Lack of beta(2)-AR improves exercise capacity and skeletal muscle oxidative phenotype in mice

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Citações na Scopus
8
Tipo de produção
article
Data de publicação
2012
Editora
WILEY-BLACKWELL
Indexadores
Título da Revista
ISSN da Revista
Título do Volume
Autores
VOLTARELLI, V. A.
BACURAU, A. V. N.
BECHARA, L. R. G.
BUENO JUNIOR, C. R.
BOZI, L. H. M.
MATTOS, K. C.
BRUM, P. C.
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
SCANDINAVIAN JOURNAL OF MEDICINE & SCIENCE IN SPORTS, v.22, n.6, p.e125-e132, 2012
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
beta(2)-adrenergic receptor (beta(2)-AR) agonists have been used as ergogenics by athletes involved in training for strength and power in order to increase the muscle mass. Even though anabolic effects of beta(2)-AR activation are highly recognized, less is known about the impact of beta(2)-AR in endurance capacity. We presently used mice lacking beta(2)-AR [beta(2)-knockout (beta(2) KO)] to investigate the role of beta(2)-AR on exercise capacity and skeletal muscle metabolism and phenotype. beta(2) KO mice and their wild-type controls (WT) were studied. Exercise tolerance, skeletal muscle fiber typing, capillary-to-fiber ratio, citrate synthase activity and glycogen content were evaluated. When compared with WT, beta 2KO mice displayed increased exercise capacity (61%) associated with higher percentage of oxidative fibers (21% and 129% of increase in soleus and plantaris muscles, respectively) and capillarity (31% and 20% of increase in soleus and plantaris muscles, respectively). In addition, beta 2KO mice presented increased skeletal muscle citrate synthase activity (10%) and succinate dehydrogenase staining. Likewise, glycogen content (53%) and periodic acid-Schiff staining (glycogen staining) were also increased in beta 2KO skeletal muscle. Altogether, these data provide evidence that disruption of beta(2)AR improves oxidative metabolism in skeletal muscle of beta 2KO mice and this is associated with increased exercise capacity.
Palavras-chave
skeletal muscle, endurance capacity, metabolism, beta(2)-adrenergic receptors, genetic animal model
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