Kato Takahide, Matsumura Yoshinori, Tsukanaka Atsuko, Harada Takeshi, Kosaka Mitsuo, Matsui Nobuo
Laboratory for Exercise Physiology and Biomechanics, Chukyo University, 101 Tokodachi, Kaizu-cho Toyota, 470-0393, Aichi, Japan.
Eur J Appl Physiol. 2004 Mar;91(2-3):296-302. doi: 10.1007/s00421-003-0975-3. Epub 2003 Oct 28.
The present study examined the effect of hypoxia-induced respiratory alkalosis on exercise-induced metabolic acidosis and increases in plasma lactate and ammonia levels. Six male subjects underwent exercise of increasing intensity until exhaustion: (1) in normoxia (20.9% O(2)) (=MAX), (2) in hypoxia (12% O(2)) (=HP) in which hypoxic condition had been maintained from 60 min before to 30 min after exercise, and (3) the same intensity of exercise as HP in normoxia (=SUB). Arterialized blood was drawn from a superficial vein. Post-exercise blood pH was significantly higher in HP than in MAX ( P<0.05), although plasma lactate was at the same level. For hypoxia as compared to normoxia, regression analysis confirmed a parallel shift of plasma lactate to higher pH levels indicating the effect of respiratory alkalosis ( P<0.01). After exercise plasma levels of ammonia were lower in HP than in MAX ( P<0.05). Regression analysis between ammonia and pH revealed nearly identical changes in hypoxia and normoxia at low pH. From these results, we conclude that: (1) hypoxia-induced respiratory alkalosis attenuated exhaustive exercise-induced metabolic acidosis, (2) plasma lactate concentration was determined by the relative exercise intensity, (3) the maximum plasma ammonia concentration under exhaustive exercise was reduced at hypoxia because of respiratory alkalosis.
本研究探讨了低氧诱导的呼吸性碱中毒对运动诱导的代谢性酸中毒以及血浆乳酸和氨水平升高的影响。六名男性受试者进行强度递增的运动直至力竭:(1) 在常氧(20.9% O₂)状态下(=MAX),(2) 在低氧(12% O₂)状态下(=HP),其中低氧状态在运动前60分钟至运动后30分钟期间持续维持,以及(3) 在常氧状态下进行与HP相同强度的运动(=SUB)。从浅表静脉采集动脉化血液。尽管血浆乳酸水平相同,但运动后HP组的血液pH值显著高于MAX组(P<0.05)。与常氧相比,回归分析证实血浆乳酸向更高pH值水平平行移动,表明呼吸性碱中毒的作用(P<0.01)。运动后HP组的血浆氨水平低于MAX组(P<0.05)。氨与pH之间的回归分析显示,在低pH值时,低氧和常氧状态下的变化几乎相同。根据这些结果,我们得出以下结论:(1) 低氧诱导的呼吸性碱中毒减轻了力竭运动诱导的代谢性酸中毒,(2) 血浆乳酸浓度由相对运动强度决定,(3) 在低氧状态下,由于呼吸性碱中毒,力竭运动时的最大血浆氨浓度降低。