View clinical trials related to Muscular Atrophy.
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Loss of muscle protein is generally a central component of weight loss in Chronic Obstructive Pulmonary Disease (COPD) patients. Gains in muscle mass are difficult to achieve in COPD unless specific metabolic abnormalities are targeted. The investigators recently observed that alterations in protein metabolism are present in normal weight COPD patients. Elevated levels of protein synthesis and breakdown rates were found in this COPD group indicating that alterations are already present before muscle wasting occurs. The investigators recently observed that in order to enhance protein anabolism, manipulation of the composition of proteins and amino acids in nutrition is required in normal-weight COPD. Intake of casein protein resulted into significant protein anabolism in these patients. The anabolic response to casein protein was even higher than after whey protein intake. A substantial number of COPD patients, underweight as well as normal weight to obese, is characterized by an increased inflammatory response. This group failed to respond to nutritional therapy. Previous experimental research and clinical studies in cachectic conditions (mostly malignancy) indicate that polyunsaturated fatty acids (PUFA) are able to attenuate protein degradation by improving the anabolic response to feeding and by decreasing the acute phase response. Eicosapentaenoic acid (EPA) (in combination with docosahexaenoic acid (DHA)) has been shown to effectively inhibit weight loss in several disease states, however weight and muscle mass gain was not present or minimal. Until now, limited research has been done examining muscle protein metabolism and the response to EPA and DHA supplementation in patients with COPD. It is the investigator's hypothesis that supplementation of 2g/day EPA+DHA in COPD patients during 4 consecutive weeks will increase the muscle anabolic response to a high quality protein supplement as compared to a placebo, and supplementation of 3.5g/day EPA+DHA will increase the anabolic response even further. In the present study both the acute and chronic effects of EPA+DHA versus a placebo on muscle and whole body protein metabolism will be examined. The principal endpoint will be the extent of stimulation of net fractional muscle protein synthesis as this is the principal mechanism by which the effect of EPA+DHA on muscle anabolism can be measured. The endpoint will be assessed by isotope methodology which is thought to be the reference method.
Atrogin-1 and muscle RING finger-1 are skeletal muscle specific genes, with ubiquitin ligase activities, that are upregulated during muscle atrophy in mice. The Akt/GSK3 and Akt/mTOR pathways are involved in muscle hypertrophy in mice. Recent studies by the investigators team and others have demonstrated the implication of these signalling pathways in the control of muscle mass in humans. However no study has yet investigated the involvement of these systems in the early stages of spinal cord injury induced human skeletal muscle atrophy. The investigators propose to investigate the level of expression of the different components of the ubiquitin-proteasome system together with the level of expression and activity of the Akt/mTOR and Akt/GSK3 signalling pathways after SCI in humans during the first months following the injury. A second aim of this project is to assess if a novel apparatus of electrical stimulation which generate movements by closed-loop electrical muscle stimulation may improve strength and muscle mass in these patients. The patients will be recruited jointly at the Clinique Romande de Réadaptation (CRR) in Sion and the Swiss paraplegic centre in Nottwil. They will be randomly divided into two groups, a first group of patients will undergo a conventional treatment of rehabilitation while a second set of patients will be treated using a brand new system of electro-stimulation called MotionMaker TM. Biopsies will be obtained in the first weeks after admission; two other biopsies will be taken respectively 3 and 6 months post-lesion. Our results will provide an increased understanding of the molecular mechanisms contributing to skeletal muscle atrophy during the early stages following SCI and a characterization of the impact of endurance training in the no more voluntary innervated muscle. Moreover this study will also investigate the potential improvement in the rehabilitation process by using a new system of electro-stimulation.
Stroke, a leading cause of disability in the aging population, increases the risk for diabetes, subsequent stroke recurrence, and cardiovascular disease complications. The downsizing of private and federal health care resources, along with the anticipated increase in stroke rates as our population ages, mandate that alternative strategies be developed to reduce the public health burden of stroke. This pilot study may facilitate our knowledge of the timing of paretic leg muscle atrophy, fiber type shift, and the progression of worsening of glucose tolerance after stroke. Knowledge of the skeletal muscle changes occurring in the sub-acute stroke period is essential to create new guidelines incorporating exercise rehabilitation, much like cardiac rehabilitation, in order to facilitate and improve the health care of veteran stroke survivors.
The proposed feasibility study is necessary to test if children and young adults will participate in and adhere to a 12-week, home-based, supervised progressive strength training exercise program and to obtain preliminary data that will subsequently allow us to determine the safety and impact of strength training in spinal muscular atrophy. Our pilot study will address 3 aims: (1) Ascertain the feasibility of, and potential barriers to, participation in and adherence to a 12-week home-based, supervised, progressive strength training exercise program in children and young adults aged 5-21 years with SMA types II and III; (2) Determine the safety and tolerability of progressive strength training in a pilot study sample of children and young adults with SMA types II and III; and (3) Determine candidate outcome measures.