Current Status of Pulmonary Rehabilitation: Introductory Remarks on Pulmonary Rehabilitation, the Importance and the Practice.

In 1994, the Pulmonary Education and Research Foundation released a VHS tape, a program for the health-care professional, entitled "Essentials of Pulmonary Rehabilitation—Taking Control of Life Aga..

Reproducibility of NIRS Assessment of Muscle Oxidative Capacity in Smokers With and Without COPD

Low muscle oxidative capacity contributes to exercise intolerance in chronic obstructive pulmonary disease (COPD). Near-infrared spectroscopy (NIRS) allows non-invasive determination of the muscle oxygen consumption (mV̇O2) recovery rate constant (k), which is proportional to oxidative capacity assuming two conditions are met: 1) exercise intensity is sufficient to fully-activate mitochondrial oxidative enzymes; 2) sufficient O2 availability. We aimed to determine reproducibility (coefficient of variation, CV; intraclass correlation coefficient, ICC) of NIRS k assessment in the gastrocnemius of 64 participants with (FEV1 64 ± 23%predicted) or without COPD (FEV1 98 ± 14%predicted). 10–15 s dynamic contractions preceded 6 min of intermittent arterial occlusions (5–10 s each, ∼250 mmHg) for k measurement. k was lower (P < 0.05) in COPD (1.43 ± 0.4 min−1; CV = 9.8 ± 5.9%, ICC = 0.88) than controls (1.74 ± 0.69 min−1; CV = 9.9 ± 8.4%; ICC = 0.93). Poor k reproducibility was more common when post-contraction mV̇O2 and deoxygenation were low, suggesting insufficient exercise intensity for mitochondrial activation and/or the NIRS signal contained little light reflected from active muscle. The NIRS assessment was well tolerated and reproducible for muscle dysfunction evaluation in COPD

Reliability and Physiological Interpretation of Pulmonary Gas Exchange by "Circulatory Equivalents" in Chronic Heart Failure

Peak ratios of pulmonary gas-exchange to ventilation during exercise (V˙O2/V˙E and V˙CO2/V˙E, termed "circulatory equivalents") are sensitive to heart failure (HF) severity, likely reflecting low and/or poorly distributed pulmonary perfusion. We tested whether peak V˙O2/V˙E and V˙CO2/V˙E would: (1) distinguish HF patients from controls; (2) be independent of incremental exercise protocol; and (3) correlate with lactate threshold (LT) and ventilatory compensation point (VCP), respectively.Twenty-four HF patients (61±11 years) with reduced ejection fraction (31±8%) and 11 controls (63±7 years) performed ramp-incremental cycle ergometry. Eighteen HF patients also performed slow (5±1 W/min), medium (9±4 W/min), and fast (19±6 W/min) ramps. Peak V˙O2/V˙E and V˙CO2/V˙E from X-Y plot, and LT and VCP from 9-panel plot, were determined by 2 independent, blinded, assessors. Peak V˙O2/V˙E (31.2±4.4 versus 41.8±4.8 mL/L; P<0.0001) and V˙CO2/V˙E (29.3±3.0 versus 36.9±4.0 mL/L; P<0.0001) were lower in HF than controls. Within individuals, there was no difference across 3 ramp rates in peak V˙O2/V˙E (P=0.62) or V˙CO2/V˙E (P=0.97). Coefficient of variation (CV) in peak V˙O2/V˙E was lower than for LT (5.1±2.1% versus 8.2±3.7%; P=0.014), and coefficient of variation in peak V˙CO2/V˙E was lower than for VCP (3.3±1.8% versus 8.7±4.2%; P<0.001). In all participants, peak V˙O2/V˙E was correlated with, but occurred earlier than, LT (r2=0.94; mean bias, -0.11 L/min), and peak V˙CO2/V˙E was correlated with, but occurred earlier than, VCP (r2=0.98; mean bias -0.08 L/min).Peak circulatory equivalents during exercise are strongly associated with (but not identical to) LT and VCP. Peak circulatory equivalents are reliable, objective, effort-independent indices of gas-exchange abnormality in HF

