I know this one has been discussed before. The full paper is now available. Looking at the changes (which are also depicted in the graphs) the increase in myogenic genes glycogen loaded and depleted is about the same, and the increase in atrogens like myostatin was significantly greater with high muscle glycogen. But then the papers conclusion is that muscle glycogen is important for hypertrophy, but how is this exemplified in this paper? I know looking at molecular stuff without looking at the big picture can be problematic, but this seems to suggest overall that low glycogen would be advantagous in the context of the time outside of working out as well. The Full text is now available here. http://jap.physiology.org/cgi/content/full/102/4/1604 Influence of preexercise muscle glycogen content on transcriptional activity of metabolic and myogenic genes in well-trained humans Emmanuel G. Churchley,1 Vernon G. Coffey,1 David J. Pedersen,1 Anthony Shield,1 Kate A. Carey,2 David Cameron-Smith,2 and John A. Hawley1 1School of Medical Sciences, RMIT University, Melbourne, Australia; and 2School of Exercise and Nutrition Sciences, Deakin University, Melbourne, Australia Submitted 6 November 2006 ; accepted in final form 8 January 2007 To determine whether preexercise muscle glycogen content influences the transcription of several early-response genes involved in the regulation of muscle growth, seven male strength-trained subjects performed one-legged cycling exercise to exhaustion to lower muscle glycogen levels (Low) in one leg compared with the leg with normal muscle glycogen (Norm) and then the following day completed a unilateral bout of resistance training (RT). Muscle biopsies from both legs were taken at rest, immediately after RT, and after 3 h of recovery. Resting glycogen content was higher in the control leg (Norm leg) than in the Low leg (435 ± 87 vs. 193 ± 29 mmol/kg dry wt; P < 0.01). RT decreased glycogen content in both legs (P < 0.05), but postexercise values remained significantly higher in the Norm than the Low leg (312 ± 129 vs. 102 ± 34 mmol/kg dry wt; P < 0.01). GLUT4 (3-fold; P < 0.01) and glycogenin mRNA abundance (2.5-fold; not significant) were elevated at rest in the Norm leg, but such differences were abolished after exercise. Preexercise mRNA abundance of atrogenes was also higher in the Norm compared with the Low leg [atrogin: 14-fold, P < 0.01; RING (really interesting novel gene) finger: 3-fold, P < 0.05] but decreased for atrogin in Norm following RT (P < 0.05). There were no differences in the mRNA abundance of myogenic regulatory factors and IGF-I in the Norm compared with the Low leg. Our results demonstrate that 1) low muscle glycogen content has variable effects on the basal transcription of select metabolic and myogenic genes at rest, and 2) any differences in basal transcription are completely abolished after a single bout of heavy resistance training. We conclude that commencing resistance exercise with low muscle glycogen does not enhance the activity of genes implicated in promoting hypertrophy.