Document Detail


Impact of exercise training on insulin sensitivity, physical fitness, and muscle oxidative capacity in first-degree relatives of type 2 diabetic patients.
MedLine Citation:
PMID:  16352678     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
First-degree relatives of type 2 diabetic patients (offspring) are often characterized by insulin resistance and reduced physical fitness (VO2 max). We determined the response of healthy first-degree relatives to a standardized 10-wk exercise program compared with an age-, sex-, and body mass index-matched control group. Improvements in VO2 max (14.1 +/- 11.3 and 16.1 +/- 14.2%; both P < 0.001) and insulin sensitivity (0.6 +/- 1.4 and 1.0 +/- 2.1 mg x kg(-1) x min(-1); both P < 0.05) were comparable in offspring and control subjects. However, VO2 max and insulin sensitivity in offspring were not related at baseline as in the controls (r = 0.009, P = 0.96 vs. r = 0.67, P = 0.002). Likewise, in offspring, exercise-induced changes in VO2 max did not correlate with changes in insulin sensitivity as opposed to controls (r = 0.06, P = 0.76 vs. r = 0.57, P = 0.01). Skeletal muscle oxidative capacity tended to be lower in offspring at baseline but improved equally in both offspring and controls in response to exercise training (delta citrate synthase enzyme activity 26 vs. 20%, and delta cyclooxygenase enzyme activity 25 vs. 23%. Skeletal muscle fiber morphology and capillary density were comparable between groups at baseline and did not change significantly with exercise training. In conclusion, this study shows that first-degree relatives of type 2 diabetic patients respond normally to endurance exercise in terms of changes in VO2 max and insulin sensitivity. However, the lack of a correlation between the VO2 max and insulin sensitivity in the first-degree relatives of type 2 diabetic patients indicates that skeletal muscle adaptations are dissociated from the improvement in VO2 max. This could indicate that, in first-degree relatives, improvement of insulin sensitivity is dissociated from muscle mitochondrial functions.
Authors:
Torben Østergård; Jesper L Andersen; Birgit Nyholm; Sten Lund; K Sreekumaran Nair; Bengt Saltin; Ole Schmitz
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Publication Detail:
Type:  Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2005-12-13
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  290     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2006 May 
Date Detail:
Created Date:  2006-04-10     Completed Date:  2006-06-19     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E998-1005     Citation Subset:  IM    
Affiliation:
Dept. of Endocrinology & Diabetes M, Aarhus Univ. Hospital, Aarhus Sygehus, Nørrebrogade 42-44, DK-8000 Aarhus C, Denmark. oest@dadlnet.dk
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MeSH Terms
Descriptor/Qualifier:
Adult
Blood Glucose / metabolism
Body Mass Index
C-Peptide / blood
Citrate (si)-Synthase / metabolism
Diabetes Mellitus, Type 2 / blood,  genetics,  physiopathology*
Electron Transport Complex IV / metabolism
Exercise / physiology*
Exercise Test
Family Health
Female
Humans
Insulin / blood
Insulin Resistance / physiology*
Lipid Metabolism / physiology
Male
Muscle, Skeletal / cytology,  metabolism*
Oxidation-Reduction
Oxygen / metabolism
Physical Fitness / physiology*
Regression Analysis
Grant Support
ID/Acronym/Agency:
R01 DK-41973/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/C-Peptide; 11061-68-0/Insulin; 7782-44-7/Oxygen; EC 1.9.3.1/Electron Transport Complex IV; EC 2.3.3.1/Citrate (si)-Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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