Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O2 uptake (V̇o2p) kinetics during exercise, which may stem from inadequate muscle O2 delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O2 delivery to uptake during exercise. We tested the hypothesis that, along with slowed V̇o2p kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Q̇t) following the onset of heavy-intensity exercise. We measured V̇o2p, Q̇t (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 V̇o2p ( r = −0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of V̇o2p (42 ± 13 vs. 73 ± 24 s) and Q̇t (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 O2 uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O2 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 O2 delivery and utilization and may contribute to the slower V̇o2p kinetics compared with age-matched controls.

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.

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 ΔTlim >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.

IMT was effective in improving ventilatory pattern, lung volume, respiratory muscle strength, and the health and vitality domains for quality of life in patients with AT. IMT may be an effective adjunct therapy to drug treatment for patients with AT.

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Exercise intolerance due to impaired oxidative metabolism is a prominent symptom in patients with mitochondrial myopathy (MM), but it is still uncertain whether L-carnitine supplementation is beneficial for patients with MM. The aim of our study was to investigate the effects of L-carnitine on exercise performance in MM. Twelve MM subjects (mean age±SD=35.4±10.8 years) with chronic progressive external ophthalmoplegia (CPEO) were first compared to 10 healthy controls (mean age±SD=29±7.8 years) before they were randomly assigned to receive L-carnitine supplementation (3 g/daily) or placebo in a double-blind crossover design. Clinical status, body composition, respiratory function tests, peripheral muscle strength (isokinetic and isometric torque) and cardiopulmonary exercise tests (incremental to peak exercise and at 70% of maximal), constant work rate (CWR) exercise test, to the limit of tolerance [Tlim]) were assessed after 2 months of L-carnitine/placebo administration. Patients with MM presented with lower mean height, total body weight, fat-free mass, and peripheral muscle strength compared to controls in the pre-test evaluation. After L-carnitine supplementation, the patients with MM significantly improved their Tlim (14±1.9 vs 11±1.4 min) and oxygen consumption (V˙O2) at CWR exercise, both at isotime (1151±115 vs 1049±104 mL/min) and at Tlim (1223±114 vs 1060±108 mL/min). These results indicate that L-carnitine supplementation may improve aerobic capacity and exercise tolerance during high-intensity CWRs in MM patients with CPEO.

Cardiopulmonary exercise testing (CPET) is often helpful to shed light on the mechanisms of exercise intolerance in different clinical populations. Although specific response patterns are rarely pathognomonic, an integrative approach considering metabolic and mechanical–ventilatory responses in addition to limiting symptoms has been valuable to guide further investigations [1].

BackgroundThe use of evaluation tools such as the manovacuometer and respirometer is frequent and disinfection is usually limited to the external surfaces, which is insufficient and raises concerns because of the potential spread of infectious diseases. Hydrophobic heat and moisture exchangers (HME) are used in mechanical ventilation and have microbiological filters, which can possibly reduce contamination, increasing the safety of related procedures. It is unknown, however, if the addition of an exchanger affects the measurements obtained. Aim of this study was to verify if the use of an HME interferes in maximal inspiratory and expiratory pressures assessed using the manovacuometer and vital capacity evaluated using the respirometer in healthy adults.MethodsA controlled transversal trial was carried out. Twenty healthy young adults were included in the study. Vital capacity by respirometer and, maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) were assessed with and without the use of HME.ResultsNo significant difference was found between the values pre and post HME use in vital capacity measurements: (3878.8 ± 202.2 mL vs. 3925.5 ± 206.0 mL, p = 0.116) and the respiratory muscle strength measurements: MIP (−99.0 ± 8.9 vs −95.5 ± 9.0 cm H2O, p = 0.149) and MEP (92.5 ± 7.5 vs 92.5 ± 7.7 cm H2O, p = 1.0) respectively.ConclusionWe conclude that the use of HME does not modify the lung volumes or respiratory muscle strength, and can be used in order to reduce the occurrence of pulmonary infection.