Adherence to walking exercise prescription during pulmonary rehabilitation in COPD with a commercial activity monitor: a feasibility trial.

BackgroundRegular exercise is important in the management of COPD. Pulmonary rehabilitation (PR) facilitates a more physically active lifestyle through exercise participation, ideally without compromising non-exercise physical activity (PA). During PR patients are advised to perform exercise defined by duration and intensity. The extent to which PR attendees participate in unsupervised exercise bouts and their adherence to the exercise prescription provided during PR is unclear. Commercially available devices have the potential to support patients to exercise at their individually prescribed intensity. Study aims were to (1) assess how adherent patients are to their prescribed walking intensity; (2) examine the pattern of overall PA and walking exercise during the course of PR; (3) determine the feasibility of prescribing exercise to PR attendees using an activity monitor; and (4) explore the relationship between exercise and non-exercise PA with routine PR outcome measures.Methods19 patients wore an activity monitor during routine walking tests and 6 weeks of PR, recording in a diary when they exercised. Exercise intensity (cadence) was prescribed from the Endurance Shuttle Walk Test. Patients completed questionnaires, walking tests and a lower limb strength test before and after PR. Repeated ANOVA compared changes in outcomes between weeks 1-6.ResultsPatients wore the monitor every day during PR (median 42 days). Exercise steps increased by 56% (Δ332 [95% CI 54-611] steps/day, p = 0.009) between weeks 1 and 6, with no significant change in non-exercise steps (Δ79 [95% CI - 22 to - 179] steps/day, p = 0.13). Patients reported exercising on 70% of days. Adherence to prescribed cadence was achieved 55% of time spent exercising, and did not change across the 6 weeks (p = 0.907). Change in total daily steps was associated with improved dyspnea (p = 0.027), Chronic Respiratory Questionnaire (CRQ) Dyspnea domain (p = 0.019), CRQ Emotional Functioning domain (p = 0.001) and CRQ Mastery domain scores (p = 0.001) but not with exercise capacity or lower limb muscle strength.ConclusionsImprovements in exercise participation, not at the expense of non-exercise PA, throughout a PR course was observed in attendees provided with a commercially available activity monitor. Wearable technology may be able to support effective remote walking exercise prescription and participation during PR. Trial registration (retrospectively registered): http://www.isrctn.com/ISRCTN15892972

Interchangeability of research and commercial wearable device data for assessing associations with cardiometabolic risk markers

Introduction: Whilst there is evidence on agreement, it is unknown whether commercial wearables can be used as surrogates for research grade devices when investigating links with markers of cardiometabolic risk. Therefore, the aim of this study was to investigate if data from a commercial wearable device could be used to assess associations between behaviour and cardiometabolic risk markers, compared to physical activity from a research grade monitor. Methods: Forty-five adults concurrently wore a wrist-worn Fitbit Charge 2 and a waist-worn ActiGraph wGT3X-BT during waking hours over 7 consecutive days. Log-linear regression models were fitted, and predictive fit via a 1-out cross-validation was performed for each device between behavioural (steps, light and moderate-to-vigorous physical activity) and cardiometabolic variables (body mass index [BMI], weight, body fat %, systolic and diastolic blood pressure, glycated haemoglobin, grip strength, estimated maximal oxygen uptake and waist circumference). Results: Overall, step count was the most consistent predictor of cardiometabolic risk factors, with negative associations across both Fitbit and ActiGraph devices for BMI (-0.017 vs. -0.020, p Conclusions: Step count data from a commercial grade wearable device showed similar associations and predictive relationships with cardiometabolic risk markers compared to a research-grade wearable device, providing preliminary support for their use in health research.</p

Changes in physical activity, sedentary behaviour, and sleep following pulmonary rehabilitation: a systematic review and network meta-analysis

No description supplie

Changes in physical activity, sedentary behaviour, and sleep following pulmonary rehabilitation: a systematic review and network meta-analysis

No description supplie

A comparison of daily physical activity profiles between adults with severe asthma and healthy controls.

Severe asthma is associated with a substantial burden of disease including premature death and reduced quality adjusted life years [1]. Care in specialist centres is associated with reduced exacerbation rates and healthcare utilisation, but at the cost of increased use of systemic steroids and increased body mass index (BMI) [2]. Common co-comorbidities such as metabolic syndrome and type 2 diabetes are associated with low levels of moderate-vigorous physical activity (MVPA) [3]. Guidelines recommend that adults accumulate either =150 minutes of moderate intensity activity or =75 minutes of vigorous intensity activity per week, accumulated in bouts of any length [4]. Adults with severe asthma may avoid MVPA due to negative expectations and fear-avoidance beliefs [5]. A few small studies have reported that daily step count and time spent in MVPA may be reduced in adults with severe asthma compared to controls [6–8]. However, results are conflicting when physical activity levels are adjusted for confounders such as age, gender, obesity and smoking [7]. Furthermore, adults with severe asthma have reduced health-related quality of life (HRQoL) but whether physical activity levels impact on HRQoL is unknown [9].</p

Pharmacodynamic Effect of Emixustat on Rod Function.

<p>The recovery of rod photoreceptor function following a photobleach was measured by ERG. Mice were treated with varied doses of emixustat (n = 4/dose group), or vehicle (n = 4/group), and ERG responses were recorded every 2 minutes for 50 minutes using a light stimulus 0.01 cd*s/m². Panel A shows representative ERG waveforms in vehicle- and emixustat-treated mice. Arrows in panel A indicate the b-wave amplitude peaks which are plotted as a function of recovery time after photobleach in panel B. B-wave response amplitudes (μV), at each corresponding time point of recovery, are shown as mean values ± SEMfor each of the treatment groups (panel B). Emixustat treatment caused a dose-dependent suppression of b-wave response amplitudes. The dose required for half-maximal suppression of ERG b-wave recovery was determined to be 0.21 mg/kg.</p

Protection from Light Damage.

