Effects of exercise training intensity on pancreatic beta-cell function.

Journal Article

OBJECTIVE: Insulin resistance and beta-cell dysfunction both are important contributors to the pathogenesis of type 2 diabetes. Exercise training improves insulin sensitivity, but its effects on beta-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) x 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 beta-cell function, we observed that both moderate- and vigorous-intensity exercise training improved beta-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.

Full Text

Duke Authors

Cited Authors

  • Slentz, CA; Tanner, CJ; Bateman, LA; Durheim, MT; Huffman, KM; Houmard, JA; Kraus, WE

Published Date

  • October 2009

Published In

Volume / Issue

  • 32 / 10

Start / End Page

  • 1807 - 1811

PubMed ID

  • 19592624

Electronic International Standard Serial Number (EISSN)

  • 1935-5548

Digital Object Identifier (DOI)

  • 10.2337/dc09-0032

Language

  • eng

Conference Location

  • United States