mitochondrial-related diseases

E-Mail Website
Guest Editor
Key Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, Shanghai, China
Interests: exercise and mitochondrial dynamics

Special Issue Information

Dear Colleagues,

It is well-known that mitochondria are highly sensitive to and changeable with exercise. Exercise promotes mitochondrial biogenesis in many organs and tissues in addition to skeletal muscle, so "exercise promotes mitochondrial biogenesis to prevent or ameliorate a disease" has become a scientific paradigm. This paradigm guides our interpretation of current data and our hypotheses for the future. However, there are many interesting questions that have not been well-addressed. For example, how can we define mitochondrial health? Does exercise promoting mitochondrial biogenesis mean that exercise promotes mitochondrial health? With the advent of single-cell gene sequencing, there is growing evidence that the emphasis on "mitochondrial number" may ignore the heterogeneity of mitochondria. In addition, "exercise-induced mitochondrial biogenesis" as a positive physiological adaptation often contradicts the interpretation of complex pathologies. The reason for this is that some diseases, such as Alzheimer's disease and tumors, may be associated with increased mitochondria, so how to evaluate the benefit of exercise remains confusing. Is it possible that mitochondria, as organelles for energy production and cell signaling, are in excess or dysregulated? Experimental and evolutionary evidence suggests that exercise promotes mitochondrial biogenesis as a cellular response to increased oxygen uptake. It may be that only mitochondria can cope with cellular damage caused by hyperoxia, but is this necessarily beneficial to ameliorating disease? How to understand the cellular phenomenon of exercise-induced mitochondrial biogenesis deserves our colleagues' consideration and attention. In addition, mitochondrial biogenesis beyond skeletal muscle is also common in exercise, but the integrative physiology of exercise between multiple organs is lacking in convincing theories.

This Special Issue welcomes manuscripts that specifically focus on exercise and mitochondria. Authors are encouraged to submit original articles and comprehensive reviews associated with this topic.

In particular, the topics of interest include, but are not limited to:

  • Exercise and mitochondrial plasticity;
  • Exercise and mitochondrial-related disease;
  • Integrative physiology of exercise;
  • Exercise and mitochondrial heterogeneity;
  • Exercise and mitochondrial adaptations beyond muscles;
  • Exercise and mitochondrial signaling;
  • Methods and technology in exploring exercise and mitochondria.

Dr. Shuzhe Ding
Dr. Zhengtang Qi
Dr. Yi Sun
Dr. Zhe Zhang
Guest Editors

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Keywords

  • exercise
  • mitochondrial
  • diseases

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Published Papers (2 papers)