FHL1 activates myostatin signalling in skeletal muscle and promotes atrophy

Myostatin is a TGFβ family ligand that reduces muscle mass. In cancer cells, TGFβ signalling is increased by the protein FHL1. Consequently, FHL1 may promote signalling by myostatin. We therefore tested the ability of FHL1 to regulate myostatin function. FHL1 increased the myostatin activity on a SMAD reporter and increased myostatin dependent myotube wasting. In mice, independent expression of myostatin reduced fibre diameter whereas FHL1 increased fibre diameter, both consistent with previously identified effects of these proteins. However, co‐expression of FHL1 and myostatin reduced fibre diameter to a greater extent than myostatin alone. Together, these data suggest that the expression of FHL1 may exacerbate muscle wasting under the appropriate conditions

Testosterone and resistance training effects on muscle nitric oxide synthase isoforms in COPD men

SummaryBackgroundSkeletal muscle dysfunction contributes to exercise limitation in COPD. The role of the nitric oxide synthase (NOS) system in muscle dysfunction is ill defined. Reduced levels of endothelial NOS (eNOS) and elevated levels of inducible NOS (iNOS) in the skeletal muscle of COPD patients have been recently reported. We hypothesized that resistance exercise training (R) and/or testosterone supplementation (T) would alter the transcription and expression of the NOS isoenzymes in COPD skeletal muscle.MethodsVastus lateralis biopsies were obtained before and after a 10-week intervention in 40 men with severe COPD(age 67.7 ± 8.3, FEV1 41.4 ± 12.6% predicted): placebo + no training (P) (n = 11), placebo + resistance training (PR) (n = 8), testosterone + no training (T) (n = 11) and testosterone + resistance training (TR) (n = 10) groups. eNOS, nNOS and iNOS mRNA and protein levels were measured in each sample. mRNA and protein levels were measured using real-time PCR and enzyme-linked immunosorbant assay, respectively.ResultseNOS mRNA increased in the TR group compared to P and T groups (P < 0.001). eNOS protein was increased in TR and T groups after intervention (P < 0.05) but not in the PR group. nNOS protein increased in the PR, T, and TR groups (P < 0.05). iNOS protein decreased only in the TR group (P = 0.01).ConclusionResistance training and testosterone supplementation increased eNOS and nNOS proteins and decreased iNOS protein in the skeletal muscles of men with COPD. These changes in NO system might explain some of the favorable effects of these therapies

A Novel Waveform to Extract Exercise Gas Exchange Response Dynamics: The Chirp Waveform

Characterizing exercise gas exchange response dynamics reveals important information about physiological control processes and cardiopulmonary dysfunction. However, current methods for extracting exercise response dynamics typically use multiple step-wise transitions, limiting applicability of this technique. PURPOSE: We designed a new protocol (chirp waveform) to extract exercise gas exchange response dynamics in a single visit. We tested the hypothesis that gas exchange response dynamics extracted from chirp forcing would be similar to those extracted from step-wise transitions. METHODS: Thirty-one participants (14 young healthy, 7 older healthy, and 10 patients with chronic obstructive pulmonary disease) visited the laboratory on three occasions. On visit 1, participants performed a ramp incremental test to determine the gas exchange threshold (GET). On visits 2-3, participants performed either a chirp or step-wise protocol in a randomized order. Chirp forcing consisted of sinusoidal fluctuations in work rate with constant amplitude and progressive shortening of sine periods. Square protocol consisted of 3 square-wave transitions each of 6 min duration. Work rate amplitude (from 20 W to ~95% of the individual’s GET) and exercise duration (30 min) were the same in both protocols. The input-output relationship was characterized using a first-order linear transfer function containing a system gain (K) and time constant (τ) [G(s)= K/(τ×s+1)]. Parameter identification was performed in Matlab using the Matlab System Identification toolbox. Agreement between measures was established using Bland-Altman analysis and Rothery’s Concordance Coefficient (RCC). RESULTS: No systematic bias (mean difference of chirp minus square-wave; Δmean) and good reliability was found for V̇O2 K [Δmean: 0.25(1.03) mL/min/W, p=0.179; RCC: 0.773, p=0.004], V̇O2 τ [Δmean: 0.30(7.08) s, p=0.815; RCC: 0.837, p2 K [Δmean: -0.19(1.57) mL/min/W, p=0.512; RCC: 0.827, pp=0.009] and good reliability (RCC: 0.794, p2 τ. CONCLUSION: The chirp waveform allows extraction of gas exchange response dynamics similar to those obtained from standard methods, thus overcoming the need for multiple tests

