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运动期间对持续性低氧的通气反应。

Ventilatory response to sustained hypoxia during exercise.

作者信息

Ward D S, Nguyen T T

机构信息

Department of Anesthesiology, University of California Los Angeles, School of Medicine, 90024-1778.

出版信息

Med Sci Sports Exerc. 1991 Jun;23(6):719-26.

PMID:1886480
Abstract

The ventilatory stimulating effects of hypoxia occurring at carotid bodies are potentiated by exercise. However, hypoxia also has central ventilatory depressive effects; the potential interactions between this hypoxic depression and exercise have not been studied. We examined the ventilatory response to a 20 min period of isocapnic hypoxia (end-tidal O2, PETO2, of 50 mm Hg), preceded and followed by a 5 min period of isocapnic hyperoxia in seven normal adult males at rest and during moderate exercise (45-75 W). When hypoxia was introduced at rest (PETO2 = 42 mmHg), ventilation initially increased from 13.73 +/- 3.04 (mean +/- SD) to 23.69 +/- 5.48 1.min-1 and then slowly declined to 19.01 +/- 4.68 1 min-1. The increase was caused by increases in tidal volume and respiratory frequency, but the decline was solely in tidal volume. During a background of moderate exercise (PETCO2 = 46 mmHg), introduction of hypoxia caused ventilation to increase from 30.84 +/- 6.31 to 56.44 +/- 10.58 1.min-1. Ventilation subsequently did not decline; at the end of the hypoxic period, ventilation was 57.06 +/- 12.59 1.min-1. The increase was also associated with an increase in tidal volume and respiratory frequency, as seen as rest, but with much larger magnitudes. Despite the absence of ventilatory decline, there was still a decline in tidal volume, but it was compensated by an increase in respiratory frequency. We conclude that exercise potentiated the acute ventilatory response to hypoxia by modifying both tidal volume and respiratory frequency but that exercise abolished or greatly reduced hypoxic decline by increasing respiratory rate.

摘要

颈动脉体处发生的低氧对通气的刺激作用会因运动而增强。然而,低氧也具有中枢性通气抑制作用;这种低氧抑制与运动之间的潜在相互作用尚未得到研究。我们在7名正常成年男性休息时和中等强度运动(45 - 75瓦)期间,检测了他们对20分钟等碳酸血症性低氧(呼气末氧分压,PETO2,为50毫米汞柱)的通气反应,该低氧期前后各有5分钟的等碳酸血症性高氧期。当在休息时引入低氧(PETO2 = 42毫米汞柱)时,通气最初从13.73 ± 3.04(平均值 ± 标准差)增加到23.69 ± 5.48升·分钟⁻¹,然后缓慢下降至19.01 ± 4.68升·分钟⁻¹。增加是由潮气量和呼吸频率增加引起的,但下降仅在于潮气量。在中等强度运动背景下(PETCO2 = 46毫米汞柱),引入低氧导致通气从30.84 ± 6.31增加到56.44 ± 10.58升·分钟⁻¹。随后通气并未下降;在低氧期结束时,通气为57.06 ± 12.59升·分钟⁻¹。这种增加也与潮气量和呼吸频率增加有关,与休息时情况相同,但幅度大得多。尽管通气没有下降,但潮气量仍有下降,不过被呼吸频率增加所补偿。我们得出结论,运动通过改变潮气量和呼吸频率增强了对低氧的急性通气反应,但运动通过增加呼吸频率消除或大大减少了低氧导致的下降。

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