CLINICAL-TESTS EXPLAIN BLUNTED CORTISOL RESPONSIVENESS BUT NOT MILD HYPERCORTISOLISM IN AMENORRHEIC RUNNERS

To investigate mechanisms of blunted adrenocortical responsiveness to exercise and mild hypercortisolism in amenorrheic runners, adrenocorti cotropic hormone [ACTH-(1-24), 0.25 mg Cortrosyn] stimulation tests we re performed in the presence and absence of overnight dexamethasone (1 mg) suppression (DX and NDX condition, respectively) in six eumenorrh eic sedentary women (ES), nine eumenorrheic runners (ER), and nine ame norrheic runners (AR). Before the NDX stimulation test, plasma cortiso l was higher (P<0.001) in AR than in ER and ES. The cortisol response to the NDX stimulation test was blunted (P<0.001) in AR but reached si milar (P>0.7) peak levels in all groups. Dexamethasone suppressed (P<0 .001) cortisol to similar (P>0.5) levels (similar to 20 nmol/l) in all groups. In AR, cortisol responses to the DX test were larger (P<0.03) than to the NDX test and similar (P>0.6) in the three groups, again r eaching comparable (P>0.8) peak levels. The blunted cortisol response to stimulation in AR in the presence of their mild hypercortisolism ap pears to be due to a normal limitation in maximal adrenal secretory ca pacity. Extrapituitary modulators of adrenal responsiveness to ACTH ma y explain the mild hypercortisolism observed in AR, but limitations of these tests prevent a central negative-feedback defect or an intrinsi c adrenal abnormality from being excluded until results of additional studies with even lower doses of dexamethasone and submaximal doses of ACTH-(1-24) are available.