Azevedo Diego de Paiva, Medeiros Wladimir Musetti, de Freitas Flávia Fernandes Manfredi, Ferreira Amorim Cesar, Gimenes Ana Cristina Oliveira, Neder Jose Alberto, Chiavegato Luciana Dias
Master's and Doctoral Program in Physical Therapy, Universidade de São Paulo (UNICID), Sao Paulo, SP, Brazil.
Pulmonary Function and Clinical Exercise Physiology Unit, Division of Respiratory Medicine, Federal University of Sao Paulo (UNIFESP), Rua Professor Francisco de Castro 54, Vila Clementino, Sao Paulo, CEP 04020-050, Brazil.
Eur J Appl Physiol. 2016 Oct;116(10):1899-910. doi: 10.1007/s00421-016-3442-7. Epub 2016 Jul 28.
It was hypothesized that patients with chronic obstructive pulmonary disease (COPD) would exhibit a slow muscle deoxygenation (HHb) recovery time when compared with sedentary controls.
Neuromuscular electrical stimulation (NMES 40 and 50 mA, 50 Hz, 400 µs) was employed to induce isometric contraction of the quadriceps. Microvascular oxygen extraction (µO2EF) and HHb were estimated by near-infrared spectroscopy (NIRS). Recovery kinetic was characterized by measuring the time constant Tau (HHb-τ). Torque and work were measured by isokinetic dynamometry in 13 non-hypoxaemic patients with moderate-to-severe COPD [SpO2 = 94.1 ± 1.6 %; FEV1 (% predict) 48.0 ± 9.6; GOLD II-III] and 13 age- and sex-matched sedentary controls.
There was no desaturation in either group during NMES. Torque and work were reduced in COPD versus control for 40 and 50 mA [torque (Nm) 50 mA = 28.9 ± 6.9 vs 46.1 ± 14.2; work (J) 50 mA = 437.2 ± 130.0 vs. 608.3 ± 136.8; P < 0.05 for all]. High µO2EF values were observed in the COPD group at both NMES intensities (corrected by muscle mass 50 mA = 6.18 ± 1.1 vs. 4.68 ± 1.0 %/kg; corrected by work 50 mA = 0.12 ± 0.05 vs. 0.07 ± 0.02 %/J; P < 0.05 for all). Absolute values of HHb-τ (50 mA = 31.11 ± 9.27 vs. 18.08 ± 10.70 s), corrected for muscle mass (50 mA 3.80 ± 1.28 vs. 2.05 ± 1.45 s/kg) and corrected for work (50 mA = 0.08 ± 0.04 vs. 0.03 ± 0.02 s/J) were reduced in COPD (P < 0.05 for all). The variables behaviour for 40 mA was similar to those of 50 mA.
COPD patients exhibited a slower muscle deoxygenation recovery time after NMES. The absence of desaturation, low torque and work, high µO2EF and high values for recovery time corrected by muscle mass and work suggest that intrinsic muscle dysfunction has an impact on muscle recovery capacity.
研究假设慢性阻塞性肺疾病（COPD）患者与久坐不动的对照组相比，肌肉脱氧（HHb）恢复时间会更慢。
采用神经肌肉电刺激（NMES，40和50 mA，50 Hz，400 μs）诱导股四头肌等长收缩。通过近红外光谱（NIRS）估算微血管氧摄取（µO2EF）和HHb。通过测量时间常数Tau（HHb-τ）来表征恢复动力学。在13例中度至重度非低氧血症COPD患者[SpO2 = 94.1 ± 1.6 %；FEV1（预测值%）48.0 ± 9.6；GOLD II-III]和13例年龄及性别匹配的久坐对照组中，使用等速测力计测量扭矩和功。
NMES期间两组均未出现血氧饱和度降低。与对照组相比，COPD患者在40和50 mA时扭矩和功降低[扭矩（Nm）50 mA = 28.9 ± 6.9 vs 46.1 ± 14.2；功（J）50 mA = 437.2 ± 130.0 vs. 608.3 ± 136.8；所有P < 0.05]。在两种NMES强度下，COPD组均观察到高µO2EF值（按肌肉质量校正50 mA = 6.18 ± 1.1 vs. 4.68 ± 1.0 %/kg；按功校正50 mA = 0.12 ± 0.05 vs. 0.07 ± 0.02 %/J；所有P < 0.05）。COPD组中HHb-τ的绝对值（校正肌肉质量后50 mA = 31.11 ± 9.27 vs. 18.08 ± 10.70 s）、按肌肉质量校正后（50 mA 3.80 ± 1.28 vs. 2.05 ± 1.45 s/kg）和按功校正后（50 mA = 0.08 ± 0.04 vs. 0.03 ± 0.02 s/J）均降低（所有P < 0.05）。40 mA时变量行为与50 mA相似。
COPD患者在NMES后肌肉脱氧恢复时间更慢。未出现血氧饱和度降低、低扭矩和功、高µO2EF以及按肌肉质量和功校正后的恢复时间高值，表明内在肌肉功能障碍对肌肉恢复能力有影响。
