77 research outputs found

    Lifestyle Behavior Change in Patients With Nonalcoholic Fatty Liver Disease:A Qualitative Study of Clinical Practice

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    Nonalcoholic fatty liver disease (NAFLD) is the most common liver condition worldwide and is linked largely to obesity and inactivity. Lifestyle modification is the primary treatment for NAFLD targeting dietary change, physical activity, and exercise to facilitate weight loss and weight loss maintenance. This has been shown to reduce steatosis and ameliorate steatohepatitis. European Clinical Practice Guidelines for the management of NAFLD highlight the importance of targeting lifestyle behavior change in all patients with NAFLD regardless of disease severity. These guidelines recommend combining dietary restriction and a progressive increase in aerobic exercise and resistance training with a focus on tailoring interventions to the individual patient. Practice guidelines published by the American Association for the Study of Liver Diseases recommend weight loss of at least 3% to 5% of body weight via hypocaloric diet or diet combined with increased physical activity but state that these lifestyle interventions should target patients with nonalcoholic steatohepatitis. Given the benefits of lifestyle behavior change, this study explored the perceptions surrounding clinical care as currently offered to patients with NAFLD. The aim of this study was to establish whether current provision of lifestyle behavior change support is sufficient, whether health care professionals believe they have the tools to target lifestyle behavior changes effectively, and how targeting diet and physical activity/exercise to facilitate weight loss and weight loss maintenance in practice can be improved from the perspective of health care professionals and patients

    A study of physical activity comparing people with Charcot Marie Tooth disease to normal control subjects

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    PURPOSE: Charcot Marie Tooth disease (CMT) describes a group of hereditary neuropathies that present with distal weakness, wasting and sensory loss. Small studies indicate that people with CMT have reduced daily activity levels. This raises concerns as physical inactivity increases the risk of a range of co- morbidities, an important consideration in the long-term management of this disease. This study aimed to compare physical activity, patterns of sedentary behavior and overall energy expenditure of people with CMT and healthy matched controls. METHODS: We compared 20 people with CMT and 20 matched controls in a comparison of physical activity measurement over seven days, using an activity monitor. Patterns of sedentary behavior were explored through a power law analysis. RESULTS: Results showed a decrease in daily steps taken in the CMT group, but somewhat paradoxically, they demonstrate shorter bouts of sedentary activity and more frequent transitions from sedentary to active behaviors. No differences were seen in energy expenditure or time spent in sedentary, moderate or vigorous activity. CONCLUSION: The discrepancy between energy expenditure and number of steps could be due to higher energy requirements for walking, but also may be due to an over-estimation of energy expenditure by the activity monitor in the presence of muscle wasting. Alternatively, this finding may indicate that people with CMT engage more in activities or movement not related to walking. Implications for Rehabilitation Charcot-Marie-Tooth disease: • People with Charcot-Marie-Tooth disease did not show a difference in energy expenditure over seven days compared to healthy controls, but this may be due to higher energy costs of walking, and/or an over estimation of energy expenditure by the activity monitor in a population where there is muscle wasting. This needs to be considered when interpreting activity monitor data in people with neuromuscular diseases. • Compared to healthy controls, people with Charcot-Marie-Tooth disease had a lower step count over seven days, but exhibited more frequent transitions from sedentary to active behaviors • High Body Mass Index and increased time spent sedentary were related factors that have implications for general health status. • Understanding the profile of physical activity and behavior can allow targeting of rehabilitation interventions to address mobility and fitness

    Estimating sleep parameters using an accelerometer without sleep diary

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    Funding Information: This work was made possible thanks to the following grants: NIH grants HL-094307 (AIP), and; MRC grant MR/ P012167/1. We would like to thank Dr. Sarah Charman, Dr. Paul Innerd, Matthew Goodman and Sara McHugh-Grant for their contributions to the collection of PSG data. Publisher Copyright: © 2018, The Author(s).Peer reviewe

    Habitual Physical Activity in Mitochondrial Disease

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    Mitochondrial disease is the most common neuromuscular disease and has a profound impact upon daily life, disease and longevity. Exercise therapy has been shown to improve mitochondrial function in patients with mitochondrial disease. However, no information exists about the level of habitual physical activity of people with mitochondrial disease and its relationship with clinical phenotype.Habitual physical activity, genotype and clinical presentations were assessed in 100 patients with mitochondrial disease. Comparisons were made with a control group individually matched by age, gender and BMI. = −0.49; 95% CI −0.33, −0.63, P<0.01). There were no systematic differences in physical activity between different genotypes mitochondrial disease.These results demonstrate for the first time that low levels of physical activity are prominent in mitochondrial disease. Combined with a high prevalence of obesity, physical activity may constitute a significant and potentially modifiable risk factor in mitochondrial disease

