Abstract
We examined the effects of graded muscle glycogen on exercise capacity and modulation of skeletal muscle signalling pathways associated with the regulation of mitochondrial biogenesis. In a repeated measures design, eight males completed a sleep-low, train-low model comprising an evening glycogen depleting cycling protocol followed by an exhaustive exercise capacity test (8 x 3 min at 80% PPO, followed by 1 min efforts at 80% PPO until exhaustion) the subsequent morning. Following glycogen depleting exercise, subjects ingested a total of 0 g kg-1 (L-CHO), 3.6 g kg-1 (M-CHO) or 7.6 g kg-1 (H-CHO) of carbohydrate during a 6 h period prior to sleeping, such that exercise was commenced the next morning with graded (P < 0.05) muscle glycogen concentrations (Mean ± SD) (L-CHO: 88 ± 43, M-CHO: 185 ± 62, H-CHO: 278 ± 47 mmol kg-1 dw). Despite differences (P < 0.05) in exercise capacity at 80% PPO between trials (L-CHO: 18 ± 7, M-CHO: 36 ± 3, H-CHO: 44 ± 9 min) exercise induced comparable AMPKThr172 phosphorylation ( 4 fold) and PGC-1a mRNA expression ( 5 fold) post- and 3 h post-exercise, respectively. In contrast, exercise nor CHO availability affected the phosphorylation of p38MAPKThr180/Tyr182, CaMKIIThr268 or mRNA expression of p53, Tfam, CPT-1, CD36 or PDK4. Data demonstrate that when exercise is commenced with muscle glycogen below 300 mmol kg-1 dw, further graded reductions of 100 mmol kg-1 dw impair exercise capacity but do not augment skeletal muscle cell signaling.