Powers S K, Martin D, Dodd S
Department of Exercise and Sport Sciences, University of Florida, Gainesville.
Sports Med. 1993 Jul;16(1):14-22. doi: 10.2165/00007256-199316010-00003.
Arterial oxygenation is well maintained in healthy untrained or moderately trained individuals during exercise. In contrast, approximately 40 to 50% of healthy elite endurance athletes (cyclists and runners) demonstrate a significant reduction in arterial oxygenation during exercise at work rates approaching VO2max. The mechanism(s) to explain this exercise-induced hypoxaemia (EIH) remain controversial. However, hypoventilation and venoarterial shunt do not appear to be involved. By elimination, this suggests that ventilation-perfusion inequality and/or pulmonary diffusion limitations must contribute to EIH in this population. Theoretical and direct experimental evidence exists to support the notion that both ventilation-perfusion inequality and diffusion disequilibrium contribute to EIH; however, the relative contribution of each factor remains to be determined. In athletes who exhibit a profound EIH, the exercise-induced decline in arterial oxygenation results in a limitation of VO2max. Further, athletes who exhibit EIH at sea level suffer more severe gas exchange impairments during short term exposure to altitude than athletes or nonathletes who do not exhibit EIH at sea level. This finding explains much of the observed variance in the decline in VO2max among individuals during short term altitude or hypoxia exposure.
在运动过程中,健康的未经训练或适度训练的个体的动脉氧合能得到良好维持。相比之下,约40%至50%的健康优秀耐力运动员(自行车运动员和跑步运动员)在接近最大摄氧量(VO2max)的工作强度下运动时,会出现动脉氧合显著降低的情况。解释这种运动诱发的低氧血症(EIH)的机制仍存在争议。然而,通气不足和静脉血动脉分流似乎并不涉及其中。通过排除法,这表明通气-灌注不均和/或肺扩散限制必定是导致该人群出现EIH的原因。存在理论和直接实验证据支持通气-灌注不均和扩散失衡均导致EIH这一观点;然而,每个因素的相对贡献仍有待确定。在表现出严重EIH的运动员中,运动诱发的动脉氧合下降导致了最大摄氧量的受限。此外,在海平面表现出EIH的运动员在短期暴露于高原环境时,比在海平面未表现出EIH的运动员或非运动员遭受更严重的气体交换损害。这一发现解释了在短期高原或低氧暴露期间个体最大摄氧量下降中观察到的大部分差异。