Aguilaniu B, Flore P, Page E, Maitre J, Lacour J R, Perrault H
UCP. X, Laboratoire de physiopathologie de l'exercice, Grenoble, France.
Eur J Appl Physiol Occup Physiol. 1998;77(1-2):81-8. doi: 10.1007/s004210050304.
We have previously reported a reduction in exercise-induced hypoxaemia following polyunsaturated fatty acid supplementation (PUFA). Although this might have been explained by increases in membrane fluidity, a clear explanation could not be provided due to potentially confounding influences of series-2 prosta- glandin mediated effects resulting from PUFA. In this investigation, ten master athletes [mean age 48.1 (SEM 6) years, maximal oxygen uptake (VO2max) 3.39 (SEM 0.21) l x min(-1)] completed a maximal cycling test (Ctrl) which was repeated after the administration of 150 mg of indomethacin to inhibit prostaglandin synthesis, both before and after 6 weeks of 3.66-g PUFA x day(-1). Cardiorespiratory parameters were obtained simultaneously with brachial arterial blood sampling for partial pressure of oxygen in arterial blood (PaO2), partial pressure of carbon dioxide in arterial blood (PaCO2), pH, oxygen saturation in arterial blood and lactate concentration determinations. A significant decrease in PaO2 (mmHg) from rest [93 (SEM 1.5)] was observed for exercise intensities of more than 40% VO2max in Ctrl reaching 75.9 (SEM 2.1) at VO2max. PUFA resulted in a 5.0 (SEM 0.68) mmHg upward shift (P < 0.05) in the PaO2-oxygen uptake relationship, reducing the difference in partial pressure of oxygen between alveolar air and arterial blood (P(A-a)O2) at VO2max [Ctrl 36 (SEM 1.6) vs PUFA 33 (SEM 2.2) mmHg] while PaCO2, remained unchanged. Indomethacin had no effect on either PaO2, ideal partial pressure of oxygen in alveolar gas or P(A-a)O2 in either Ctrl or after PUFA. In contrast, the fall in pH was significantly reduced after indomethacin while VCO2, PaCO2 and lactacidaemia remained unchanged. These observations confirm an effect of PUFA on exercise PaO2 behaviour which does not appear to be mediated by the influence of a series-2 prostaglandin.
我们之前曾报道过，补充多不饱和脂肪酸（PUFA）后运动诱发的低氧血症有所减轻。尽管这可能是由于膜流动性增加所致，但由于PUFA产生的2系列前列腺素介导效应存在潜在的混杂影响，因此无法给出明确的解释。在本研究中，10名优秀运动员[平均年龄48.1（标准误6）岁，最大摄氧量（VO2max）3.39（标准误0.21）升/分钟]完成了一次最大骑行测试（对照），在服用150毫克消炎痛以抑制前列腺素合成后重复该测试，测试分别在每日补充3.66克PUFA为期6周之前和之后进行。在采集肱动脉血样的同时获取心肺参数，用于测定动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）、pH值、动脉血氧饱和度和乳酸浓度。在对照测试中，对于运动强度超过40%VO2max的情况，静息时的PaO2（毫米汞柱）[93（标准误1.5）]显著下降，在VO2max时降至75.9（标准误2.1）。PUFA使PaO2与摄氧量的关系向上偏移5.0（标准误0.68）毫米汞柱（P<0.05），在VO2max时减小了肺泡气与动脉血之间的氧分压差值[对照36（标准误1.6）与PUFA 33（标准误2.2）毫米汞柱]，而PaCO2保持不变。消炎痛对对照测试或补充PUFA后的PaO2、肺泡气理想氧分压或P(A-a)O2均无影响。相比之下，消炎痛使用后pH值的下降显著减少，而二氧化碳排出量、PaCO2和血乳酸水平保持不变。这些观察结果证实了PUFA对运动时PaO2行为的影响，这种影响似乎不是由2系列前列腺素的作用介导的。
