Rice A J, Scroop G C, Gore C J, Thornton A T, Chapman M A, Greville H W, Holmes M D, Scicchitano R
Department of Thoracic Medicine, Royal Adelaide Hospital, Australia.
Eur J Appl Physiol Occup Physiol. 1999 Mar;79(4):353-9. doi: 10.1007/s004210050520.
A group of 15 competitive male cyclists [mean peak oxygen uptake, VO2peak 68.5 (SEM 1.5 ml x kg(-1) x min(-1))] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% VO2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (VO2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P(A)O2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P(A-a)O2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At VO2peak PaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P(A)O2 and P(A-a)O2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and VO2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and P(A)O2 with the first exercise intensity and at VO2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.
15名有竞争力的男性自行车运动员（平均峰值摄氧量，VO₂峰值为68.5（标准误1.5毫升·千克⁻¹·分钟⁻¹））按照如下方案在自行车测力计上进行运动：运动起始强度为150瓦，之后每2分钟增加25瓦，直至受试者力竭。在每个运动强度结束时，从桡动脉采集血样，以测定血气分压和氧合血红蛋白饱和度（SaO₂），所有数值均校正为直肠温度。同时通过耳部血氧测定法持续监测SaO₂。在第一个运动强度（150瓦，约为VO₂峰值的40%）时，动脉血氧分压（PaO₂）出现显著下降。在200瓦时PaO₂进一步显著下降，此后保持稳定，但仍显著低于静息值，最低值在350瓦时测得[87.0（标准误1.9）毫米汞柱]。动脉血二氧化碳分压（PaCO₂）在运动强度达到250瓦之前保持不变，此后呈现显著下降趋势，在运动强度为375瓦时达到最低值[34.5（标准误0.5）毫米汞柱]。在第一个运动强度（150瓦）和最终运动强度（VO₂峰值）时，PaO₂与肺泡气氧分压（P(A)O₂，相关系数分别为0.81和0.70）以及肺泡 - 动脉氧分压差值（P(A - a)O₂，相关系数分别为0.63和0.86）均显著相关，但与PaCO₂无关。在VO₂峰值时，PaO₂与摄氧量和二氧化碳排出量的通气当量均显著相关（相关系数分别为0.58和0.53）。当将P(A)O₂和P(A - a)O₂纳入多元线性回归模型时，在150瓦和VO₂峰值时，至少95%的PaO₂方差可以得到解释。随着运动强度增加，SaO₂呈现显著下降趋势，在375瓦时达到最低值[94.6（标准误0.3）%]。在整个运动过程中，耳部血氧测定法估算的SaO₂始终显著高于血液测量值，直到350瓦时才出现与静息值相比的显著下降。PaO₂与P(A)O₂在第一个运动强度和VO₂峰值时的显著相关性得出结论：通气不足是运动诱发低氧血症的主要原因。
