Changes in insulin sensitivity, glucose effectiveness, and B-cell function in regularly exercising subjects
Abstract
To determine the relative contributions of changes in glucose effectiveness, B-cell function, and insulin sensitivity to changes in glucose tolerance upon exercise cessation in regularly exercising individuals, we studied seven young subjects who were performing aerobic exercise on a regular schedule. Each subject was studied 12 and 84 hours after the last bout of exercise with an intravenous glucose tolerance test (IVGTT) to quantify insulin sensitivity and glucose effectiveness at zero insulin (GEZI) using the minimal model of glucose kinetics. Additionally, B-cell function was quantified as the acute insulin response to glucose (AIRglucose), and intravenous glucose tolerance as the glucose disappearance constant (Kg). Twelve hours after the last bout of exercise, SI was 8.47 +/- 1.12 x 10(-5) min-1/pmol/L, as compared with 6.98 +/- 1.17 x 10(-5) min-1/pmol/L 84 hours after exercise (mean +/- SE, P = .005). No changes was observed in GEZI (0.020 +/- 0.004 min-1 at 12 hours v 0.019 +/- 0.002 min-1 at 84 hours, P = NS) or AIRglucose (588 +/- 213 pmol/L at 12 hours v 687 +/- 271 pmol/L at 84 hours, P = NS). Thus, the difference in intravenous glucose tolerance observed 12 hours after exercise as compared with 84 hours after the last bout of exercise (Kg, 2.91 +/- 0.70%/min at 12 hours v 2.23 +/- 0.60%/min at 84 hours, P < .05) would appear to be entirely related to a difference in SI and not to differences in glucose effectiveness or B-cell function.
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Insulin sensitivity is influenced by genetics, age, acute exercise, physical fitness, dietary nutrients, medications, obesity and body fat distribution.
“insulin sensitivity is influenced by a number of different factors such as genetics [20], age [21, 22], acute exercise [23], physical fitness [24], dietary nutrients [25], medications [26, 27, 28], obesity [9, 10, 29, 30, 31, 32] and body fat distribution [31, 33, 34, 35, 36, 37, 38].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [23]
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References 32 · Cited by 30
- Authors
- Prigeon, R. L., Kahn, S. E., & Porte, D.
- Affiliations
- University of Washington (US)
- Corresponding author
- Prigeon, Ronald L.
- ORCID
- Kahn, Steven E.
- Venue
- Metabolism
- Publisher
- Elsevier BV
- Published
- 1995-10
- Volume
- 44
- Issue
- 10
- Pages
- 1259-1263
- ISSN
- 0026-0495 (ISSN-L)
- OpenAlex
- W2004268883
- Cited by
- 30
- References
- 32
- Citations by year
- 2022: 1 · 2021: 1 · 2015: 1 · 2012: 2
- FWCI
- 0.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- National Institutes of Health (2r01dk012829-36)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 12829, DK-17047, P30DK017047)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Physiology › Physical Activity and Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- insulin sensitivity, glucose effectiveness, B cell function, exercise cessation, glucose tolerance, acute insulin response to glucose, aerobic exercise, insulin sensitivity index, glucose kinetics
- MeSH terms
- Adult, Blood Glucose, Epinephrine, Glucose, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Islets of Langerhans, Male, Norepinephrine, Time Factors, Exercise
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