Acute effects of physical exercise and phosphodiesterase’s type 5 inhibition on serum 11β-hydroxysteroid dehydrogenases related glucocorticoids metabolites: a pilot study

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 11b-hydroxysteroid
dehydrogenases (11b-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 11b-HSDs activity during acute exercise.
Additional researches on the effects of both exercise and
PDE5i on tissue-specific 11b-HSDs activity at rest and
during physiological adaptation are warranted.