Participação dos receptores β2-adrenérgicos na expressão de genes tróficos da musculatura esquelética em resposta ao exercício resistido

Abstract

Although stimulation of the sympathetic nervous system (SNS) is a well-established response during exercise, the role of catecholamines in resistance exercise (RE)-induced changes in skeletal muscle protein metabolism remains unclear. This study investigated the effects of β2-adrenergic receptor (β2-AR) blockade on the acute molecular responses induced by a single RE session in skeletal muscles of rodents. Male C57BL6/J mice underwent a single session of progressive RE on a vertical ladder under β2-AR blockade with ICI 118,551 (ICI; 10 mg.kg-1, i.p.) or vehicle (sterile saline; 0.9%, i.p.) and gene expression analyzed in tibialis anterior (TA) and/or gastrocnemius (GAS) muscles. We demonstrated that a single RE session acutely increased circulating levels of the stress-associated hormones norepinephrine (NE) and corticosterone and levels of AMPK, p38-MAPK and CREB phosphorylation only in GAS muscles. The acute increase in CREB phosphorylation levels was accompanied by upregulation of CREB target genes Sik1 and Nr4a3.3h after the RE session. On the other hand, β2-AR blockade completely prevented the Sik1 increase and attenuated Nr4a3 mRNA levels. Furthermore, a single RE session stimulated mRNA levels of genes related to autophagy (Map1lc3b and Gabarapl1) and myostatin, but did not alter gene expression of igf-1 or il-6, while genes related to atrophy (Murf1 and Atrogin-1) were increased only in mice under β2-AR blockade. Interestingly, performing a single RE session under β2-AR blockade amplified the increase in myostatin mRNA levels in GAS muscles of exercised mice. In conclusion, our data suggest that at least part of the acute molecular changes induced by RE depend on the activation of β2-ARs in skeletal muscle.