Abstract

AMPK is activated by exercise, particularly when it elicits a concomitant rise in AMP/ATP ratio. Activated AMPK decreases ATP-consuming processes and stimulates ATP-producing processes. Sprint exercise induces Thr172-AMP-activated protein kinase (AMPK) phosphorylation and increased PGC-1a mRNA, by an unknown mechanism. SIRT1 plays an important role in mitochondrial biogenesis, fatty acid oxidation and glucose homeostasis through deacetylation of PGC-1a. However, it remains unknown if AMPK phosphorylation through sprint exercise may affect SIRT1 protein expression in human skeletal muscle and how this may influence PGC-1a protein levels. PURPOSE: To determine if SIRT1 and PGC-1a protein expression is increased by AMPK phosphorylation in response to a single bout of sprint exercise and the effect of glucose ingestion prior to the sprint exercise may have on this response. METHODS: Muscle biopsies were obtained in fifteen young healthy men in response to a 30 s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n=7, C), and the glucose group (n=8, G), who ingested 75g of glucose one hour before exercising to downregulate AMPKa phosphorylation. RESULTS: Thirty min after the control sprint, compared to pre-exercise values, Thr172-AMPKa phosphorylation was enhanced 5-fold (from 100 ± 4% to 531 ± 215%, P < 0.05). Moreover, under control conditions, SIRT1 protein expression was increased by 72% (from 100 ± 6.5% to 172.8 ± 21.8%, P < 0.05) and PGC-1a protein expression was decreased by 38% (from 100 ± 12% to 61.6 ± 8.7%, P < 0.05), 120 min into the recovery period. These effects were prevented by the ingestion of glucose prior to exercise. CONCLUSIONS: SIRT1 and PGC-1a protein expression was increased and reduced, respectively, in response to a single bout of sprint exercise performed in fasting conditions, and this effect appears to be mediated by AMPKa phosphorylation. Glucose ingestion prior to a sprint exercise profoundly affects Thr172-AMPKa phosphorylation and its downstream signaling during the recovery period. Granted by Ministerio de Educación y Ciencia of Spain (DEP2009-11638).

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