Changes in Muscle Protein Synthesis Following Resistance Exercise

Abstract

In order to gain better insight into the possible mechanisms that influence resistance training-induced muscle hypertrophy, two groups of subjects were examined for changes in muscle protein synthesis, and protein, total RNA, and DNA content 4 (group A) and 24 (group B) hours following an isolated bout of unilateral elbow flexor resistance training. Subjects trained one arm by performing 3 different biceps exercises consisting of 4 sets of 6-12 repetitions to failure while the contralateral arm served as a control. Both groups received a primed-constant infusion of L-[1-¹³C] leucine (group A infused 0.68h post-exercise for 5.4h; group B infused 20.41h post:-exercise for 6.38h) and muscle protein synthesis was determined by the increment in L-[1-¹³C] leucine abundance in muscle biopsy samples relative to the mean plasma α-KIC enrichment at isotopic plateau. Protein, total RNA, and DNA were~ determined with standard methods and RNA capacity (total RNA (ug)/protein (ug)) and RNA activity (ug protein synthesized/hour/ug RNA) were calculated to assess changes in gene transcription and translation. Possible muscle damage was assessed by changes between pre and 15 minute post-exercise maximal voluntary elbow flexor torque (measured at 30°/S and 180°/S) and by 22 hour post-exercise changes in serum CK activity (assessed in group B only). Both groups had significantly elevated muscle protein synthetic rates (group A 43% ↑; group B 80% ↑) and RNA activities (group A 25% ↑ ; group B 89% ↑) in the exercised biceps compared to the control biceps. In addition, post-exercise torque declined by 22% at 30°/S and by 24% at 180°/S and mean serum CK activity increased by 35% in group B. It is concluded that an intense bout of resistance training stimulates increases in muscle protein synthesis 4 and 24 hours post-exercise. The elevations in muscle protein synthesis of the exercised arm are probably related to increases in translation with contractile protein damage being one possible signal for increasing protein synthetic rates.