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Relationship Between Cortisol and Free Testosterone in Response to Exhaustive Endurance Exercise
Author(s) -
Lane Amy,
Anderson Travis,
Hackney Anthony
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.677.18
Subject(s) - medicine , endocrinology , free testosterone , basal (medicine) , endurance training , testosterone (patch) , hormone , negative correlation , androgen , sex hormone binding globulin , insulin
Research has shown intensive exercise to induce significant changes in cortisol (C) and testosterone (T). Typically, increases in C are witnessed concurrently to decreases in T. To determine whether there was the existence of a relationship between the changes observed in these two hormones, we measured the change scores (Δ) for 12 healthy, endurance trained males (X±SD: age 22.8±3.1y; VO 2max 66.3±4.8 mL/kg/min) in response to an exhaustive exercise session (EES) (96.9±10.8 min at 74.7±4.6% of VO 2max ). The change scores were determined for basal levels of C and free T from pre to post EES (Δ0), post to +24h (Δ24), +48h (Δ48) and +72h (Δ72) into recovery. All basal hormonal levels were within acceptable clinical ranges for these subjects. The EES induced highly significant C increases (pre: 326.5±29.3nmol/L, post: 700.8±177.7nmol/L; p <0.001) and free T decreases (pre: 162.3±23.6pmol/L, post: 106.1±38.6 pmol/L; p <0.001) at Δ0. A significant negative correlation existed between C (Δ 374.3 nmol/L) and free T (Δ ‐56.2 pmol/L) at Δ0 ( p =0.028, r s = ‐0.629; Spearman rho ). No additional significant changes were detected into recovery. Cumming et al (J Clin Endocrinol Metab. 57:671, 1983) illustrated the phenomenon of C induced T reduction via pharmaceutical intervention. This study indicates a single bout of EES will induce similar effects endogenously, i.e., with elevated levels of C being associated with suppressed free T, perhaps through mechanisms directly associated with T production inhibition.