title: A 2-wk reduction of ambulatory activity attenuates peripheral insulin sensitivity.
abstract: US adults take between approximately 2,000 and approximately 12,000 steps per day, a wide range of ambulatory activity that at the low range could increase risk for developing chronic metabolic diseases. Dramatic reductions in physical activity induce insulin resistance; however, it is uncertain if and how low ambulatory activity would influence peripheral insulin sensitivity. We aimed to explore if healthy, nonexercising subjects who went from a normal to a low level of ambulatory activity for 2 wk would display metabolic alterations including reduced peripheral insulin sensitivity. To do this, ten healthy young men decreased their daily activity level from a mean of 10,501+/-808 to 1,344+/-33 steps/day for 2 wk. Hyperinsulinemic-euglycemic clamps with stable isotopes and muscle biopsies, maximal oxygen consumption (VO2 max) tests, and blood samples were performed pre- and postintervention. A reduced number of daily steps induced a significant reduction of 17% in the glucose infusion rate (GIR) during the clamp. This reduction was due to a decline in peripheral insulin sensitivity with no effect on hepatic endogenous glucose production. The insulin-stimulated ratio of pAktthr308/total Akt decreased after step reduction, with a post hoc analysis revealing the most pronounced effect after 4 h of insulin infusion. In addition, the 2-wk period induced a 7% decline in VO2 max (ml/min; cardiovascular fitness). Lean mass of legs, but not arms and trunk, decreased concurrently. Taken together, one possible biological cause for the public health problem of Type 2 diabetes has been identified. Reduced ambulatory activity for 2 wk in healthy, nonexercising young men significantly reduced peripheral insulin sensitivity, cardiovascular fitness, and lean leg mass.
authors.affiliation: Centre of Inflammation and Metabolism, Department of Infectious Diseases, Rigshospitalet-Section 7641, Blegdamsvej 9, Faculty of Health Sciences, University of Copenhagen, DK-2100 Copenhagen, Denmark. krogh-madsen@inflammation-metabolism.dk
authors.forename: Rikke
authors.initials: R
authors.lastname: Krogh-Madsen
authors.forename: John P
authors.initials: JP
authors.lastname: Thyfault
authors.forename: Christa
authors.initials: C
authors.lastname: Broholm
authors.forename: Ole Hartvig
authors.initials: OH
authors.lastname: Mortensen
authors.forename: Rasmus H
authors.initials: RH
authors.lastname: Olsen
authors.forename: Remi
authors.initials: R
authors.lastname: Mounier
authors.forename: Peter
authors.initials: P
authors.lastname: Plomgaard
authors.forename: Gerrit
authors.initials: G
authors.lastname: van Hall
authors.forename: Frank W
authors.initials: FW
authors.lastname: Booth
authors.forename: Bente K
authors.initials: BK
authors.lastname: Pedersen
mesh_terms: D056044:Actigraphy / Q000295:instrumentation; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001706:Biopsy; D001786:Blood Glucose / Q000378:metabolism*; D001823:Body Composition; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D004734:Energy Metabolism; D015309:Glucose Clamp Technique; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood; D007328:Insulin / Q000008:administration & dosage / Q000378:metabolism*; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D009043:Motor Activity; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000503:physiopathology; D010101:Oxygen Consumption; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D057185:Sedentary Behavior; D013997:Time Factors; D055815:Young Adult
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D018836:Inflammation Mediators; D007328:Insulin; D051057:Proto-Oncogene Proteins c-akt