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Research

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18 pages, 3509 KiB  
Article
Aerobic Exercise Delays Alzheimer’s Disease by Regulating Mitochondrial Proteostasis in the Cerebral Cortex and Hippocampus
by Kaiyin Cui, Chaoyang Li and Guoliang Fang
Life 2023, 13(5), 1204; https://doi.org/10.3390/life13051204 - 17 May 2023
Cited by 5 | Viewed by 1977
Abstract
In clinical practice, Alzheimer’s disease (AD), as one of the main neurodegenerative diseases globally, currently has no cure. Recently, the delaying and improving effects of physical exercise on AD have gradually been confirmed; however, the specific mechanism involved needs further clarification. (1) Objective: [...] Read more.
In clinical practice, Alzheimer’s disease (AD), as one of the main neurodegenerative diseases globally, currently has no cure. Recently, the delaying and improving effects of physical exercise on AD have gradually been confirmed; however, the specific mechanism involved needs further clarification. (1) Objective: Explore the mechanism aerobic exercise plays in delaying AD by regulating mitochondrial proteostasis and provide new theoretical bases for improving and delaying AD through aerobic exercise in the future. (2) Methods: Male APP/PS1 mice were randomly divided into a normal group (NG, n = 20), activation group (AG, n = 20), and inhibition group (SG, n = 20). Then, the mice in each group were randomly divided into control group and exercise group (n = 10 mice each), yielding the normal control group (CNG), normal exercise group (ENG), active control group (CAG), active exercise group (EAG), inhibitive control group (CSG), and inhibitive exercise group (ESG). After adaptive training, the mice in the exercise groups were trained on an aerobic treadmill for 12 weeks; we conducted behavioral tests and sampled the results. Then, quantitative real-time PCR (Q-PCR) and Western blot analysis were performed. (3) Results: In the Morris water maze (MWM) test, the latency was significantly reduced and the number of platform crossings was significantly increased in the CAG and ENG compared with the CNG, while the result of the CSG was contrary to this. Compared with the ENG, latency was significantly reduced and the number of platform crossings was significantly increased in the EAG, while the opposite occurred for ESG. Compared with the CAG, the latency was significantly reduced and the number of platform crossings was significantly increased in the EAG, while the results for CSG were contrary. In the step-down test, compared with the CNG, the latency was significantly increased and the number of errors was significantly reduced in the CAG and ENG, respectively, while the results for CSG were contrary. Compared with the ENG, the latency was significantly increased and the number of errors was significantly reduced in the EAG, while the results for ESG were contrary. Compared with the CAG, the latency was significantly increased and the number of errors was significantly reduced in the EAG, while the results for CSG were contrary. Mitochondrial unfolded protein reactions (UPRmt), mitochondrial autophagy, and mitochondrial protein import levels in each group of mice were detected using Q-PCR and Western blot experiments. Compared with the CNG, the UPRmt and mitochondrial autophagy levels in the CAG and ENG were significantly increased and the mitochondrial protein import levels were significantly reduced, while the results for the CSG were contrary. Compared with the ENG, the UPRmt and mitochondrial autophagy levels in the EAG were significantly increased and the mitochondrial protein import levels were significantly reduced, while the results for ESG were contrary. Compared with the CAG, the UPRmt and mitochondrial autophagy levels in the EAG were significantly increased and the mitochondrial protein import levels were significantly reduced, while the results for CSG were contrary. (4) Conclusions: Aerobic exercise can improve cognitive function levels and delay the symptoms of AD in APP/PS1 mice by regulating mitochondrial proteostasis. Full article
(This article belongs to the Special Issue Exercise and Mitochondrial Health)
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23 pages, 3106 KiB  
Review
Exercise Improves the Coordination of the Mitochondrial Unfolded Protein Response and Mitophagy in Aging Skeletal Muscle
by Yan Wang, Jialin Li, Ziyi Zhang, Runzi Wang, Hai Bo and Yong Zhang
Life 2023, 13(4), 1006; https://doi.org/10.3390/life13041006 - 13 Apr 2023
Cited by 7 | Viewed by 3017
Abstract
The mitochondrial unfolded protein response (UPRmt) and mitophagy are two mitochondrial quality control (MQC) systems that work at the molecular and organelle levels, respectively, to maintain mitochondrial homeostasis. Under stress conditions, these two processes are simultaneously activated and compensate for each other when [...] Read more.
The mitochondrial unfolded protein response (UPRmt) and mitophagy are two mitochondrial quality control (MQC) systems that work at the molecular and organelle levels, respectively, to maintain mitochondrial homeostasis. Under stress conditions, these two processes are simultaneously activated and compensate for each other when one process is insufficient, indicating mechanistic coordination between the UPRmt and mitophagy that is likely controlled by common upstream signals. This review focuses on the molecular signals regulating this coordination and presents evidence showing that this coordination mechanism is impaired during aging and promoted by exercise. Furthermore, the bidirectional regulation of reactive oxygen species (ROS) and AMPK in modulating this mechanism is discussed. The hierarchical surveillance network of MQC can be targeted by exercise-derived ROS to attenuate aging, which offers a molecular basis for potential therapeutic interventions for sarcopenia. Full article
(This article belongs to the Special Issue Exercise and Mitochondrial Health)
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