PHYSICAL PERFORMANCE AND BODY COMPOSITION IN MAINTENANCE HEMODIALYSIS (MHD) PATIENTS

BackgroundMHD patients (pts) often display protein-energy wasting, sarcopenia & diminished physical performance. This study was undertaken to assess the relationship between body composition & physical performance in MHD pts.MethodsBody composition, assessed by dual energy x-ray absorptiometry and body mass index (BMI), were compared to 3 measures of physical performance: 6-minute walking distance (6-MW), sit-to-stand testing and stair climb. 52 clinically stable MHD pts (≥6 mo) and 21 matched normal controls were examined in this ongoing study.ResultsPts were 53±13SD yrs, 33% female; 38% diabetic; dialysis vintage was 62±52 months. Normals were 52 years and 43% female. MHD pts had higher % body fat than Normals. 6-MW and sit to stand cycles were much lower in MHD men and women than in Normal men and women. 6MW in MHD and Normals were 445 vs 630 meters, respectively (p<.001). In men but not women, time to climb 22 stairs was greater in MHD pts then in Normals (p=.03). Unadjusted analyses in MHD indicated that 6-MW distance correlated negatively with lean body mass index (LBMI, kg of LBM/m2; r=-0.37; p<0.01) and % body fat (r=-0.33; p= 0.02); stair climb time correlated negatively with lean leg mass (r=-0.32, p=0.03) and total leg mass (r=-0.29, p=0.045).). Sit-to-stand did not correlate with any body composition measure. 6-MW adjusted for age and gender correlated negatively with LBMI (r=-0.29; p=0.04).There were no associations between BMI (range, 19.8-44.2 kg/m2) and physical performance.ConclusionsThese findings indicate that adult MHD pts had a higher % body fat. Measures of physical performance were markedly reduced in MHD pts as compared to Normals. Physical performance in MHD, measured especially by 6-MW, correlated negatively with some measures of body composition, particularly with LBMI

Skeletal muscle power and fatigue at the tolerable limit of ramp-incremental exercise in COPD

Muscle fatigue (a reduced power for a given activation) is common following exercise in COPD. Whether muscle fatigue, and reduced maximal voluntary locomotor power, are sufficient to limit whole-body exercise in COPD is unknown. We hypothesized in COPD: 1) exercise is terminated with a locomotor muscle power reserve; 2) reduction in maximal locomotor power is related to ventilatory limitation; and 3) muscle fatigue at intolerance is less than age-matched controls. We used a rapid switch from hyperbolic to isokinetic cycling to measure the decline in peak isokinetic power at the limit of incremental exercise ('performance fatigue') in 13 COPD (FEV1 49±17 %pred) and 12 controls. By establishing the baseline relationship between muscle activity and isokinetic power, we apportioned performance fatigue into the reduction in muscle activation and muscle fatigue. Peak isokinetic power at intolerance was ~130% of peak incremental power in controls (274±73 vs 212±84W, p<0.05), but ~260% in COPD (187±141 vs 72±34W, p<0.05) - greater than controls (p<0.05). Muscle fatigue as a fraction of baseline peak isokinetic power was not different in COPD vs controls (0.11±0.20 vs 0.19±0.11). Baseline to intolerance, the median frequency of maximal isokinetic muscle activity was unchanged in COPD but reduced in controls (+4.3±11.6 vs -5.5±7.6%, p<0.05). Performance fatigue as a fraction of peak incremental power was greater in COPD vs controls and related to resting (FEV1/FVC) and peak exercise (V̇E/MVV) pulmonary function (r2=0.47, r2=0.55, p<0.05). COPD patients are more fatigable than controls, but this fatigue is insufficient to constrain locomotor power and define exercise intolerance

