Search

Interval exercise delays critical mechanical-ventilatory constraints with positive consequences on Dyspnoea and exercise tolerance in COPD. We hypothesized that those advantages of interval exercise would be partially off-set in patients showing excessive ventilation (V˙E) to metabolic demand (V˙CO 2 ). Sixteen men (FEV 1  = 42.3 ± 8.9%) performed, on different days, 30 s and 60 s bouts at 100% peak (on) interspersed by moderate exercise at 40% (off). Nine patients did not sustain exercise for 30 min irrespective of on duration. They presented with higher V˙E/V˙CO 2 nadir (35 ± 3 vs. 30 ± 5) and dead space/tidal volume (0.39 ± 0.05 vs. 0.34 ± 0.06) compared to their counterparts (p < 0.05). [Lactate], operating lung volumes and symptom burden (dyspnoea and leg effort) were also higher (p < 0.05). Unloading off decreased the metabolic-ventilatory demands, thereby allowing 7/9 patients to exercise for 30 min. Increased wasted ventilation accelerates the rate at which critical mechanical constraints and limiting dyspnoea are reached during interval exercise in patients with COPD., (Copyright © 2018 Elsevier B.V. All rights reserved.)

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.

Background: High-frequency neuromuscular electrical stimulation increases exercise tolerance in patients with advanced chronic obstructive pulmonary disease (COPD patients). However, it is conceivable that its benefits are more prominent in patients with better-preserved peripheral muscle function and structure., Objective: To investigate the effects of high-frequency neuromuscular electrical stimulation in COPD patients with better-preserved peripheral muscle function., Design: Prospective and cross-over study., Methods: Thirty COPD patients were randomly assigned to either home-based, high-frequency neuromuscular electrical stimulation or sham stimulation for six weeks. The training intensity was adjusted according to each subject's tolerance. Fat-free mass, isometric strength, six-minute walking distance and time to exercise intolerance (Tlim) were assessed., Results: Thirteen (46.4%) patients responded to high-frequency neuromuscular electrical stimulation; that is, they had a post/pre Δ Tlim >10% after stimulation (unimproved after sham stimulation). Responders had a higher baseline fat-free mass and six-minute walking distance than their seventeen (53.6%) non-responding counterparts. Responders trained at higher stimulation intensities; their mean amplitude of stimulation during training was significantly related to their fat-free mass (r = 0.65; p<0.01). Logistic regression revealed that fat-free mass was the single independent predictor of Tlim improvement (odds ratio [95% CI] = 1.15 [1.04-1.26]; p<0.05)., Conclusions: We conclude that high-frequency neuromuscular electrical stimulation improved the exercise capacity of COPD patients with better-preserved fat-free mass because they tolerated higher training stimulus levels. These data suggest that early training with high-frequency neuromuscular electrical stimulation before tissue wasting begins might enhance exercise tolerance in patients with less advanced COPD.

Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O(2) uptake (Vo(2)(p)) kinetics during exercise, which may stem from inadequate muscle O(2) delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O(2) delivery to uptake during exercise. We tested the hypothesis that, along with slowed Vo(2)(p) kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Qt) following the onset of heavy-intensity exercise. We measured Vo(2)(p), Qt (impedance cardiography), and muscle deoxygenation (near-infrared spectroscopy) during heavy-intensity exercise performed to the limit of tolerance by 10 patients with moderate-to-severe COPD and 11 age-matched sedentary controls. Variables were analyzed by standard nonlinear regression equations. Time to exercise intolerance was significantly (P < 0.05) lower in patients and related to the kinetics of Vo(2)(p) (r = -0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of Vo(2)(p) (42 +/- 13 vs. 73 +/- 24 s) and Qt (67 +/- 11 vs. 96 +/- 32 s), and faster overall kinetics of muscle deoxy-Hb (19.9 +/- 2.4 vs. 16.5 +/- 3.4 s). Consequently, the time constant ratio of O(2) uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O(2) delivery. In conclusion, our data show that patients with moderate-to-severe COPD have impaired central and peripheral cardiovascular adjustments following the onset of heavy-intensity exercise. These cardiocirculatory disturbances negatively impact the dynamic matching of O(2) delivery and utilization and may contribute to the slower Vo(2)(p) kinetics compared with age-matched controls.

Study Objective: To determine the structural and functional consequences of high-frequency neuromuscular electrical stimulation (hf-NMES) in a group of moderately impaired outpatients with chronic obstructive pulmonary disease (COPD)., Design: A prospective, cross-over randomized trial., Setting: An university-based, tertiary center., Patients and Materials: Seventeen patients (FEV(1)=49.6+/-13.4% predicted, Medical Research Council dyspnoea grades II-III) underwent 6-weeks hf-NMES (50Hz) and sham stimulation of the quadriceps femoris in a randomized, cross-over design. Knee strength was measured by isokinetic dynamometry (peak torque) and leg muscle mass (LMM) by DEXA; in addition, median cross-sectional area (CSA) of type I and II fibres and capillary-fibre ratio were evaluated in the vastus lateralis. The 6-min walking distance (6MWD) was also determined., Results: At baseline, patients presented with well-preserved functional capacity, muscle strength and mass: there was a significant relationship between strength and type II CSA (P<0.05). NMES was not associated with significant changes in peak torque, LMM or 6MWD as compared to sham (P>0.05). At micro-structural level, however, electrical stimulation increased type II, but decreased type I, CSA; no change, however, was found in the relative fibre distribution or capillary:fibre ratio (P<0.05). There was no significant association between individual changes in structure and function with training (P>0.05). Post-NMES increase in type II CSA was inversely related to baseline mass and strength (P<0.05)., Conclusion: NMES may promote a modest degree of type II muscle fibre hypertrophy in COPD patients with well-preserved functional status. These micro-structural changes, however, were not translated into increased volitional strength in this sub-population.