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高强度低氧循环运动不会改变竞技男性自行车运动员的肺密度。

Intense hypoxic cycle exercise does not alter lung density in competitive male cyclists.

作者信息

MacNutt M J, Guenette J A, Witt J D, Yuan R, Mayo J R, McKenzie D C

机构信息

School of Human Kinetics, University of British Columbia, Vancouver, Canada.

出版信息

Eur J Appl Physiol. 2007 Apr;99(6):623-31. doi: 10.1007/s00421-006-0388-1. Epub 2007 Jan 12.

Abstract

We tested the hypothesis that intense short duration hypoxic exercise would result in an increase in extravascular lung water (EVLW), as evidenced by an increase in lung density. Using computed tomography (CT), baseline lung density was obtained in eight highly trained male cyclists (mean +/- SD: age = 28 +/- 8 years; height = 180 +/- 9 cm; mass = 71.6 +/- 8.2 kg; VO2max= 65.0 +/- 5.2 ml kg min(-1)). Subjects then completed an intense hypoxic exercise challenge on a cycle ergometer and metabolic data, HR and %S(p)O2 were recorded throughout. While breathing 15% O2, subjects performed five 3 km cycling intervals (mean power, 286 +/- 20 W; HR = 91 +/- 4% HRmax) separated by 5 min of recovery. From a resting hypoxic S(p)O2 of 92 +/- 4%, subjects further desaturated during exercise to 76 +/- 3%. CT scans were repeated 76 +/- 10 min (range 63-88 min) following the completion of exercise. There was no change in lung density from pre (0.18 +/- 0.02 g ml(-1)) to post-exercise (0.18 +/- 0.04 g ml(-1)). The substantial reduction in S(p)O2 may be explained by a number of potential mechanisms, including decreased pulmonary diffusion capacity, alveolar hypoventilation, reduced red cell transit time, ventilation/perfusion inequality or a temperature and pH induced rightward-shift in the oxyhaemoglobin dissociation curve. Alternatively, the integrity of the blood gas barrier may have been disrupted without any measurable increase in lung density.

摘要

我们验证了这样一个假设

高强度短时间的低氧运动将导致血管外肺水(EVLW)增加,这可通过肺密度增加得以证明。使用计算机断层扫描(CT),在八名训练有素的男性自行车运动员中获取了基线肺密度(平均值±标准差:年龄 = 28±8岁;身高 = 180±9厘米;体重 = 71.6±8.2千克;最大摄氧量 = 65.0±5.2毫升·千克·分钟⁻¹)。受试者随后在自行车测力计上完成了一次高强度低氧运动挑战,并在整个过程中记录了代谢数据、心率和脉搏血氧饱和度(%S(p)O2)。在呼吸15%氧气的情况下,受试者进行了五个3千米的骑行间歇(平均功率,286±20瓦;心率 = 91±4%最大心率),中间间隔5分钟的恢复时间。从静息时92±4%的低氧脉搏血氧饱和度开始,受试者在运动过程中进一步降至76±3%。运动结束后76±10分钟(范围63 - 88分钟)重复进行CT扫描。肺密度从运动前(0.18±0.02克/毫升)到运动后(0.18±0.04克/毫升)没有变化。脉搏血氧饱和度的大幅下降可能由多种潜在机制解释,包括肺弥散能力下降、肺泡通气不足、红细胞通过时间缩短、通气/血流不均或温度和pH值导致的氧合血红蛋白解离曲线右移。或者,血气屏障的完整性可能已被破坏,但肺密度没有任何可测量的增加。

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