Noninvasive prediction of Blood Lactate through a machine learning-based approach.

We hypothesized that blood lactate concentration([Lac]blood) is a function of cardiopulmonary variables, exercise intensity and some anthropometric elements during aerobic exercise. This investigation aimed to establish a mathematical model to estimate [Lac]blood noninvasively during constant work rate (CWR) exercise of various intensities. 31 healthy participants were recruited and each underwent 4 cardiopulmonary exercise tests: one incremental and three CWR tests (low: 35% of peak work rate for 15 min, moderate: 60% 10 min and high: 90% 4 min). At the end of each CWR test, venous blood was sampled to determine [Lac]blood. 31 trios of CWR tests were employed to construct the mathematical model, which utilized exponential regression combined with Taylor expansion. Good fitting was achieved when the conditions of low and moderate intensity were put in one model; high-intensity in another. Standard deviation of fitting error in the former condition is 0.52; in the latter is 1.82 mmol/liter. Weighting analysis demonstrated that, besides heart rate, respiratory variables are required in the estimation of [Lac]blood in the model of low/moderate intensity. In conclusion, by measuring noninvasive cardio-respiratory parameters, [Lac]blood during CWR exercise can be determined with good accuracy. This should have application in endurance training and future exercise industry

Exercise Training in Patients With Non-Small Cell Lung Cancer During In-Hospital Chemotherapy Treatment: A RANDOMIZED CONTROLLED TRIAL.

PurposeThe aim of this study was to perform a randomized trial to assess the impact of exercise training in patients with non-small cell lung cancer during chemotherapy on several outcomes in comparison to a control group (CG).MethodsThe exercise training group (ETG) consisted of 20 patients and the CG consisted of 10 patients. In the ETG, a 4-wk in-hospital exercise training program was performed in 2-wk cycles interspersed with consecutive rounds of chemotherapy with cytostatic drugs. The exercise training program was individualized and included warm-up, respiratory muscle exercise, training on a cycle ergometer or treadmill, and Nordic walking. CG participants were assessed before and after 6 wk of chemotherapy alone.ResultsComparing pre- and post-intervention values, the ETG demonstrated an increase in 6-min walk distance (486 ± 92 vs 531 ± 103 m, P = .01). In a battery of physical performance tests: Up and Go Test (6.3 ± 1.0 vs 6.0 ± 1.1 sec, P = .01); chair stand (13.3 ± 2.8 vs 14.3 ± 3.4 repetitions, P = .001); and arm curl (18.4 ± 3.1 vs 20.4 ± 3.5 repetitions, P = .001) all improved significantly. Spirometry values also improved: FEV1 % predicted (76 ± 16 vs 84 ± 15, P = .01), FVC % predicted (87 ± 14 vs 95 ± 13, P = .01), and FEV1/FVC (73 ± 13% vs 76 ± 12%, P = .04). The exercise training was well tolerated, without any adverse events due to exercise. There were no significant improvements in the CG.ConclusionsThis study suggests that planned, individualized, and supervised exercise programs in patients with advanced lung cancer during chemotherapy are a practical and beneficial intervention for enhancing mobility and physical fitness

Nano-optical observation of cascade switching in a parallel superconducting nanowire single photon detector

The device physics of parallel-wire superconducting nanowire single photon detectors is based on a cascade process. Using nano-optical techniques and a parallel wire device with spatially-separate pixels we explicitly demonstrate the single- and multi-photon triggering regimes. We develop a model for describing efficiency of a detector operating in the arm-trigger regime. We investigate the timing response of the detector when illuminating a single pixel and two pixels. We see a change in the active area of the detector between the two regimes and find the two-pixel trigger regime to have a faster timing response than the one-pixel regime.Comment: 11 pages, 2 figure

Relationship between diffusion capacity and small airway abnormality in COPDGene.

