Effects of differing antecedent increases of plasma cortisol on counterregulatory responses during subsequent exercise in type 1 diabetes.
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.


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.
Bao
Shichun
S
Department of Medicine, Division of Diabetes, Endocrinology, and Metabolism, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Briscoe
Vanessa J
VJ
Tate
Donna B
DB
Davis
Stephen N
SN
D000328:Adult; D001341:Autonomic Nervous System / Q000502:physiology*; D001786:Blood Glucose / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology*; D004837:Epinephrine / Q000097:blood; D015444:Exercise / Q000502:physiology*; D005260:Female; D015309:Glucose Clamp Technique; D006801:Humans; D006854:Hydrocortisone / Q000008:administration & dosage* / Q000097:blood*; D006946:Hyperinsulinism / Q000097:blood / Q000503:physiopathology; D007003:Hypoglycemia / Q000097:blood / Q000503:physiopathology*; D007262:Infusions, Intravenous; D007328:Insulin / Q000097:blood; D008297:Male
D001786:Blood Glucose; D007328:Insulin; D006854:Hydrocortisone; D004837:Epinephrine