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低强度静力收缩过程中的肌肉内压力和组织氧合并非肌肉疲劳的原因。

Intramuscular pressure and tissue oxygenation during low-force static contraction do not underlie muscle fatigue.

作者信息

Blangsted A K, Vedsted P, Sjøgaard G, Søgaard K

机构信息

Department of Physiology, National Institute of Occupational Health, Copenhagen, Denmark.

出版信息

Acta Physiol Scand. 2005 Apr;183(4):379-88. doi: 10.1111/j.1365-201X.2005.01411.x.

Abstract

AIM

To test the hypothesis that time-wise increase in intramuscular pressure (IMP) and subsequent decrease in muscle tissue oxygenation (TO(2)) results in muscle fatigue development during a non-exhaustive, low-force contraction evidenced by changes in electromyogram (EMG) and particular mechanomyogram (MMG).

METHODS

Seven subjects performed static elbow flexion at 10% maximal voluntary contraction (MVC) for 10 min (10% MVC(10 min)). Surface EMG, MMG, IMP and TO(2) measured by near-infrared spectroscopy was recorded from m. biceps brachii during 10% MVC(10 min) and during 5% MVC test contractions of 1 min duration performed before 10% MVC(10 min), 10 and 30 min post-exercise. EMG and MMG were analysed for root mean square (rms) and mean power frequency (mpf).

RESULTS

During 10% MVC(10 min) MMGrms increased from initial level of 0.04 +/- 0.01 to 0.11 +/- 0.07 m s(-2) in the last minute and MMGmpf and EMGmpf decreased from 34.9 +/- 8.2 to 21.3 +/- 3.8 Hz and from 71.7 +/- 10.9 to 61.7 +/- 10.0 Hz respectively. Similar changes were present in 5% MVC test contractions 30 min post-exercise. Initially, TO(2) decreased by 6.9 +/- 6.5% of resting level but returned to rest within 1 min. IMP remained constant during the contraction after an initial fourfold increase from resting level of 12.2 +/- 10.4 mmHg.

CONCLUSIONS

IMP was anticipated to increase with time of contraction due to e.g. increased muscle water content; but this was not confirmed. Consequently, muscle blood flow was unlikely to be impeded with contraction time, which may account for the maintenance of TO(2). Thus, decreased TO(2) did not underlie either acute or long-term muscle fatigue development evidenced by changes in EMG and particular MMG variables.

摘要

目的

验证以下假设,即在非竭尽全力的低强度收缩过程中,肌内压(IMP)随时间增加,随后肌肉组织氧合(TO₂)降低,导致肌肉疲劳,这可通过肌电图(EMG)和特定的机械肌电图(MMG)变化得以证明。

方法

7名受试者以最大自主收缩(MVC)的10%进行静态屈肘10分钟(10%MVC₁₀min)。在10%MVC₁₀min期间以及在10%MVC₁₀min之前、运动后10分钟和30分钟进行的持续1分钟的5%MVC测试收缩期间,从肱二头肌记录表面肌电图、机械肌电图、肌内压和通过近红外光谱测量的组织氧合。对肌电图和机械肌电图进行均方根(rms)和平均功率频率(mpf)分析。

结果

在10%MVC₁₀min期间,机械肌电图均方根在最后一分钟从初始水平0.04±0.01增加到0.11±0.07m·s⁻²,机械肌电图平均功率频率和肌电图平均功率频率分别从34.9±8.2Hz降至21.3±3.8Hz,从71.7±10.9Hz降至61.7±10.0Hz。运动后30分钟的5%MVC测试收缩中也出现了类似变化。最初,组织氧合降低了静息水平的6.9±6.5%,但在1分钟内恢复到静息水平。肌内压在收缩期间保持恒定,最初从静息水平12.2±10.4mmHg增加了四倍。

结论

预计肌内压会因例如肌肉含水量增加等因素而随收缩时间增加,但未得到证实。因此,肌肉血流不太可能因收缩时间而受阻,这可能是组织氧合得以维持的原因。因此,组织氧合降低并非由肌电图和特定机械肌电图变量变化所证明的急性或长期肌肉疲劳发展的基础。

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