<p>The ability of emixustat to provide protection from light damage was assessed as described in <i>Methods</i>. Mice received a single dose of emixustat, or vehicle, prior to light exposure (8,000 lux white light, 1 hour). Histological analyses and determination of ONL thickness was performed following a 2-week recovery period. Panel A shows tissue sections prepared from untreated, dark-adapted mice, untreated light-exposed mice, and mice pre-treated with either 0.3 or 1.0 mg/kg emixustat (ONL, outer nuclear layer; INL, inner nuclear layer; GCL, ganglion cell layer). Quantitative analysis of ONL layer thickness (panel B) was used to calculate the ED₅₀ for preservation of the ONL in emixustat-treated mice (ED₅₀ = 0.20 mg/kg). There was a statistically significant preservation of ONL thickness in mice treated with 1.0 or 3.0 mg/kg emixustat compared to the vehicle-treated, light control group (*, p<0.01).</p

Processing of Vitamin A in The Visual Cycle.

<p>Enzymatic processing within the visual cycle begins with delivery of vitamin A (all-<i>trans</i>-retinol) from the blood circulation. Upon entry into the RPE, all-<i>trans</i>-retinol is converted to a retinyl ester through the activity of lecithin retinol acyl transferase (1). The resulting all-<i>trans</i>-retinyl ester pool represents a storage form of vitamin A upon which RPE65 acts to generate 11-<i>cis</i>-retinol (2); 11-<i>cis</i>-retinol is then oxidized by an 11-<i>cis</i>-specific retinol dehydrogenase to form the visual chromophore, 11-<i>cis</i>-retinal (3). The visual chromophore is delivered to rod and cone outer segments (4) where it combines with opsins to form visual pigments (e.g., rhodopsin). Light activation of rhodopsin initiates visual transduction processes and liberates all-<i>trans</i>-retinal as a photoproduct. Reduction of all-<i>trans</i>-retinal, via all-<i>trans</i>-retinal dehydrogenase, produces all-<i>trans</i>-retinol (5), which is transferred back to the RPE for recycling. The continued activity of RPE65 in the light state ensures sustained levels of rhodopsin, closure of ion channels through transducin activation, and reduced oxygen demand.</p

Reduced Lipofuscin Autofluorescence and A2E Accumulation.

<p>The effect of emixustat on lipofuscin autofluorescence and A2E levels was examined in an animal model of autosomal recessive Stargardt disease (<i>Abca4</i>^-/- mice). Histological analysis of lipofuscin autofluorescence in untreated, strain- and age-matched wild-type mice, and <i>Abca4</i>^-/- mice treated with either vehicle or emixustat (0.3 or 3.0 mg/kg) is shown in panels A—D, respectively. All mice were 5 months of age. Lipofuscin fluorophores were extracted from RPE eyecups and analyzed by HPLC as described in <i>Methods</i>. Representative chromatograms from eyecup extracts of mice treated with emixustat (3 mg/kg for 3 months) and vehicle (red and black tracings, respectively) are shown in panel E. UV-vis spectra associated with the indicated peaks (numbered 1–5) are shown in the panel inset. Peak 1 in the chromatogram was determined to be A2E based upon spectral identity and co-elution with an authentic A2E standard. Quantitative analysis of A2E levels (based on area units of peak 1) in <i>Abca4</i>^-/- mice is shown in panel F (peaks 2–4 were not quantified). Numbers of mice analyzed for A2E quantitation are as follows: Day 0: n = 17; Vehicle: n = 6; 0.03 mg/kg: n = 6; 0.1 mg/kg: n = 7; 0.3 mg/kg, n = 8 1.0 mg/kg, n = 8; 3 mg/kg, n = 8. A2E levels increased from ~5 to ~20 pmoles/eye over a 3-month period in vehicle-treated <i>Abca4</i>^-/- mice. <i>Abca4</i>^-/- mice treated with emixustat showed a dose-dependent reduction of A2E which was statistically significant at doses ≥ 0.30 mg/kg/day, relative to vehicle treated <i>Abca4</i>^-/- mice (*, p<0.05). The ED₅₀ for the effect of emixustat on reducing accumulation of A2E was 0.47 mg/kg/day.</p

Reduced Retinal Neovascularization.

<p>The effect of emixustat on retinal neovascularization was studied in the mouse OIR model. Seven day-old mouse pups were subjected to hyperoxia (75% oxygen) for 5 days. On P12, the mice were returned to room air and daily treatments with ruboxistaurin (10 mg/kg), emixustat (0.03–3.0 mg/kg), or appropriate vehicles were administered as described in <i>Methods</i>. Retinal flat mounts were prepared and areas of NV were quantified; these data were compared to data from control mice that were maintained in a normoxic environment (21% oxygen). Mice that were moved from a hyperoxic to normoxic environment, without treatment, showed a significant extent of retinal NV (~30% of the retinal area). Treatment with the ruboxistaurin (positive control) reduced the area of NV to ~20% of the total retinal area. In mice treated with emixustat, a dose-dependent reduction in retinal NV was observed. The reduction in NV at the highest emixustat dose (3.0 mg/kg/day) approached a level that was comparable to that obtained with ruboxistaurin (Fig 6A; *, t-test, p<0.05). The ED₅₀ for reduction of retinal NV in emixustat-treated mice was 0.46 mg/kg/day. Representative retinal flat mounts from an untreated, normoxic control, an untreated OIR control, and in a 3 mg/kg emixustat-treated mouse are shown in panels B, C, and D, respectively. Areas of NV, outlined in red tracings, were identified and quantified using Adobe Photoshop software.</p