title: Exercise counteracts the effects of short-term overfeeding and reduced physical activity independent of energy imbalance in healthy young men.
abstract: Physical activity can affect many aspects of metabolism but it is unclear to what extent this relies on manipulation of energy balance. Twenty-six active men age 25 ± 7 years (mean ± SD) were randomly assigned either to consume 50% more energy than normal by over-consuming their habitual diet for 7 days whilst simultaneously restricting their physical activity below 4000 steps day(-1) to induce an energy surplus (SUR group; n = 14) or to the same regimen but with 45 min of daily treadmill running at 70% of maximum oxygen uptake (SUR+EX group; n = 12). Critically, the SUR+EX group received additional dietary energy intake to account for the energy expended by exercise, thus maintaining a matched energy surplus. At baseline and follow-up, fasted blood samples and abdominal subcutaneous adipose tissue biopsies were obtained and oral glucose tolerance tests conducted. Insulinaemic responses to a standard glucose load increased 2-fold from baseline to follow-up in the SUR group (17 ± 16 nmol (120 min) l(-1); P = 0.002) whereas there was no change in the SUR+EX group (1 ± 6 nmol (120 min) l(-1)). Seven of 17 genes within adipose tissue were differentially expressed in the SUR group; expression of SREBP-1c, FAS and GLUT4 was significantly up-regulated and expression of PDK4, IRS2, HSL and visfatin was significantly down-regulated (P ≤ 0.05). The pAMPK/AMPK protein ratio in adipose tissue was significantly down-regulated in the SUR group (P = 0.005). Vigorous-intensity exercise counteracted most of the effects of short-term overfeeding and under-activity at the whole-body level and in adipose tissue, even in the face of a standardised energy surplus.
authors.affiliation: D. Thompson: Department for Health, University of Bath, Bath BA2 7AY, UK. d.thompson@bath.ac.uk.
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Walhin
authors.forename: Judith D
authors.initials: JD
authors.lastname: Richardson
authors.forename: James A
authors.initials: JA
authors.lastname: Betts
authors.forename: Dylan
authors.initials: D
authors.lastname: Thompson
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000293:Adolescent; D000328:Adult; D015536:Down-Regulation; D002149:Energy Intake; D004734:Energy Metabolism; D015444:Exercise; D005215:Fasting / Q000378:metabolism; D018149:Glucose Intolerance; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D054409:Nicotinamide Phosphoribosyltransferase / Q000235:genetics / Q000378:metabolism; D010101:Oxygen Consumption; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D000081382:Pyruvate Dehydrogenase Acetyl-Transferring Kinase; D002787:Sterol Esterase / Q000235:genetics / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism; D019014:fas Receptor / Q000235:genetics / Q000378:metabolism
chemical_list: C491901:FAS protein, human; D051275:Glucose Transporter Type 4; C526297:IRS2 protein, human; D055504:Insulin Receptor Substrate Proteins; C000631432:PDK4 protein, human; D000081382:Pyruvate Dehydrogenase Acetyl-Transferring Kinase; D051780:Sterol Regulatory Element Binding Protein 1; D019014:fas Receptor; D054409:Nicotinamide Phosphoribosyltransferase; D017346:Protein Serine-Threonine Kinases; D002787:Sterol Esterase