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Metabolic and Molecular Framework for the Enhancement of Endurance by Intermittent Fasting

ABSTRACT: Evolutionary considerations suggest that the body has been optimized to perform at a high level in the fasted state when fatty acids and their ketone metabolites are a major fuel source for muscle cells. Because fasting is the most potent physiological stimulus for ketosis, we designed a study to determine the impact of intermittent fasting during endurance training on performance, and to elucidate the underlying cellular and molecular mechanisms. Male mice were randomly assigned to either ad libitum feeding or alternate-day fasting (AF) groups, and half of the mice in each diet group were trained daily on a treadmill for 1 month (45 minutes of running with increasing speed or incline each week). A run to exhaustion endurance test performed at the end of the training period revealed superior performance in the mice maintained on AF during training compared to mice fed ad libitum during training. VO2max was increased similarly by treadmill training in mice on AF or ad libitum diets, whereas respiratory exchange ratio (RER) was reduced in AF mice on fasting days and during running. Analyses of gene expression in liver and soleus tissues, and metabolomics analysis of blood suggest that the metabolic switch invoked by AF and potentiated by exercise strongly modulate molecular pathways involved in mitochondrial biogenesis, metabolism and cellular plasticity. Our findings demonstrate intermittent fasting engages metabolic and cellular signaling pathways that result in increased metabolic efficiency and endurance capacity.

ORGANISM(S): Mus musculus

PROVIDER: GSE104079 | GEO | 2018/09/10

REPOSITORIES: GEO

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Project description:We investigated the effects of diabetes, physical training, and their combination on the gene expression of cardiac muscle. Mice were divided to control (C), training (T), streptozotocin-induced diabetic (D), and diabetic training (DT) groups. Training groups performed 1, 3, or 5 weeks of endurance training on a motor-driven treadmill. Muscle samples from T and DT groups together with respective controls were collected 24 hours after the last training session. Gene expression of cardiac muscles were analyzed using Affymetrix Gene chip MG U74Av2 (Affymetrix , Inc., Santa Clara, CA). Experiment was performed on 10 to 15 weeks old male NMRI mice (Harlan, Holland) housed in standard conditions (temperature 22°C, humidity 60 ± 10 %, artificial light from 8.00 am to 8.00 pm, normally 5 animals per cage). Animals had free access to tap water and food pellets (R36, Labfor, Stockholm, Sweden). Animals were randomly divided into healthy and diabetic groups. The diabetic group received a single peritoneal injection of streptozotocin (STZ, Sigma-Aldrich, France, 180 mg/kg) dissolved in sodium citrate buffer solution (0.1 mol/l, pH 4.5) to induce experimental diabetes similar to type 1. The other group received injection of an equal volume of buffer. Diabetes was confirmed 72 hours after the injection by urine glucose testing (Glukotest(r), Roche, Germany), and mice were characterized diabetic when urine glucose values were greater than 200 mg/dl. Diabetic and healthy animals were randomly assigned into 12 groups (n = 5 per group), which were sedentary or trained for one, three or five weeks. Training groups performed 1 hour per day of treadmill running at 21 m/min and 2.5° incline. After one day of familiarization on a rodent treadmill, the mice ran as described above 5 days per week. Mice were sacrificed 24 hours after the last training bout (respective sedentary controls at the same time) by cervical dislocation followed by decapitation. Cardiac muscle was removed, weighed, snap frozen in liquid nitrogen and stored at -80°C for further analysis.

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Metabolic and Molecular Framework for the Enhancement of Endurance by Intermittent Fasting

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