title: Acute effects of physical exercise and phosphodiesterase's type 5 inhibition on serum 11β-hydroxysteroid dehydrogenases related glucocorticoids metabolites: a pilot study.
abstract: Endogenous glucocorticoids (GC) rapidly increase after acute exercise, and the phosphodiesterase's type 5 inhibitor (PDE5i) tadalafil influences this physiological adaptation. No data exist on acute effects of both acute exercise and PDE5i administration on 11β-hydroxysteroid dehydrogenases (11β-HSDs)-related GC metabolites. We aimed to investigate the rapid effects of exercise on serum GC metabolites, with and without tadalafil administration. A double blind crossover study was performed in eleven healthy male volunteers. After the volunteers randomly received a short-term administration of placebo or tadalafil (20 mg/die for 2 days), a maximal exercise test to exhaustion on cycle ergometer was performed. Then, after a 2-week washout period, the volunteers were crossed over. Blood samples were collected before starting exercise and at 5 and 30 min of recovery (+5-Rec, +30-Rec). Serum ACTH, corticosterone (Cn), cortisol (F), cortisone (E), tetrahydrocortisol (THF), tetrahydrocortisone (THE), cortols, cortolones and respective ratios were evaluated. Pre-Ex THF was higher after tadalafil. Exercise increased ACTH, Cn, F, E, THE, cortols and cortolones after both placebo and tadalafil, and THF after placebo. The F/E ratio increased at +5-Rec and decreased at +30-Rec after placebo. Compared to placebo, after tadalafil lower ACTH, F and Cn, higher THF/F and THE/E, and not E (at +5-Rec) and F/E modifications were observed. Acute exercise rapidly influences serum GC metabolites concentrations. Tadalafil influences both GC adaptation and 11β-HSDs activity during acute exercise. Additional researches on the effects of both exercise and PDE5i on tissue-specific 11β-HSDs activity at rest and during physiological adaptation are warranted.
authors: Department of Movement, Human and Health Sciences, University of Rome "Foro Italico", Piazza Lauro de Bosis, 15, 00135, Rome, Italy, luigi.diluigi@uniroma4.it.
authors: Luigi
authors: L
authors: Di Luigi
authors: Francesco
authors: F
authors: Botrè
authors: Stefania
authors: S
authors: Sabatini
authors: Massimiliano
authors: M
authors: Sansone
authors: Monica
authors: M
authors: Mazzarino
authors: Laura
authors: L
authors: Guidetti
authors: Carlo
authors: C
authors: Baldari
authors: Andrea
authors: A
authors: Lenzi
authors: Daniela
authors: D
authors: Caporossi
authors: Francesco
authors: F
authors: Romanelli
authors: Paolo
authors: P
authors: Sgrò
mesh_terms: D042842:11-beta-Hydroxysteroid Dehydrogenases / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D002243:Carbolines / Q000494:pharmacology*; D003345:Corticosterone / Q000097:blood; D003348:Cortisone / Q000097:blood; D018592:Cross-Over Studies; D004311:Double-Blind Method; D015444:Exercise / Q000502:physiology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D058986:Phosphodiesterase 5 Inhibitors / Q000494:pharmacology*; D010865:Pilot Projects; D000068581:Tadalafil; D013760:Tetrahydrocortisol / Q000097:blood; D013761:Tetrahydrocortisone / Q000097:blood; D055815:Young Adult
chemical_list: D002243:Carbolines; D058986:Phosphodiesterase 5 Inhibitors; D013761:Tetrahydrocortisone; D000068581:Tadalafil; D013760:Tetrahydrocortisol; D000324:Adrenocorticotropic Hormone; D042842:11-beta-Hydroxysteroid Dehydrogenases; D003348:Cortisone; D003345:Corticosterone; D006854:Hydrocortisone