Author(s): GOMES BERNARDES, A., GABARDO, J.M.2, OLIVEIRA, L.S.3, MITAMURA, F.M.3, AGUIAR, A.F.3, ALTIMARI, L.R.2, DELL’ANNA, S.1, DE GIORGIO, A.1, BALDARI, C.1, BUZZACHERA, C.F.4, Institution: UNIVERSITÀ DEGLI STUDI DI E-CAMPUS , Country: ITALY, Abstract-ID: 2208

INTRODUCTION:
The nitric oxide (NO)-3′5′cyclic guanosine monophosphate (cGMP) signaling pathway plays a plethora of important roles in the human body. Recent studies suggest that increased NO production can enhance skeletal muscle function and improve exercise performance in some circumstances. The effects of elevated cGMP production on exercise performance, however, are less clear. While some authors have demonstrated improvements, others have shown no effect on exercise tolerance following the inhibition of phosphodiesterase-5, a member of a larger group of phosphodiesterase enzymes that deactivate cGMP. The inconsistencies found in previous studies are not well understood and warrant further research. We, therefore, investigated the effects of phosphodiesterase-5 on exercise tolerance and the physiological responses to moderate- and severe-intensity exercise.
METHODS:
Twelve recreationally active men (mean age 23 ± 4 years) volunteered for this study. Each participant visited the laboratory on five separate occasions. On Day 1, they underwent a ramp incremental exercise test on an electronically braked cycle ergometer to establish gas exchange threshold (GET) and peak oxygen uptake (V̇O2peak). Subsequently, on Days 2-5, participants were administered, in a randomized, double-blind, crossover manner, a single tablet containing either placebo or tadalafil citrate (20 mg) 80 minutes prior to completing three “step” exercise bouts: two at moderate intensity followed by one at severe intensity. Following a 7-d washout period, participants repeated the tests to complete a total of four moderate-intensity exercise bouts and two severe-intensity exercise bouts for each experimental condition. Pulmonary gas exchange and ventilation and NIRS-derived muscle oxygenation were continuously monitored throughout the tests. Blood samples were collected to determine blood lactate concentration 20 seconds before the onset of the first step exercise bout and 20 seconds following exhaustion during the severe-intensity exercise bout.
RESULTS:
Pulmonary gas exchange and ventilation and NIRS-derived muscle oxygenation responses to either moderate- or severe-intensity exercise did not show significant differences between the two experimental conditions. However, the phosphodiesterase-5 inhibition improved tolerance to severe-intensity exercise (399 ± 81 vs. 438 ± 110 sec; p < 0.05). Similarly, changes in blood lactate concentration differed between the two experimental conditions (7.0 ± 2.0 vs. 8.3 ± 2.4 mmol/L for placebo and phosphodiesterase-5 inhibition, respectively; p < 0.05).
CONCLUSION:
Our findings indicate that acute administration of a phosphodiesterase-5 inhibitor, tadalafil, improved exercise tolerance without affecting the physiological responses to submaximal exercise in humans. This ergogenicity is possibly associated with the augmented activation of anaerobic sources of energy by the skeletal muscles mediated through the NO/CGMP signaling pathway.