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Purpose: 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., Methods: 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., Results: 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., Conclusions: 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.

This study addressed whether O(2) delivery during recovery from high-intensity, supra-gas exchange threshold exercise would be matched to O(2) utilization at the microvascular level in patients with mitochondrial myopathy (MM). Off-exercise kinetics of (1) pulmonary O(2) uptake VO(2P) (2) an index of fractional O(2) extraction by near-infrared spectroscopy (Δ[deoxy-Hb + Mb]) in the vastus lateralis and (3) cardiac output (Q'(T)) by impedance cardiography were assessed in 12 patients with biopsy-proven MM (chronic progressive external ophthalmoplegia) and 12 age- and gender-matched controls. Kinetics of VO(2P) were significantly slower in patients than controls (τ = 53.8 ± 16.5 vs. 38.8 ± 7.6 s, respectively; p < 0.05). Q'(T), however, declined at similar rates (τ = 64.7 ± 18.8 vs. 73.0 ± 21.6 s; p > 0.05) being typically slower than [Formula: see text] in both groups. Importantly, Δ[deoxy-Hb + Mb] dynamics (MRT) were equal to, or faster than, τVO(2P) in patients and controls, respectively. In fact, there were no between-group differences in τVO(2P)MRTΔ[deoxy-Hb + Mb] (1.1 ± 0.4 vs. 1.0 ± 0.2, p > 0.05) thereby indicating similar rates of microvascular O(2) delivery. These data indicate that the slower rate of recovery of muscle metabolism after high-intensity exercise is not related to impaired microvascular O(2) delivery in patients with MM. This phenomenon, therefore, seems to reflect the intra-myocyte abnormalities that characterize this patient population.