    Cardiorespiratory fitness is associated with hard and light intensity physical activity but not time spent sedentary in 10–14 year old schoolchildren: the HAPPY study

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    Sedentary behaviour is a major risk factor for developing chronic diseases and is associated with low cardiorespiratory fitness in adults. It remains unclear how sedentary behaviour and different physical activity subcomponents are related to cardiorespiratory fitness in children. The purpose of this study was to assess how sedentary behaviour and different physical activity subcomponents are associated with 10–14 year-old schoolchildren's cardiorespiratory fitness

    Pathophysiology of exercise intolerance in chronic diseases: the role of diminished cardiac performance in mitochondrial and heart failure patients

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    Objective: Exercise intolerance is a clinical hallmark of chronic conditions. The present study determined pathophysiological mechanisms of exercise intolerance in cardiovascular, neuromuscular, and metabolic disorders. Methods: In a prospective cross-sectional observational study 152 patients (heart failure reduced ejection fraction, n=32; stroke, n=34; mitochondrial disease, n=28; type two diabetes, n=28; and healthy controls, n=30) performed cardiopulmonary exercise testing with metabolic and haemodynamic measurements. Peak exercise O2 consumption and cardiac power output were measures of exercise tolerance and cardiac performance. Results: Exercise tolerance was significantly diminished in patients compared with controls (ie, by 45% stroke, 39% mitochondria disease, and 33% diabetes and heart failure, p&lt;0.05). Cardiac performance was only significantly reduced in heart failure (due to reduced heart rate, stroke volume, and blood pressure) and mitochondrial patients (due reduced stroke volume) compared with controls (ie, by 53% and 26%, p&lt;0.05). Ability of skeletal muscles to extract oxygen (ie, arterial-venous O2 difference) was diminished in mitochondrial, stroke, and diabetes patients (by 24%, 22%, and 18%, p&lt;0.05), but increased by 21% in heart failure (p&lt;0.05) compared with controls. Cardiac output explained 65% and 51% of the variance in peak O2 consumption (p&lt;0.01) in heart failure and mitochondrial patients, whereas arterial-venous O2 difference explained 69% (p&lt;0.01) of variance in peak O2 consumption in diabetes, and 65% and 48% in stroke and mitochondrial patients (p&lt;0.01). Conclusions: Different mechanisms explain exercise intolerance in patients with heart failure, mitochondrial dysfunction, stroke and diabetes. Their better understanding may improve management of patients, their stress tolerance and quality of life

    Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists

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    The purpose of this study was to define the effect of glucose ingestion compared with sucrose ingestion on liver and muscle glycogen depletion during prolonged endurance-type exercise. Fourteen cyclists completed two 3-h bouts of cycling at 50% of peak power output while ingesting either glucose or sucrose at a rate of 1.7 g/min (102 g/h). Four cyclists performed an additional third test for reference in which only water was consumed. We employed C-13 magnetic resonance spectroscopy to determine liver and muscle glycogen concentrations before and after exercise. Expired breath was sampled during exercise to estimate whole body substrate use. After glucose and sucrose ingestion, liver glycogen levels did not show a significant decline after exercise (from 325 +/- 168 to 345 +/- 205 and 321 +/- 177 to 348 +/- 170 mmol/l, respectively; P > 0.05), with no differences between treatments. Muscle glycogen concentrations declined (from 101 +/- 49 to 60 +/- 34 and 114 +/- 48 to 67 +/- 34 mmol/l, respectively; P < 0.05), with no differences between treatments. Whole body carbohydrate utilization was greater with sucrose (2.03 +/- 0.43 g/min) vs. glucose (1.66 +/- 0.36 g/min; P < 0.05) ingestion. Both liver (from 454 +/- 33 to 283 +/- 82 mmol/l; P < 0.05) and muscle (from 111 +/- 46 to 67 +/- 31 mmol/l; P < 0.01) glycogen concentrations declined during exercise when only water was ingested. Both glucose and sucrose ingestion prevent liver glycogen depletion during prolonged endurance-type exercise. Sucrose ingestion does not preserve liver glycogen concentrations more than glucose ingestion. However, sucrose ingestion does increase whole body carbohydrate utilization compared with glucose ingestion
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