title: Altered adrenal steroid metabolism underlying hypercortisolism in female endurance athletes.
abstract: OBJECTIVE
  To explore possible changes in adrenal steroid metabolism and androgenic-anabolic status in female endurance athletes as a mechanism for their hypercortisolism.
  
  
  METHODS
  Adrenal steroids and androgenic-anabolic factors were studied during basal conditions and in response to ACTH stimulation related to menstrual status.
  
  
  METHODS
  Department of Obstetrics and Gynecology, Karolinska Hospital, Stockholm, Sweden.
  
  
  METHODS
  Thirteen female elite middle to long distance runners (six eumenorrheic, seven oligoamenorrheic) and seven regularly menstruating controls.
  
  
  METHODS
  Blood samples were collected before and after an injection of 250 micrograms IV synthetic ACTH 1-24. Body weight, height, and body fat were measured.
  
  
  METHODS
  Basal serum concentrations of cortisol, androstenedione (A), DHEA, DHEAS, 17 alpha-hydroxyprogesterone (17-OHP), T, steroid-binding proteins, and insulin-like growth factor I and ACTH-induced response (area under the curve) of cortisol, DHEA, and 17-OHP.
  
  
  RESULTS
  Oligoamenorrheic athletes had higher basal cortisol and A concentrations compared with healthy controls, whereas basal levels of DHEA and DHEAS were normal. Important findings in the oligoamenorrheic athletes were a significantly lower ratio between the ACTH-induced increments of DHEA and 17-OHP and an increased ratio between basal A and DHEAS. Insulin-like growth factor I was correlated negatively to sex hormone-binding globulin and to the amount of body fat in the combined material.
  
  
  CONCLUSIONS
  The results indicate a redistribution of adrenal steroid metabolism in favor of glucocorticoid production in female endurance athletes. We suggest that hypercortisolism in female endurance athletes is a physiological adaptation to maintain adequate blood glucose levels during a condition of energy deficiency.
authors.affiliation: Department of Obstetrics and Gynecology, Karolinska Hospital, Stockholm, Sweden.
authors.forename: C
authors.initials: C
authors.lastname: Lindholm
authors.forename: A L
authors.initials: AL
authors.lastname: Hirschberg
authors.forename: K
authors.initials: K
authors.lastname: Carlström
authors.forename: B
authors.initials: B
authors.lastname: von Schoultz
mesh_terms: D019326:17-alpha-Hydroxyprogesterone; D000305:Adrenal Cortex Hormones / Q000097:blood*; D000308:Adrenocortical Hyperfunction / Q000097:blood* / Q000209:etiology; D000328:Adult; D000568:Amenorrhea / Q000097:blood / Q000209:etiology; D000735:Androstenedione / Q000097:blood; D003366:Cosyntropin; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D006908:Hydroxyprogesterones / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D010807:Physical Endurance / Q000502:physiology*; D012420:Running; D013739:Testosterone / Q000097:blood
chemical_list: D000305:Adrenal Cortex Hormones; D006908:Hydroxyprogesterones; D003366:Cosyntropin; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D007334:Insulin-Like Growth Factor I; D019326:17-alpha-Hydroxyprogesterone; D006854:Hydrocortisone