Bourdillon Nicolas, Fan Jui-Lin, Uva Barbara, Müller Hajo, Meyer Philippe, Kayser Bengt
Faculty of Biology and Medicine, Institut des Sciences du Sport de l'Université de Lausanne, University of Lausanne Lausanne, Switzerland ; Department of Physiology, Faculty of Biology and Medicine, University of Lausanne Lausanne, Switzerland.
Faculty of Biology and Medicine, Institut des Sciences du Sport de l'Université de Lausanne, University of Lausanne Lausanne, Switzerland ; Department of Physiology, Faculty of Biology and Medicine, University of Lausanne Lausanne, Switzerland ; Lemanic Neuroscience Doctoral School, University of Lausanne Lausanne, Switzerland.
Front Physiol. 2015 Oct 14;6:288. doi: 10.3389/fphys.2015.00288. eCollection 2015.
Hypoxia-induced pulmonary vasoconstriction increases pulmonary arterial pressure (PAP) and may impede right heart function and exercise performance. This study examined the effects of oral nitrate supplementation on right heart function and performance during exercise in normoxia and hypoxia. We tested the hypothesis that nitrate supplementation would attenuate the increase in PAP at rest and during exercise in hypoxia, thereby improving exercise performance.
Twelve trained male cyclists [age: 31 ± 7 year (mean ± SD)] performed 15 km time-trial cycling (TT) and steady-state submaximal cycling (50, 100, and 150 W) in normoxia and hypoxia (11% inspired O2) following 3-day oral supplementation with either placebo or sodium nitrate (0.1 mmol/kg/day). We measured TT time-to-completion, muscle tissue oxygenation during TT and systolic right ventricle to right atrium pressure gradient (RV-RA gradient: index of PAP) during steady state cycling.
During steady state exercise, hypoxia elevated RV-RA gradient (p > 0.05), while oral nitrate supplementation did not alter RV-RA gradient (p > 0.05). During 15 km TT, hypoxia lowered muscle tissue oxygenation (p < 0.05). Nitrate supplementation further decreased muscle tissue oxygenation during 15 km TT in hypoxia (p < 0.05). Hypoxia impaired time-to-completion during TT (p < 0.05), while no improvements were observed with nitrate supplementation in normoxia or hypoxia (p > 0.05).
Our findings indicate that oral nitrate supplementation does not attenuate acute hypoxic pulmonary vasoconstriction nor improve performance during time trial cycling in normoxia and hypoxia.
缺氧诱导的肺血管收缩会增加肺动脉压(PAP),并可能妨碍右心功能和运动表现。本研究探讨了口服硝酸盐补充剂对常氧和缺氧状态下运动时右心功能和表现的影响。我们检验了以下假设:补充硝酸盐会减弱缺氧时静息和运动期间PAP的升高,从而改善运动表现。
12名训练有素的男性自行车运动员[年龄:31±7岁(平均值±标准差)]在口服安慰剂或硝酸钠(0.1 mmol/kg/天)3天后,于常氧和缺氧(吸入氧浓度11%)状态下进行15公里计时赛骑行(TT)以及稳态次最大强度骑行(50、100和150瓦)。我们测量了TT的完成时间、TT期间的肌肉组织氧合以及稳态骑行期间的收缩期右心室至右心房压力梯度(RV-RA梯度:PAP指标)。
在稳态运动期间,缺氧使RV-RA梯度升高(p>0.05),而口服硝酸盐补充剂未改变RV-RA梯度(p>0.05)。在15公里TT期间,缺氧降低了肌肉组织氧合(p<0.05)。在缺氧状态下进行15公里TT时,补充硝酸盐进一步降低了肌肉组织氧合(p<0.05)。缺氧损害了TT期间的完成时间(p<0.05),而在常氧或缺氧状态下补充硝酸盐均未观察到改善(p>0.05)。
我们的研究结果表明,口服硝酸盐补充剂不会减弱急性缺氧性肺血管收缩,也不会改善常氧和缺氧状态下计时赛骑行期间的表现。