Document Detail

Effects of differing antecedent increases of plasma cortisol on counterregulatory responses during subsequent exercise in type 1 diabetes.
MedLine Citation:
PMID:  19509020     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Antecedent hypoglycemia can blunt neuroendocrine and autonomic nervous system responses to next-day exercise in type 1 diabetes. The aim of this study was to determine whether antecedent increase of plasma cortisol is a mechanism responsible for this finding.
RESEARCH DESIGN AND METHODS: For this study, 22 type 1 diabetic subjects (11 men and 11 women, age 27 +/- 2 years, BMI 24 +/- 1 kg/m(2), A1C 7.9 +/- 0.2%) underwent four separate randomized 2-day protocols, with overnight normalization of blood glucose. Day 1 consisted of morning and afternoon 2-h hyperinsulinemic- (9 pmol x kg(-1) x min(-1)) euglycemic clamps (5.1 mmol/l), hypoglycemic clamps (2.9 mmol/l), or euglycemic clamps with a physiologic low-dose intravenous infusion of cortisol to reproduce levels found during hypoglycemia or a high-dose infusion, which resulted in further twofold greater elevations of plasma cortisol. Day 2 consisted of 90-min euglycemic cycling exercise at 50% Vo(2max).
RESULTS: During exercise, glucose levels were equivalently clamped at 5.1 +/- 0.1 mmol/l and insulin was allowed to fall to similar levels. Glucagon, growth hormone, epinephrine, norepinephrine, and pancreatic polypeptide responses during day 2 exercise were significantly blunted following antecedent hypoglycemia, low- and high-dose cortisol, compared with antecedent euglycemia. Endogenous glucose production and lipolysis were also significantly reduced following day 1 low- and high-dose cortisol.
CONCLUSIONS: Antecedent physiologic increases in cortisol (equivalent to levels occurring during hypoglycemia) resulted in blunted neuroendocrine, autonomic nervous system, and metabolic counterregulatory responses during subsequent exercise in subjects with type 1 diabetes. These data suggest that prior elevations of cortisol may play a role in the development of exercise-related counterregulatory failure in those with type 1 diabetes.
Shichun Bao; Vanessa J Briscoe; Donna B Tate; Stephen N Davis
Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural     Date:  2009-06-09
Journal Detail:
Title:  Diabetes     Volume:  58     ISSN:  1939-327X     ISO Abbreviation:  Diabetes     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-09-01     Completed Date:  2009-09-30     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  0372763     Medline TA:  Diabetes     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2100-8     Citation Subset:  AIM; IM    
Department of Medicine, Division of Diabetes, Endocrinology, and Metabolism, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
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MeSH Terms
Autonomic Nervous System / physiology*
Blood Glucose / metabolism
Diabetes Mellitus, Type 1 / blood,  physiopathology*
Epinephrine / blood
Exercise / physiology*
Glucose Clamp Technique
Hydrocortisone / administration & dosage*,  blood*
Hyperinsulinism / blood,  physiopathology
Hypoglycemia / blood,  physiopathology*
Infusions, Intravenous
Insulin / blood
Grant Support
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 50-23-7/Hydrocortisone; 51-43-4/Epinephrine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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