High oxygen extraction and slow recovery of muscle deoxygenation kinetics after neuromuscular electrical stimulation in COPD patients
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Date
2016
Authors
Azevedo, Diego de Paiva
Medeiros, Wladimir Musetti [UNIFESP]
Manfredi de Freitas, Flavia Fernandes
Amorim, Cesar Ferreira
Gimenes, Ana Cristina Oliveira [UNIFESP]
Neder, Jose Alberto [UNIFESP]
Chiavegato, Luciana Dias [UNIFESP]
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Abstract
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 A mu s) was employed to induce isometric contraction of the quadriceps. Microvascular oxygen extraction (A mu O2EF) and HHb were estimated by near-infrared spectroscopy (NIRS). Recovery kinetic was characterized by measuring the time constant Tau (HHb-tau). Torque and work were measured by isokinetic dynamometry in 13 non-hypoxaemic patients with moderate-to-severe COPD [SpO(2) = 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 A mu O2EF 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-tau (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 A mu O2EF and high values for recovery time corrected by muscle mass and work suggest that intrinsic muscle dysfunction has an impact on muscle recovery capacity.
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 A mu O2EF 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-tau (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 A mu O2EF and high values for recovery time corrected by muscle mass and work suggest that intrinsic muscle dysfunction has an impact on muscle recovery capacity.
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Citation
European Journal Of Applied Physiology. New York, v. 116, n. 10, p. 1899-1910, 2016.