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急性低氧、高氧和常氧状态下运动时的心肺反应。

Cardiorespiratory responses to exercise in acute hypoxia, hyperoxia and normoxia.

作者信息

Peltonen J E, Tikkanen H O, Rusko H K

机构信息

Unit for Sports and Exercise Medicine, Institute of Clinical Medicine, University of Helsinski, Finland.

出版信息

Eur J Appl Physiol. 2001 Jul;85(1-2):82-8. doi: 10.1007/s004210100411.

DOI:10.1007/s004210100411
PMID:11513325
Abstract

There is a prevailing hypothesis that an acute change in the fraction of oxygen in inspired air (F(I)O2) has no effect on maximal cardiac output (Qcmax), although maximal oxygen uptake (VO2max) and exercise performance do vary along with F(I)O2. We tested this hypothesis in six endurance athletes during progressive cycle ergometer exercise in conditions of hypoxia (FI(O)2 = 0.150), normoxia (F(I)O2 = 0.209) and hyperoxia (F(I)O2=0.320). As expected, VO2max decreased in hypoxia [mean (SD) 3.58 (0.45)l.min(-1), P<0.05] and increased in hyperoxia [5.17 (0.34) l.min(-1), P<0.05] in comparison with normoxia [4.55 (0.32)l.min(-1)]. Similarly, maximal power (Wmax) decreased in hypoxia [334 (41) W, P< 0.05] and tended to increase in hyperoxia [404 (58) W] in comparison with normoxia [383 (46) W]. Contrary to the hypothesis, Qcmax was 25.99 (3.37) l.min(-1) in hypoxia (P<0.05 compared to normoxia and hyperoxia), 28.51 (2.36) l.min(-1) in normoxia and 30.13 (2.06)l.min(-1) in hyperoxia. Our results can be interpreted to indicate that (1) the reduction in VO2max in acute hypoxia is explained both by the narrowing of the arterio-venous oxygen difference and reduced Qcmax, (2) reduced Qcmax in acute hypoxia may be beneficial by preventing a further decrease in pulmonary and peripheral oxygen diffusion, and (3) reduced Qcmax and VO2max in acute hypoxia may be the result rather than the cause of the reduced Wmax and skeletal muscle recruitment, thus supporting the existence of a central governor.

摘要

有一种普遍的假设认为,吸入空气中氧气分数(F(I)O2)的急性变化对最大心输出量(Qcmax)没有影响,尽管最大摄氧量(VO2max)和运动表现确实会随F(I)O2而变化。我们在六名耐力运动员进行递增式自行车测力计运动时,在低氧(FI(O)2 = 0.150)、常氧(F(I)O2 = 0.209)和高氧(F(I)O2 = 0.320)条件下对这一假设进行了测试。正如预期的那样,与常氧[4.55(0.32)l.min(-1)]相比,低氧时VO2max降低[均值(标准差)3.58(0.45)l.min(-1),P<0.05],高氧时升高[5.17(0.34)l.min(-1),P<0.05]。同样,与常氧[383(46)W]相比,低氧时最大功率(Wmax)降低[334(41)W,P<0.05],高氧时趋于升高[404(58)W]。与该假设相反,低氧时Qcmax为25.99(3.37)l.min(-1)(与常氧和高氧相比,P<0.05),常氧时为28.51(2.36)l.min(-1),高氧时为30.13(2.06)l.min(-1)。我们的结果可以解释为表明:(1)急性低氧时VO2max的降低既可以通过动静脉氧差的缩小来解释,也可以通过Qcmax的降低来解释;(2)急性低氧时Qcmax的降低可能通过防止肺和外周氧扩散的进一步降低而有益;(3)急性低氧时Qcmax和VO2max的降低可能是Wmax和骨骼肌募集减少的结果而非原因,从而支持了中枢调控者的存在。

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