Low-intensity resistance training attenuates dexamethasone-induced atrophy in the flexor hallucis longus muscle

Autor(es)

Macedo, Anderson G. ^[1] ; Krug, Andre L. O. ^[1] ; Herrera, Naiara A. ^[2] ; Zago, Anderson S. ^[2] ; Rush, James W. E. ^[3] ; Amaral, Sandra L. ^{[2, 1]}

Afiliação do(s) autor(es)

^[1] PIPGCF UFSCar UNESP, Joint Grad Program Physiol Sci, BR-676 Sao Carlos, SP - Brazil

^[2] UNESP, Dept Phys Educ, Fac Sci, Bauru, SP - Brazil

^[3] Univ Waterloo, Fac Appl Hlth Sci, Dept Kinesiol, Waterloo, ON N2L 3G1 - Canada

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY; v. 143, p. 357-364, SEP 2014.
• Citações Web of Science: 14

Resumo

This study investigated the potential protective effect of low-intensity resistance training (RT) against dexamethasone (DEX) treatment induced muscle atrophy. Rats underwent either an 8 week period of ladder climbing RT or remained sedentary. During the last 10 days of the exercise protocol, animals were submitted to a DEX treatment or a control saline injection. Muscle weights were assessed and levels of mTOR, FOXO3a, Atrogin-1 and MuRF-1 proteins were analyzed in flexor hallucis longus (FHL), tibialis anterior (TA), and soleus muscles. DEX induced blood glucose increase (+46%), body weight reduction (-19%) and atrophy in FHL (-28%) and TA (-21%) muscles, which was associated with a decrease in AKT and an increase in MuRF-1 proteins levels. Low-intensity RT prevented the blood glucose increase, attenuated the FHL atrophy effects of DEX, and was associated with increased mTOR and reductions in Atrogin-1 and MuRF-1 in FHL. In contrast, TA muscle atrophy and signaling proteins were not affected by RT. These are the first data to demonstrate that low-intensity ladder-climbing RT specifically mitigates the FHL atrophy, which is the main muscle recruited during the training activity, while not preventing atrophy in other limb muscle not as heavily recruited. The recruitment-dependent prevention of atrophy by low intensity RT likely occurs by a combination of attenuated muscle protein degradation signals and enhanced muscle protein synthesis signals including mTOR, Atrogin-1 and MuRF-1. (C) 2014 Elsevier Ltd. All rights reserved. (AU)

• Processo FAPESP: 12/21820-3 - Papel do exercício resistido na atrofia muscular induzida por dexametasona
• Beneficiário: André Luis de Oliveira Krug
• Modalidade de apoio: Bolsas no Brasil - Mestrado
• Processo FAPESP: 11/21522-0 - Papel do sistema renina-angiotensina e do sistema nervoso simpático na hipertensão induzida por dexametasona: efeitos preventivos do exercício físico
• Beneficiário: Sandra Lia do Amaral Cardoso
• Modalidade de apoio: Auxílio à Pesquisa - Regular