View clinical trials related to Glycogen Depletion.
Filter by:The aim of the study is to investigate the role of exercise-induced IL-6 in regulating energy stores and energy metabolism during recovery after an acute exercise bout. To achieve this, 30 men will be randomized to infusion placebo or tocilizumab (IL-6 receptor antibody) combined with a 2-hour exercise bout. Stable isotope tracers will be infused to determine substrate kinetics. Indirect calorimetry will be applied to determine substrate oxidation, and muscle biopsies will be taken to determine substrate uptake and storage.
To determine if modalities designed to improve blood flow combined with post-exercise nutrient intake will improve replenishment of muscle glycogen better than nutrient intake alone. A secondary objective is to compare the effectiveness of heat therapy and intermittent pneumatic compression on glycogen replenishment.
Excessive fat in the liver is associated with impairments in metabolic health. Low levels of DNL and high levels of hepatic fat oxidation are considered to be protective. A decrease in glycogen stores has been causally linked to improved whole body fat oxidation. Also on an organ level, it is suggested that hepatic fat oxidation is stimulated by low hepatic glycogen stores. Next to hepatic fat oxidation, DNL may be influenced by hepatic glycogen stores. Some studies have shown that prolongation of fasting time lowers hepatic glycogen content. It is therefore hypothesized that prolonging fasting time will lower glycogen content and thereby increases fat oxidation and decreases DNL in the liver. To this end, hepatic fat oxidation (plasma marker beta-hydroxybutyrate), de novo lipogenesis, hepatic glycogen content and intrahepatic fat content, will be measured upon a short overnight fast and an extended overnight fast in 13 overweight/obese subjects with hepatic steatosis.
Nine healthy, moderately fit male volunteers participated in the study. The subjects gave written informed consent after having been informed of any possible risk and discomfort associated with the study. The study was approved by the regional ethics committee in Denmark (Journal number: H-4-2013-071) and performed in accordance with the Declarations of Helsinki II. All subjects underwent 3 clinical investigations (day 1, day 2 and day 5) during a 5 day glycogen supercompensation regime. The subjects were asked to refrain from physical activity and to eat a controlled diet containing 60% carbohydrates (CHO) for 4 days prior to the initial experiments. Upon arrival at the laboratory on day 1, the subjects performed one-legged knee extensor exercise for 1 hour at 80% of PWL interspersed by 5 min bouts at 90% of PWL. This was followed by interval exercise until exhaustion containing 4 min bouts starting at 100% PWL followed by 1 min at 50% of PWL. Upon cessation of exercise the subjects showered and rested in the supine position for 4 hours. Then a 120 min hyperinsulinemic euglycemic clamp was initiated by a bolus insulin injection (9.0 mU/kg, Actrapid, Novo Nordisk, Denmark) followed by continuous insulin infusion (1.42 mU/kg/min insulin) reaching a level of plasma insulin around 100 µU/mL (n=9). At least 2 hours before the insulin clamp, catheters were placed in both femoral, one antecubital and one dorsal hand vein. A heat pad was placed around the lower part of the arm and hand in order to "arterialize" blood drawn from the hand vein. Substrate uptake/release across the legs was calculated by multiplying the arterial-venous (AV) difference in blood substrate concentration by femoral arterial blood flow (measured by ultrasound, Philips DICOM). Blood glucose levels were maintained at the euglycemic predefined target by continuously adjusting the glucose infusion rate (GIR) (20% glucose solution; Fresenius Kabi, Sweden). Concurrent measures of substrate AV differences and blood flow were performed every 20 min. Muscle biopsies from m. vastus lateralis were obtained under local anaesthesia (3-5 ml of Xylocaine, 20 mg/ml.) in the basal- and insulin-stimulated state (120 min) by use of needle biopsy technique. Muscle specimen were frozen within 20 sec in liquid nitrogen and stored at -80°C for further analysis. A new incision was made for every biopsy and spaced 4-5 cm apart. This insulin clamp procedure in combination with basal and insulin stimulated muscle biopsies was repeated in the rested state (without prior exercise) on day 2 and day 5. The subjects arrived in the morning in the overnight fasted state at day 1, day 2 and day 5. During the 5 day supercompensation regime the subjects were provided a predefined isocaloric diet containing 80% carbohydrates, 10% fat and 10% proteins. All food items were handle out to the subjects and compliance of the diet regime was ensured by survey.
This investigation will examine the impact of skeletal muscle glycogen stores on skeletal muscle and circulating microRNA expression and exogenous carbohydrate oxidation. Primary Objective Determine the influence of carbohydrate availability (e.g., glycogen depletion and repletion) on skeletal muscle microRNA expression, and if changes in circulating microRNA are reflective of changes in skeletal muscle microRNA. Secondary Objective Determine how initiation of exercise with adequate or low glycogen stores effects exogenous carbohydrate efficiency.
The aim of this experiment is to investigate if intake of stevioside in addition to a carbohydrate-containing composition after work related depletion of muscle glycogen will increase the rate of glycogen re-synthesis as compared with intake of the carbohydrate-containing composition alone.