A new bronchodilator response grading strategy ıdentifies distinct patient populations

Rationale: A positive bronchodilator response (BDR) according to American Thoracic Society/European Respiratory Society (ATS/ERS) guidelines require both 200 ml and 12% increase in forced expiratory volume in 1 second (FEV1) or forced vital capacity (FVC) after bronchodilator inhalation. This dual criterion is insensitive in those with high or low FEV1. Objectives: To establish BDR criteria with volume or percentage FEV1 change. Methods: The largest FEV1 and FVC were identified fromthree pre- and three post-bronchodilator maneuvers in COPDGene (Genetic Epidemiology of COPD) participants. A total of 7,741 individuals with coefficient of variation less than 15% for both FEV1 and FVC formed bronchodilator categories of FEV1 response: negative (0.00% to 0.00 L to 9.00% to 16.00% to 0.16 L to 26.00% or >0.26 L). These response size categories are based on empirical limits considering average FEV1 increase of approximately 160 ml and the clinically important difference for FEV1. To compare flow and volume response characteristics, BDR-FEV1 category assignments were applied for the BDR-FVC response. Results: Twenty percent met mild and 31% met moderate or marked BDR-FEV1 criteria, whereas 12% met mild and 33% met moderate or marked BDR-FVC criteria. In contrast, only 20.6% met ATS/ERS positive criteria. Compared with the negative BDR-FEV1 category, the minimal, mild, moderate, and marked BDR-FEV1 categories were associated with greater 6-minute-walk distance and lower St. George's Respiratory Questionnaire and modified Medical Research Council dyspnea scale scores. Compared with negative BDR, moderate and marked BDR-FEV1 categories were associated with fewer exacerbations, and minimal BDR was associated with lower computed tomography airway wall thickness. Compared with the negative category, all BDR-FVC categories were associated with increasing emphysema percentage and gas trapping percentage. Moderate and marked BDR-FVC categories were associated with higher St. George's Respiratory Questionnaire scores but fewer exacerbations and lower dyspnea scores. Conclusions: BDR grading by FEV1 volume or percentage response identified subjects otherwise missed by ATS/ERS criteria. BDR grades were associated with functional exercise performance, quality of life, exacerbation frequency, dyspnea, and radiological airway measures. BDR grades in FEV1 and FVC indicate different clinical and radiological characteristics.United States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Heart Lung & Blood Institute (NHLBI)National Center for Advancing Translational Sciences through UCLA CTSI Gran

ERS statement on standardisation of cardiopulmonary exercise testing in chronic lung diseases

The objective of this document was to standardise published cardiopulmonary exercise testing (CPET) protocols for improved interpretation in clinical settings and multicentre research projects. This document: 1) summarises the protocols and procedures used in published studies focusing on incremental CPET in chronic lung conditions; 2) presents standard incremental protocols for CPET on a stationary cycle ergometer and a treadmill; and 3) provides patients’ perspectives on CPET obtained through an online survey supported by the European Lung Foundation. We systematically reviewed published studies obtained from EMBASE, Medline, Scopus, Web of Science and the Cochrane Library from inception to January 2017. Of 7914 identified studies, 595 studies with 26 523 subjects were included. The literature supports a test protocol with a resting phase lasting at least 3 min, a 3-min unloaded phase, and an 8- to 12-min incremental phase with work rate increased linearly at least every minute, followed by a recovery phase of at least 2–3 min. Patients responding to the survey (n=295) perceived CPET as highly beneficial for their diagnostic assessment and informed the Task Force consensus. Future research should focus on the individualised estimation of optimal work rate increments across different lung diseases, and the collection of robust normative data.The document facilitates standardisation of conducting, reporting and interpreting cardiopulmonary exercise tests in chronic lung diseases for comparison of reference data, multi-centre studies and assessment of interventional efficacy. http://bit.ly/31SXeB