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Effects of Exercise Training Intensity on Pancreatic β-Cell Function

OBJECTIVE: Insulin resistance and β-cell dysfunction both are important contributors to the pathogenesis of type 2 diabetes. Exercise training improves insulin sensitivity, but its effects on β-cell function are less well studied. RESEARCH DESIGN AND METHODS: Sedentary, overweight adults were random...

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Autores principales: Slentz, Cris A., Tanner, Charles J., Bateman, Lori A., Durheim, Michael T., Huffman, Kim M., Houmard, Joseph A., Kraus, William E.
Formato: Texto
Lenguaje:English
Publicado: American Diabetes Association 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752909/
https://www.ncbi.nlm.nih.gov/pubmed/19592624
http://dx.doi.org/10.2337/dc09-0032
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author Slentz, Cris A.
Tanner, Charles J.
Bateman, Lori A.
Durheim, Michael T.
Huffman, Kim M.
Houmard, Joseph A.
Kraus, William E.
author_facet Slentz, Cris A.
Tanner, Charles J.
Bateman, Lori A.
Durheim, Michael T.
Huffman, Kim M.
Houmard, Joseph A.
Kraus, William E.
author_sort Slentz, Cris A.
collection PubMed
description OBJECTIVE: Insulin resistance and β-cell dysfunction both are important contributors to the pathogenesis of type 2 diabetes. Exercise training improves insulin sensitivity, but its effects on β-cell function are less well studied. RESEARCH DESIGN AND METHODS: Sedentary, overweight adults were randomized to control or one of three 8-month exercise programs: 1) low amount/moderate intensity, 2) low amount/vigorous intensity, or 3) high amount/vigorous intensity. Of 387 randomized, 260 completed the study and 237 had complete data. Insulin sensitivity (S(i)), acute insulin response to glucose (AIRg), and the disposition index (DI = S(i) × AIRg) were modeled from an intravenous glucose tolerance test. RESULTS: Compared with control subjects, all three training programs led to increases in DI. However, the moderate-intensity group experienced a significantly larger increase in DI than either of the vigorous-intensity groups and through a different mechanism. The high-amount/vigorous-intensity group improved S(i) and had a compensatory reduction in AIRg, whereas the moderate-intensity group had a similar improvement in S(i) but almost no reduction in AIRg. Importantly, the inactive control group experienced a significant increase in fasting glucose. CONCLUSIONS: To the extent that the DI accurately reflects β-cell function, we observed that both moderate- and vigorous-intensity exercise training improved β-cell function, albeit through distinct mechanisms. It is not clear which of these mechanisms is preferable for maintenance of metabolic health. While moderate-intensity exercise led to a larger improvement in DI, which may reflect a transition toward a more normal DI, longer-term investigations would be necessary to determine which was more effective at reducing diabetes risk.
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spelling pubmed-27529092010-10-01 Effects of Exercise Training Intensity on Pancreatic β-Cell Function Slentz, Cris A. Tanner, Charles J. Bateman, Lori A. Durheim, Michael T. Huffman, Kim M. Houmard, Joseph A. Kraus, William E. Diabetes Care Original Research OBJECTIVE: Insulin resistance and β-cell dysfunction both are important contributors to the pathogenesis of type 2 diabetes. Exercise training improves insulin sensitivity, but its effects on β-cell function are less well studied. RESEARCH DESIGN AND METHODS: Sedentary, overweight adults were randomized to control or one of three 8-month exercise programs: 1) low amount/moderate intensity, 2) low amount/vigorous intensity, or 3) high amount/vigorous intensity. Of 387 randomized, 260 completed the study and 237 had complete data. Insulin sensitivity (S(i)), acute insulin response to glucose (AIRg), and the disposition index (DI = S(i) × AIRg) were modeled from an intravenous glucose tolerance test. RESULTS: Compared with control subjects, all three training programs led to increases in DI. However, the moderate-intensity group experienced a significantly larger increase in DI than either of the vigorous-intensity groups and through a different mechanism. The high-amount/vigorous-intensity group improved S(i) and had a compensatory reduction in AIRg, whereas the moderate-intensity group had a similar improvement in S(i) but almost no reduction in AIRg. Importantly, the inactive control group experienced a significant increase in fasting glucose. CONCLUSIONS: To the extent that the DI accurately reflects β-cell function, we observed that both moderate- and vigorous-intensity exercise training improved β-cell function, albeit through distinct mechanisms. It is not clear which of these mechanisms is preferable for maintenance of metabolic health. While moderate-intensity exercise led to a larger improvement in DI, which may reflect a transition toward a more normal DI, longer-term investigations would be necessary to determine which was more effective at reducing diabetes risk. American Diabetes Association 2009-10 2009-07-10 /pmc/articles/PMC2752909/ /pubmed/19592624 http://dx.doi.org/10.2337/dc09-0032 Text en © 2009 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
spellingShingle Original Research
Slentz, Cris A.
Tanner, Charles J.
Bateman, Lori A.
Durheim, Michael T.
Huffman, Kim M.
Houmard, Joseph A.
Kraus, William E.
Effects of Exercise Training Intensity on Pancreatic β-Cell Function
title Effects of Exercise Training Intensity on Pancreatic β-Cell Function
title_full Effects of Exercise Training Intensity on Pancreatic β-Cell Function
title_fullStr Effects of Exercise Training Intensity on Pancreatic β-Cell Function
title_full_unstemmed Effects of Exercise Training Intensity on Pancreatic β-Cell Function
title_short Effects of Exercise Training Intensity on Pancreatic β-Cell Function
title_sort effects of exercise training intensity on pancreatic β-cell function
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752909/
https://www.ncbi.nlm.nih.gov/pubmed/19592624
http://dx.doi.org/10.2337/dc09-0032
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