β-Adrenoceptors activation regulates muscle trophic-related genes following acute resistance exercise in mice.

Resistance exercise (RE) training and pharmacological stimulation of β-Adrenoceptors (β-ARs) alone can promote muscle hypertrophy and prevent muscle atrophy. Although the activation of the sympathetic nervous system (SNS) is a well-established response during RE, the physiological contribution of the endogenous catecholamines and β-ARs to the RE-induced changes on skeletal muscle protein metabolism remains unclear. This study investigated the effects of the β-ARs blockade on the acute molecular responses induced by a single bout of RE in rodent skeletal muscles. Male C57BL6/J mice were subjected to a single bout of progressive RE (until exhaustion) on a vertical ladder under β-AR blockade with ICI 118,551 (ICI; 10 mg kg, i. p.), or vehicle (sterile saline; 0.9%, i. p.), and the gene expression was analyzed in (GAS) muscles by qPCR. We demonstrated that a single bout of RE acutely increased the circulating levels of stress-associated hormones norepinephrine (NE) and corticosterone (CORT), as well as the muscle phosphorylation levels of AMPK, p38 MAPK and CREB, immediately after the session. The acute increase in the phosphorylation levels of CREB was followed by the upregulation of CREB-target genes , and (a central regulator of the acute RE response), 3 h after the RE session. Conversely, β-AR blockade reduced significantly the and mRNA levels in muscles of exercised mice. Furthermore, a single bout of RE stimulated the mRNA levels of the atrophic genes and (autophagy-related genes) and (a well-known negative regulator of muscle growth). Unexpectedly, the gene expression of or were not affected by RE, while the atrophic genes and (ubiquitin-ligases) were increased only in muscles of exercised mice under β-AR blockade. Interestingly, performing a single bout of RE under β-AR blockade increased the mRNA levels of in muscles of exercised mice. These data suggest that β-ARs stimulation during acute RE stimulates the hypertrophic gene and prevents the overexpression of atrophic genes such as , , and in the first hours of postexercise recovery, indicating that he SNS may be physiologically important to muscle adaptations in response to resistance training.