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

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Summary

Introduction

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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