Abstract
Background: Skeletal muscle adaptations are affected by resistance training (RT)-induced acute and chronic transcriptional responses. An under-explored gene target involved in mechanotransduction is the expression of the G protein-coupled receptor 56 (GPR56). However, studies investigating the acute and chronic effects of RT manipulations on GPR56 mRNA are scarce. Methods: Twenty subjects had each leg randomly assigned to a standard ((CON) no specific manipulation) or a variable RT (manipulations in load, volume, muscle action, and pause in a session-by-session fashion (VAR)). GPR56 mRNA expression was assessed before and after 16 training sessions (chronic effect) and 24 h after a 17th session (acute effect). Results: Acute GPR56 mRNA expression increased at 24 h (p < 0.01) without differences between CON and VAR (p > 0.05). No differences were found in GPR56 mRNA expression when comparing each VAR condition (load vs. sets vs. eccentric actions vs. pause) nor with CON at 24 h (p > 0.05). Chronic GPR56 mRNA expression increased at Post compared with Pre (p < 0.02) for VAR only, with a tendency (p = 0.058) toward higher expression for VAR as compared with CON. Conclusion: GPR56 mRNA expression is acutely and chronically modulated by RT. Additionally, chronic GPR56 mRNA expression is modulated by RT variable manipulations.
Highlights
Resistance training (RT) induces acute and chronic transcriptional changes, which are suggested to affect skeletal muscle adaptations [1,2,3,4].In recent years, several studies have explored novel transcriptional targets that could be modulated by RT [5,6,7,8]
No significant differences were found between CON and VAR at 24 h for G protein-coupled receptor 56 (GPR56) mRNA
We found tendencyfor fora ahigher higherincrease increaseininGPR56
Summary
Resistance training (RT) induces acute (after a single bout) and chronic (after several bouts) transcriptional changes, which are suggested to affect skeletal muscle adaptations [1,2,3,4]. Several studies have explored novel transcriptional targets that could be modulated by RT [5,6,7,8]. The mechanisms involved in mechanotransduction have garnered interest in the field. Membrane proteins translate RT-induced mechanical tension in the cell membrane into chemical signaling, activating protein synthesis pathways [9,10]. The upstream regulators of mechanotransduction are currently unclear, the adhesion G protein-coupled receptor family (GPCR). May be a candidate activator of anabolic signaling pathways [11,12].
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