Effects of tadalafil administration on plasma markers of exercise-induced muscle damage, IL6 and antioxidant status capacity

Introduction Physical exercise is associated with enhanced
production of reactive oxygen species, which if uncontrolled
can result in tissue injury. Phosphodiesterase type 5 inhibitors
(PDE5i) exhibit protective effect against oxidative stress,
both in animals and healthy/unhealthy humans. However, the
effect of a chronic administration of PDE5i, particularly combined
with physical exercise, has never been investigated.
Purpose The present study was designed to evaluate the
effect of the long-acting PDE5i tadalafil on oxidative status
and muscle damage after exhaustive exercise in healthy
males included in a double-blind crossover trial.
Hypothesis Tadalafil, having a putative antioxidant activity,
may reduce oxidative damage after strenuous exercise.
Methods Each volunteer randomly received two tablets
of placebo or tadalafil (20 mg/day) with 36 h of interval
before performing exhaustive exercise. After 2 weeks of
washout, the volunteers were crossed over. Blood samples
were collected immediately before exercise, immediately after, and during recovery (15, 30, 60 min). Plasma total
antioxidant status, glutathione homeostasis (GSH/GSSG),
malondialdehyde (MDA), protein carbonyls, creatine
kinase (CK), lactate dehydrogenase (LDH) and the inflammatory
cytokine interleukin 6 were assessed.
Results Tadalafil administration per se affected redox
homeostasis (GSH/GSSG −36 %; p < 0.05), cellular (CK
+75 % and LDH +36 %; p < 0.05) and oxidative damage
(MDA +41 % and protein carbonyls +50 %; p < 0.05)
markers. The exhaustive exercise increased all the abovereported
biochemical parameters, with subjects from the
tadalafil group showing significantly higher values with
respect to the placebo group.
Conclusions A prolonged exposure to tadalafil decreases
antioxidant capacity at resting condition, therefore making
subjects more susceptible to the oxidative stress induced by
an exhaustive bout of exercise.