11 research outputs found
Creatine ingestion augments dietary carbohydrate mediated muscle glycogen supercomposition during the initial 24 hrs of recovery following prolonged exhaustive exercise in humans
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 (20g.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
Regulation of glycogen synthase by glucose and glycogen: A possible role for AMP-activated protein kinase
Discrete effects of glimepiride and metformin on preprandial and postprandial glucose and contributions to the amelioration of chronic hyperglycemia
Decreased neuroinflammation and increased brain energy homeostasis following environmental enrichment after mild traumatic brain injury is associated with improvement in cognitive function
Lipopolysaccharide-Induced Loss of Cultured Rat Myenteric Neurons - Role of AMP-Activated Protein Kinase
Long-term T cell fitness and proliferation is driven by AMPK-dependent regulation of reactive oxygen species
Maintenance of skeletal muscle energy homeostasis during prolonged wintertime fasting in the raccoon dog (Nyctereutes procyonoides)
Dietary Enrichment with Fish Oil Prevents High Fat-Induced Metabolic Dysfunction in Skeletal Muscle in Mice
Sixty Years of Drug Discovery for Type 2 Diabetes: Where Are We Now?
The control of blood glucose is a dynamic interplay involving several complex systems. In diabetes these systems are perturbed, resulting in a disease continuum of progressive decline over many years. Today, excluding insulin, there are eight classes of anti-diabetic agent which have taken over 60 years to add to the pharmacy chest. In this review I have examined each of these classes with some bias towards drug discovery thinking. Based on history, future science here will be strong, progressive and innovative; the huge test for industry is their response to enormous challenges besetting drug discovery and successfully turn the drug discovery praxis into affordable, effective and safe medicines