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Clinical Trial
, 48 (8), 1831-42

Creatine Ingestion Augments Dietary Carbohydrate Mediated Muscle Glycogen Supercompensation During the Initial 24 H of Recovery Following Prolonged Exhaustive Exercise in Humans

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Clinical Trial

Creatine Ingestion Augments Dietary Carbohydrate Mediated Muscle Glycogen Supercompensation During the Initial 24 H of Recovery Following Prolonged Exhaustive Exercise in Humans

Paul A Roberts et al. Amino Acids.

Abstract

Muscle glycogen availability can limit endurance exercise performance. We previously demonstrated 5 days of creatine (Cr) and carbohydrate (CHO) ingestion augmented post-exercise muscle glycogen storage compared to CHO feeding alone in healthy volunteers. Here, we aimed to characterise the time-course of this Cr-induced response under more stringent and controlled experimental conditions and identify potential mechanisms underpinning this phenomenon. Fourteen healthy, male volunteers cycled to exhaustion at 70 % VO2peak. Muscle biopsies were obtained at rest immediately post-exercise and after 1, 3 and 6 days of recovery, during which Cr or placebo supplements (20 g day(-1)) were ingested along with a prescribed high CHO diet (37.5 kcal kg body mass(-1) day(-1), >80 % calories CHO). Oral-glucose tolerance tests (oral-GTT) were performed pre-exercise and after 1, 3 and 6 days of Cr and placebo supplementation. Exercise depleted muscle glycogen content to the same extent in both treatment groups. Creatine supplementation increased muscle total-Cr, free-Cr and phosphocreatine (PCr) content above placebo following 1, 3 and 6 days of supplementation (all P < 0.05). Creatine supplementation also increased muscle glycogen content noticeably above placebo after 1 day of supplementation (P < 0.05), which was sustained thereafter. This study confirmed dietary Cr augments post-exercise muscle glycogen super-compensation, and demonstrates this occurred during the initial 24 h of post-exercise recovery (when muscle total-Cr had increased by <10 %). This marked response ensued without apparent treatment differences in muscle insulin sensitivity (oral-GTT, muscle GLUT4 mRNA), osmotic stress (muscle c-fos and HSP72 mRNA) or muscle cell volume (muscle water content) responses, such that another mechanism must be causative.

Keywords: Glucose tolerance; Glycogen storage; Insulin sensitivity; Phosphocreatine.

Figures

Fig. 1
Fig. 1
Diagrammatic overview of the experimental protocol
Fig. 2
Fig. 2
Skeletal muscle total-creatine (TCr) content during 6 days of creatine + carbohydrate (Creatine, n = 7) or glycine + carbohydrate (Placebo, n = 7) supplementation following glycogen-depleting exercise in man. Results are expressed as means ± SEM with units of mmol kg−1 dry muscle. Different from the pre-supplementation time point (post-exercise, time 0) within the same treatment group ( P < 0.05, †† P < 0.01); different from placebo at the corresponding time point (*P < 0.05, **P < 0.01)
Fig. 3
Fig. 3
Skeletal muscle glycogen content during 6 days of creatine + carbohydrate (Creatine, n = 7) or glycine + carbohydrate (Placebo, n = 7) supplementation following glycogen-depleting exercise in man. Results are expressed as means ± SEM with units of mmol kg−1 dry muscle. Different from the pre-supplementation (post-exercise, time 0) time point within the same treatment group ( P < 0.05, †† P < 0.01); different from placebo at the corresponding time point (*P < 0.05, **P < 0.01)
Fig. 4
Fig. 4
Area under the curve during an oral glucose tolerance test (GTT) for blood glucose (a), serum insulin (b) and blood lactate (c) before (pre-exercise) and after 1, 3 and 6 days of Cr + carbohydrate or glycine + carbohydrate supplementation following glycogen-depleting exercise in man. Results are expressed as means ± SEM. Area under plasma glucose and lactate curve expressed as (mmol l−1 min−1), area under serum insulin curve expressed as (mU l−1 min−1). different from the pre-exercise time point within the same treatment group (P < 0.05); * different from placebo group at the corresponding time point (P < 0.05)

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