Impaired single breath carbon monoxide diffusing capacity (DLCO) is associated with emphysema. Small airways disease (SAD) may be a precursor lesion to emphysema, but the relationship between SAD and DLCO is undescribed. We hypothesized that in mild COPD, functional SAD (fSAD) defined by computed tomography (CT) and Parametric Response Mapping methodology would correlate with impaired DLCO. Using data from ever-smokers in the COPDGene cohort, we established that fSAD correlated significantly with lower DLCO among both non-obstructed and GOLD 1-2 subjects. The relationship between DLCO with CT-defined emphysema was present in all GOLD stages, but most prominent in severe disease. TRIAL REGISTRATION: NCT00608764. Registry: COPDGene. Registered 06 February 2008, retrospectively registered

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

Protocol for a randomized controlled trial of moderate intensity interval training in individuals with chronic obstructive pulmonary disease and obstructive sleep apnea overlap syndrome who have excessive daytime sleepiness.

BACKGROUND: The term Overlap Syndrome (OS) describes the presence of both chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) in a single individual. Excessive daytime sleepiness (EDS) is a common symptom of OS shown to be associated with an increased risk of cardiovascular disease (CVD) that could be reduced through exercise. Thus, we propose to investigate a novel exercise intervention in individuals with the EDS-OS phenotype as they are at highest risk of CVD yet have the greatest barriers to exercise. METHODS: We will conduct a single-site, randomized, two-arm, parallel group-controlled exercise trial in individuals with EDS-OS. The Epworth Sleepiness Scale (ESS) will be assessed at baseline. Individuals with OS and the EDS-OS phenotype (ESS &gt;10) (n&nbsp;=&nbsp;46) will be randomized to a moderate intensity interval training (MIIT, i.e. intervals of 5&nbsp;min at 50% VO2peak followed by 3&nbsp;min of active recovery at 10% VO2peak) or a control group of standard of care. We will investigate if MIIT intervention decreases the risk of CVD in EDS-OS, which will be assessed by: 1) quality of life, measured by the 36-Item Short Form Health Survey; 2) physical activity, measured by daily step counts; and 3) cardiovascular health, assessed as VO2peak, flow-mediated dilation and serum high sensitivity C-reactive protein, lipids, and glucose. CONCLUSION: Our findings will guide future development and implementation of exercise interventions that could reduce the risk of CVD in the understudied EDS-OS phenotype

Heme metabolism genes Downregulated in COPD Cachexia.

IntroductionCachexia contributes to increased mortality and reduced quality of life in Chronic Obstructive Pulmonary Disease (COPD) and may be associated with underlying gene expression changes. Our goal was to identify differential gene expression signatures associated with COPD cachexia in current and former smokers.MethodsWe analyzed whole-blood gene expression data from participants with COPD in a discovery cohort (COPDGene, N = 400) and assessed replication (ECLIPSE, N = 114). To approximate the consensus definition using available criteria, cachexia was defined as weight-loss &gt; 5% in the past 12 months or low body mass index (BMI) (&lt; 20 kg/m2) and 1/3 criteria: decreased muscle strength (six-minute walk distance &lt; 350 m), anemia (hemoglobin &lt; 12 g/dl), and low fat-free mass index (FFMI) (&lt; 15 kg/m2 among women and &lt; 17 kg/m2 among men) in COPDGene. In ECLIPSE, cachexia was defined as weight-loss &gt; 5% in the past 12 months or low BMI and 3/5 criteria: decreased muscle strength, anorexia, abnormal biochemistry (anemia or high c-reactive protein (&gt; 5 mg/l)), fatigue, and low FFMI. Differential gene expression was assessed between cachectic and non-cachectic subjects, adjusting for age, sex, white blood cell counts, and technical covariates. Gene set enrichment analysis was performed using MSigDB.ResultsThe prevalence of COPD cachexia was 13.7% in COPDGene and 7.9% in ECLIPSE. Fourteen genes were differentially downregulated in cachectic versus non-cachectic COPD patients in COPDGene (FDR &lt; 0.05) and ECLIPSE (FDR &lt; 0.05).DiscussionSeveral replicated genes regulating heme metabolism were downregulated among participants with COPD cachexia. Impaired heme biosynthesis may contribute to cachexia development through free-iron buildup and oxidative tissue damage