Hemostatic Effects of Exercise-Related Hypoglycemia in Male Persons With Type 1 Diabetes

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CONTEXT: People with type 1 diabetes (T1D) are at increased risk of thrombosis, however, the underlying mechanisms remain unclear. Hypoglycemia induced at rest can induce coagulation activation, but little is known about the hemostatic effects of exercise-related hypoglycemia in people with T1D.

OBJECTIVE: We compared hemostatic profiles of individuals with T1D with healthy controls and explored hemostatic effects of hypoglycemia, induced with or without exercise, in participants with T1D.

METHODS: Thrombelastography (TEG) was used for a baseline hemostatic comparison between fifteen men with T1D and matched healthy controls. In addition, the participants with T1D underwent two euglycemic-hypoglycemic clamp days in a randomized, crossover fashion. Hypoglycemia was induced with the participants at rest (Hypo-rest) or during exercise (Hypo-exercise). TEG provides data on the rate of coagulation activation (R-time), the rate of clot formation (K-time, α-Angle), the maximum clot amplitude (MA), the functional fibrinogen contribution to the clot strength (MA-FF) and the fibrinolysis (LY-30).

RESULTS: The T1D group exhibited shorter R-time and K-time and a greater α-Angle compared to the controls. During the clamp experiments, Hypo-exercise induced an increased clot strength (MA) with a mean difference from baseline of 2.77 mm [95% confidence interval 2.04; 3.51] accompanied with a decreased fibrinolysis (LY-30) of -0.45 percentage points [-0.60; -0.29]. Hypo-rest resulted in increased functional fibrinogen (MA-FF) of 0.74 mm [0.13; 1.36] along with an increased fibrinolysis (LY-30) of 0.54 percentage points [0.11; 0.98].

CONCLUSION: Individuals with T1D exhibit a hypercoagulable hemostatic profile compared to healthy controls and exercise-related hypoglycemia may increase the susceptibility to thrombosis via both procoagulant and antifibrinolytic effects.

Original languageEnglish
JournalThe Journal of clinical endocrinology and metabolism
ISSN0021-972X
DOIs
Publication statusE-pub ahead of print - 2024

Bibliographical note

© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society.

ID: 390396176