Graded reductions in preexercise muscle glycogen impair exercise capacity but do not augment skeletal muscle cell signaling: implications for CHO periodization

May 4, 2019Journal of applied physiology (Bethesda, Md. : 1985)

Lower muscle energy stores before exercise reduce performance but do not increase muscle cell signals: implications for carbohydrate timing

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Abstract

Graded reductions in muscle glycogen below 300 mmol/kg dry wt are associated with a decrease in exercise capacity of 20-50%.

Muscle glycogen concentrations were measured at 88 ± 43, 185 ± 62, and 278 ± 47 mmol/kg dry weight for low, medium, and high carbohydrate intake, respectively.
Exercise capacity at 80% peak power output varied significantly between different glycogen levels, with times of 18 ± 7, 36 ± 3, and 44 ± 9 minutes for low, medium, and high carbohydrate trials.
AMPK phosphorylation increased approximately 4-fold following exercise, regardless of carbohydrate availability.
PGC-1α mRNA expression rose about 5-fold after exercise and 3 hours later, independent of glycogen levels.
No significant effects were observed on p38MAPK or CaMKII phosphorylation or on the mRNA expression of several key metabolic regulators.

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We examined the effects of graded muscle glycogen on exercise capacity and modulation of skeletal muscle signaling pathways associated with the regulation of mitochondrial biogenesis. In a repeated-measures design, eight men completed a sleep-low, train-low model comprising an evening glycogen-depleting cycling protocol followed by an exhaustive exercise capacity test [8 × 3 min at 80% peak power output (PPO), followed by 1-min efforts at 80% PPO until exhaustion] the subsequent morning. After glycogen-depleting exercise, subjects ingested a total of 0 g/kg (L-CHO), 3.6 g/kg (M-CHO), or 7.6 g/kg (H-CHO) of carbohydrate (CHO) during a 6-h period before sleeping, such that exercise was commenced the next morning with graded (< 0.05) muscle glycogen concentrations (means ± SD: L-CHO: 88 ± 43, M-CHO: 185 ± 62, H-CHO: 278 ± 47 mmol/kg dry wt). Despite differences (< 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 AMPKphosphorylation (~4-fold) and PGC-1α mRNA expression (~5-fold) after exercise and 3 h after exercise, respectively. In contrast, neither exercise nor CHO availability affected the phosphorylation of p38MAPKor CaMKIIor mRNA expression of p53, Tfam, CPT-1, CD36, or PDK4. Data demonstrate that when exercise is commenced with muscle glycogen < 300 mmol/kg dry wt, further graded reductions of 100 mmol/kg dry weight impair exercise capacity but do not augment skeletal muscle cell signaling.We provide novel data demonstrating that when exercise is commenced with muscle glycogen below 300 mmol/kg dry wt (as achieved with the sleep-low, train-low model) further graded reductions in preexercise muscle glycogen of 100 mmol/kg dry wt reduce exercise capacity at 80% peak power output by 20-50% but do not augment skeletal muscle cell signaling. P P Thr172Thr180/Tyr182Thr268NEW & NOTEWORTHY

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Graded reductions in preexercise muscle glycogen impair exercise capacity but do not augment skeletal muscle cell signaling: implications for CHO periodization

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