The Ergogenic Effect of Recombinant Human Erythropoietin on V̇O2max Depends on the Severity of Arterial Hypoxemia
The Ergogenic Effect of Recombinant Human Erythropoietin on V̇O2max Depends on the Severity of Arterial Hypoxemia
复制标题
重组人促红细胞生成素对 V̇O2max 的强效作用取决于动脉低氧血症的严重程度
作者：
P. Robach;J. Calbet;J. J. Thomsen;R. Boushel;P. Mollard;P. Rasmussen;C. Lundby
用重组人促红细胞生成素（rhEpo）治疗可诱导血液携氧能力（CaO 2）的升高，这明确地增强了常氧运动期间的最大摄氧量（V ~ O2 max），但在严重急性缺氧条件下进行运动时则不然。这意味着应该有一个阈值高度，在该高度下，V_（O_2）_（max）对CaO_2的依赖性较小。为了确定解释缺氧、CaO 2和V_（max）之间相互作用的机制，我们在常氧和不同程度急性缺氧的情况下，对8名rhEpo治疗的受试者进行了递增负荷运动至力竭过程中全身和腿部O2转运和利用的测定。在长期rhEpo治疗后，在常氧条件下观察到的全身V_（2 max）增益（6-7%）在轻度缺氧期间持续（在吸入O2分数（FIO 2）为0.173时为8%），在中度缺氧期间甚至更大（在FIO 2 = 0.153-0.134时为14-17%）。 当缺氧进一步增加到FIO_2 = 0.115时，rhEpo对全身V_（TO）_（2 max）和下肢V_（TO）_（2 max）均无明显增强作用。 我们的数据所强调的机制是，除了其对CaO 2的强烈影响，rhEpo被发现在常氧下通过优先重新分配心输出量到运动腿来提高腿部V ~ O2 max，而这种有利的效果在严重缺氧时消失，只留下增加的CaO 2不足以改善腿部峰值O2输送和V ~ O2。最后，中度缺氧时VtoO_2max主要依赖于CaO_2，但随着缺氧程度的增加，VtoO_2max突然变得不依赖于CaO_2，这可能是中枢疲劳出现的间接证据。
Treatment with recombinant human erythropoietin (rhEpo) induces a rise in blood oxygen-carrying capacity (CaO2) that unequivocally enhances maximal oxygen uptake (V̇O2max) during exercise in normoxia, but not when exercise is carried out in severe acute hypoxia. This implies that there should be a threshold altitude at which V̇O2max is less dependent on CaO2. To ascertain which are the mechanisms explaining the interactions between hypoxia, CaO2 and V̇O2max we measured systemic and leg O2 transport and utilization during incremental exercise to exhaustion in normoxia and with different degrees of acute hypoxia in eight rhEpo-treated subjects. Following prolonged rhEpo treatment, the gain in systemic V̇O2max observed in normoxia (6–7%) persisted during mild hypoxia (8% at inspired O2 fraction (FIO2) of 0.173) and was even larger during moderate hypoxia (14–17% at FIO2 = 0.153–0.134). When hypoxia was further augmented to FIO2 = 0.115, there was no rhEpo-induced enhancement of systemic V̇O2max or peak leg V̇O2. The mechanism highlighted by our data is that besides its strong influence on CaO2, rhEpo was found to enhance leg V̇O2max in normoxia through a preferential redistribution of cardiac output toward the exercising legs, whereas this advantageous effect disappeared during severe hypoxia, leaving augmented CaO2 alone insufficient for improving peak leg O2 delivery and V̇O2. Finally, that V̇O2max was largely dependent on CaO2 during moderate hypoxia but became abruptly CaO2-independent by slightly increasing the severity of hypoxia could be an indirect evidence of the appearance of central fatigue.