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体内缺血性肌肉收缩期间的肌细胞内氧合作用。

Intramyocellular oxygenation during ischemic muscle contractions in vivo.

作者信息

Tevald Michael A, Lanza Ian R, Befroy Douglas E, Kent-Braun Jane A

机构信息

Kinesiology Department, University of Massachusetts, Amherst, MA, 01003, USA.

出版信息

Eur J Appl Physiol. 2009 Jun;106(3):333-43. doi: 10.1007/s00421-009-1021-x. Epub 2009 Mar 11.

Abstract

There is some evidence that the fall in intramyocellular oxygen content during ischemic contractions is less than during ischemia alone. We used proton magnetic resonance spectroscopy to determine whether peak deoxy-myoglobin (dMb) obtained during ischemic ankle dorsiflexion contractions attained the maximal dMb level observed during a separate trial of ischemia alone (resting max). In six healthy young men, the rate of myoglobin desaturation was rapid at the onset of ischemic contractions and then slowed as contractions continued, attaining only 75 +/- 3.3% (mean +/- SE) of resting max dMb by the end of contractions (p = 0.03). Myoglobin continued to desaturate while ischemia was maintained following contractions, reaching 98 +/- 1.8% of resting max within 10 min (p = 0.03 vs. end of contractions). Notably, contractions performed after 10 min of ischemia did not affect dMb (dMb = 100 +/- 1.5% of resting max, p > 0.99), suggesting that full desaturation had already been achieved. The blunting of desaturation during ischemic contractions is likely a result of slowed mitochondrial oxygen consumption due to limited oxygen availability.

摘要

有证据表明,缺血性收缩期间肌细胞内氧含量的下降幅度小于单纯缺血期间。我们使用质子磁共振波谱来确定在缺血性踝关节背屈收缩期间获得的脱氧肌红蛋白(dMb)峰值是否达到在单独的单纯缺血试验(静息最大值)中观察到的最大dMb水平。在6名健康年轻男性中,缺血性收缩开始时肌红蛋白去饱和速率很快,然后随着收缩持续而减慢,到收缩结束时仅达到静息最大dMb的75±3.3%(平均值±标准误)(p = 0.03)。收缩后维持缺血状态时,肌红蛋白继续去饱和,在10分钟内达到静息最大值的98±1.8%(与收缩结束时相比,p = 0.03)。值得注意的是,缺血10分钟后进行的收缩不影响dMb(dMb为静息最大值的100±1.5%,p > 0.99),这表明已经实现了完全去饱和。缺血性收缩期间去饱和的减弱可能是由于氧供应有限导致线粒体氧消耗减慢的结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e26/2716118/65eca9adc36f/nihms-117789-f0001.jpg

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