Does cerebral oxygen delivery limit incremental exercise performance?
Does cerebral oxygen delivery limit incremental exercise performance?
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脑氧输送会限制增量运动表现吗？
DOI：
10.1152/japplphysiol.00569.2011
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发表时间：
2011
期刊：
影响因子：
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通讯作者：
Roach,RobertC
中科院分区：
文献类型：
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作者：
Subudhi,AndrewW;Olin,JTod;Dimmen,AndrewC;Polaner,DavidM;Kayser,Bengt;Roach,RobertC
以前的研究表明，大脑氧气供应的减少可能会限制运动，特别是在缺氧条件下，氧气运输受到损害。我们假设，在递增负荷运动中，增加呼气末二氧化碳分压(PetCO2)将增加脑血流量(CBF)和氧气供应，从而改善峰值功率输出(Wak)。业余自行车手按平衡顺序进行了两次坡道运动试验(25W/min)，以比较正常的POI-KO_2反应和夹持状态，在夹持状态下，PetCO2在整个运动过程中保持在50托。试验在常压(大气压=630 mm Hg，1650 m)和低氧(大气压=425 mm Hg，4,875 m)条件下进行。另一项低氧试验研究了夹在较低的PetCO2(40Torr)下的效果，从∼75到100%Wpek，以减少因夹住PetCO2在50Torr时造成的呼吸性酸中毒和肌肉疲劳的潜在影响。试验期间监测代谢气体、通气量、大脑中动脉脑血流速度(经颅多普勒)、额部脉搏血氧饱和度以及大脑(前额)和肌肉(股外侧肌)的血红蛋白氧合(近红外光谱)。在常氧(n=9)和低氧(n=11)下，夹闭PETCO_2至50Torr均可增加脑血流速度(∼40%)和改善脑血红蛋白氧合(∼15%)，但降低W峰(6%)和峰值氧耗量(11%)。在低氧状态下，钳制在40Torr附近的最大努力(n=6)也改善了脑氧合(∼为15%)，但再次限制了W峰(5%)。这些发现表明，通过二氧化碳介导的血管扩张增加大量脑氧供应并不能改善递增运动能力，至少在伴有呼吸性酸中毒的情况下是这样。
Previous studies have suggested that a reduction in cerebral oxygen delivery may limit motor drive, particularly in hypoxic conditions, where oxygen transport is impaired. We hypothesized that raising end-tidal Pco2(PetCO2) during incremental exercise would increase cerebral blood flow (CBF) and oxygen delivery, thereby improving peak power output (Wpeak). Amateur cyclists performed two ramped exercise tests (25 W/min) in a counterbalanced order to compare the normal, poikilocapnic response against a clamped condition, in which PetCO2was held at 50 Torr throughout exercise. Tests were performed in normoxia (barometric pressure = 630 mmHg, 1,650 m) and hypoxia (barometric pressure = 425 mmHg, 4,875 m) in a hypobaric chamber. An additional trial in hypoxia investigated effects of clamping at a lower PetCO2(40 Torr) from ∼75 to 100% Wpeakto reduce potential influences of respiratory acidosis and muscle fatigue imposed by clamping PetCO2at 50 Torr. Metabolic gases, ventilation, middle cerebral artery CBF velocity (transcranial Doppler), forehead pulse oximetry, and cerebral (prefrontal) and muscle (vastus lateralis) hemoglobin oxygenation (near infrared spectroscopy) were monitored across trials. Clamping PetCO2at 50 Torr in both normoxia (n= 9) and hypoxia (n= 11) elevated CBF velocity (∼40%) and improved cerebral hemoglobin oxygenation (∼15%), but decreased Wpeak(6%) and peak oxygen consumption (11%). Clamping at 40 Torr near maximal effort in hypoxia (n= 6) also improved cerebral oxygenation (∼15%), but again limited Wpeak(5%). These findings demonstrate that increasing mass cerebral oxygen delivery via CO2-mediated vasodilation does not improve incremental exercise performance, at least when accompanied by respiratory acidosis.