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.

Background: Obese subjects are at increased risk of developing obstructive sleep apnea syndrome (OSAS). However, the individual role of local (i.e., upper airway-related) and general (clinical and whole-body anthropometric) characteristics in determining OSAS in obese patients is still controversial. Objectives: To contrast the clinical, anthropometric and upper airway anatomical features of obese subjects presenting or not presenting with OSAS. Methods: Thirty-seven obese (BMI ≧30 kg/m²) males with OSAS and 14 age- and gender-matched obese controls underwent clinical and anthropometric (BMI, waist-to-hip ratio and neck circumference) evaluation. In a subgroup of subjects (18 and 11 subjects, respectively), magnetic resonance imaging (MRI) during wakefulness was used to study the upper airway anatomy. Results: OSAS patients showed significantly higher BMI, waist-to-hip ratio and neck circumference as compared to controls (p < 0.05). They also referred to nonrepairing sleep, impaired attention, and previous car accidents more frequently (p < 0.05). The transversal diameter of the airways (TDAW) at the retroglossal level by MRI was found to be an independent predictor of the presence and severity of OSAS (p < 0.05). Parapharyngeal fat increase, however, was not related to OSAS. A TDAW >12 mm was especially useful to rule out severe OSAS (apnea-hypopnea index >30, negative predictive value = 88.9%, likelihood ratio for a negative test result = 0.19). Conclusions: MRI of the upper airway can be used in association with clinical and anthropometric data to identify obese males at increased risk of OSAS.

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The purpose of this study was to investigate the relationships between peripheral muscle structure (mass) and function (strength, endurance, and maximal aerobic capacity) in patients with chronic obstructive pulmonary disease (COPD) with different nutritional states. Thirty-nine patients (31 male) with moderate-severe COPD (63.5 ± 7.3 [SD] years) and 17 controls (14 male; 64.7 ± 5.5 [SD] years) underwent isokinetic (peak torque [PT]), isometric (isometric torque [IT]), and endurance strength (total work [TW]) measurements of the knee extensor muscles and a maximal cardiopulmonary exercise test to evaluate the maximal aerobic capacity (peak oxygen uptake [VO(2)] peak). Muscle mass (MM) was determined using dual-energy x-ray absorptiometry. Patients with COPD presented with reduced muscle function as compared with the healthy controls: PT (105.9 ± 33.9 vs. 134.3 ± 30.9, N·m(-1), respectively, p < 0.05), TW (1,446.3 ± 550.8 vs. 1,792.9 ± 469.1 kJ, respectively, p < 0.05), and VO(2)peak (68.1 ± 15.1 vs. 93.7 ± 14.5, % pred, respectively, p < 0.05). Significant relationships were found between muscle structure and function (strength and endurance) in the patient subgroup with preserved MM and in the control group: PT·MM(r(2) = 0.36; p = 0.01 vs. r(2) = 0.32; p = 0.01, respectively) and TW·MM (r(2) = 0.32; p = 0.01 vs. r(2) = 0.22; p = 0.05, respectively). Strength corrected for mass normalized this function in both patient subgroups, whereas endurance was normalized only in the patient subgroup without muscle depletion. Maximal aerobic capacity remained reduced, despite the correction, in both patient subgroups (depleted or nondepleted) compared with the healthy controls (VO(2)peak.MM: 9.1 ± 3.7 vs. 21.8 ± 4.9 vs. 28.5 ± 4.2 ml·min·kg, respectively, with p < 0.01 among groups). Muscle atrophy seems to be the main determinant of strength reduction among patients with moderate-severe COPD, whereas endurance reduction seems to be more related to imbalance between oxygen delivery and consumption than to the local muscle structure itself. Peripheral MM did not constitute a good predictor for maximal aerobic capacity in this population. The main practical application of this study is to point out a crucial role for the strategies able to ameliorate cardiorespiratory and muscular fitness in patients with COPD, even in those patients with preserved MM.