Intense Exercise Has Unique Effects on Both Insulin Release and Its Roles in Glucoregulation
Open accessAbstract
In intense exercise (>80% Vo2max), unlike at lesser intensities, glucose is the exclusive muscle fuel. It must be mobilized from muscle and liver glycogen in both the fed and fasted states. Therefore, regulation of glucose production (GP) and glucose utilization (GU) have to be different from exercise at <60% Vo2max, in which it is established that the portal glucagon-to-insulin ratio causes the less than or equal to twofold increase in GP. GU is subject to complex regulation by insulin, plasma glucose, alternate substrates, other humoral factors, and muscle factors. At lower intensities, plasma glucose is constant during postabsorptive exercise and declines during postprandial exercise (and often in persons with diabetes). During such exercise, insulin secretion is inhibited by β-cell α-adrenergic receptor activation. In contrast, in intense exercise, GP rises seven- to eightfold and GU rises three- to fourfold; therefore, glycemia increases and plasma insulin decreases minimally, if at all. Indeed, even an increase in insulin during α-blockade or during a pancreatic clamp does not prevent this response, nor does pre-exercise hyperinsulinemia due to a prior meal or glucose infusion. At exhaustion, GU initially decreases more than GP, which leads to greater hyperglycemia, requiring a substantial rise in insulin for 40–60 min to restore pre-exercise levels. Absence of this response in type 1 diabetes leads to sustained hyperglycemia, and mimicking it by intravenous infusion restores the normal response. Compelling evidence supports the conclusion that the marked catecholamine responses to intense exercise are responsible for both the GP increment (that occurs even during glucose infusion and postprandially) and the restrained increase of GU. These responses are normal in persons with type 1 diabetes, who often report exercise-induced hyperglycemia, and in whom the clinical challenge is to reproduce the recovery period hyperinsulinemia. Intense exercise in type 2 diabetes requires additional study.
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Hyperglycemia can result from brief, intense aerobic exercise and persist for up to 1-2 h.
“Hyperglycemia can result from such activity and persist for up to 1–2 h, likely because plasma catecholamine levels and glucose production do not return to normal immediately with cessation of the activity ( 184 ).”
From Exercise and Type 2 Diabetes (2010) · cites this paper as [184]
The paper’s discussion of glucoregulatory responses reports that hyperglycemia after intense exercise persists for up to 1 hour in normal subjects. In “Intense exercise in diabetes,” it reports persistence through a 2-hour recovery period in subjects with type 1 diabetes receiving unchanged insulin infusion. The cited sentence does not distinguish those groups, and the paper attributes prolonged hyperglycemia in type 1 diabetes to insufficient postexercise insulin, not simply to catecholamines and glucose production remaining elevated. (LLM, conf=0.86)
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- Authors
- Marliss, E. B., & Vranic, M.
- Affiliations
- McGill University Health Centre (CA)
- Departments of Physiology and Medicine, University of Toronto, Toronto, Ontario, Canada
- ORCID
- Marliss, Errol B.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2002-02-01
- Volume
- 51
- Issue
- suppl_1
- Pages
- S271-S283
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2400357431
- Cited by
- 390
- References
- 61
- Citations by year
- 2026: 15 · 2025: 10 · 2024: 14 · 2023: 19 · 2022: 19 · 2021: 24 · 2020: 18 · 2019: 24 · 2018: 25 · 2017: 24 · 2016: 29 · 2015: 23 · 2014: 20 · 2013: 15 · 2012: 18
- FWCI
- 0.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Washington
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- high-intensity exercise, insulin secretion, glucose regulation, glucose production, glucose utilization, type 1 diabetes, type 2 diabetes, exercise-induced hyperglycemia, catecholamines, alpha-adrenergic receptors, beta-cell function, glycogen mobilization, postprandial exercise, hyperinsulinemia
- MeSH terms
- Blood Glucose, Diabetes Mellitus, Type 2, Humans, Insulin, Exercise
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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