Moderate, but Not Excessive, Training Attenuates Autophagy Machinery in Metabolic Tissues

Autor: Adelino Sanchez Ramos da Silva, Donato A. Rivas, Giovana R. Teixeira, Rafael L. Rovina, José Rodrigo Pauli, Allice Santos Cruz Veras, Ana P. Pinto, Alisson L. da Rocha, Gustavo P. Morais, Leandro Pereira de Moura, Dennys E. Cintra, Bruno B. Marafon, Eduardo R. Ropelle
Přispěvatelé: Universidade de São Paulo (USP), Universidade Estadual Paulista (Unesp), Universidade Estadual de Campinas (UNICAMP), Tufts University
Rok vydání: 2020
Předmět:
Male
Overtraining
Autophagy-Related Proteins
lcsh:Chemistry
Mice
Basal (phylogenetics)
endurance training
Concurrent training
lcsh:QH301-705.5
Spectroscopy
exercise
General Medicine
Adaptation
Physiological
Endurance training
Computer Science Applications
Cell biology
medicine.anatomical_structure
Liver
Organ Specificity
concurrent training
METABOLISMO
autophagy
Physical exercise
Biology
Models
Biological
Article
colchicine
Catalysis
Inorganic Chemistry
In vivo
Physical Conditioning
Animal
Autophagy
medicine
Animals
RNA
Messenger
Physical and Theoretical Chemistry
Muscle
Skeletal
Exercise
Molecular Biology
Myocardium
Organic Chemistry
Skeletal muscle
medicine.disease
Resistance training
Mice
Inbred C57BL
overtraining
lcsh:Biology (General)
lcsh:QD1-999
Physical Endurance
resistance training
Colchicine
Flux (metabolism)
Zdroj: International Journal of Molecular Sciences
Volume 21
Issue 22
International Journal of Molecular Sciences, Vol 21, Iss 8416, p 8416 (2020)
Scopus
Repositório Institucional da UNESP
Universidade Estadual Paulista (UNESP)
instacron:UNESP
Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual)
Universidade de São Paulo (USP)
instacron:USP
ISSN: 1422-0067
DOI: 10.3390/ijms21228416
Popis: The protective effects of chronic moderate exercise-mediated autophagy include the prevention and treatment of several diseases and the extension of lifespan. In addition, physical exercise may impair cellular structures, requiring the action of the autophagy mechanism for clearance and renovation of damaged cellular components. For the first time, we investigated the adaptations on basal autophagy flux in vivo in mice&rsquo
s liver, heart, and skeletal muscle tissues submitted to four different chronic exercise models: endurance, resistance, concurrent, and overtraining. Measuring the autophagy flux in vivo is crucial to access the functionality of the autophagy pathway since changes in this pathway can occur in more than five steps. Moreover, the responses of metabolic, performance, and functional parameters, as well as genes and proteins related to the autophagy pathway, were addressed. In summary, the regular exercise models exhibited normal/enhanced adaptations with reduced autophagy-related proteins in all tissues. On the other hand, the overtrained group presented higher expression of Sqstm1 and Bnip3 with negative morphological and physical performance adaptations for the liver and heart, respectively. The groups showed different adaptions in autophagy flux in skeletal muscle, suggesting the activation or inhibition of basal autophagy may not always be related to improvement or impairment of performance.
Databáze: OpenAIRE
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