View clinical trials related to Skeletal Muscle.
Filter by:To highlight the importance of protein quality rather than the total protein content of a meal, the investigators will demonstrate that unlike high quality proteins, a single meal containing 30 g of an incomplete protein source does not stimulate skeletal muscle protein synthesis. Secondly, the investigators will directly challenge a prevalent, but untested, assertion that has the potential to negatively impact health. The goal is to demonstrate that complementary plant-proteins (i.e., two or more incomplete protein sources) must be consumed at the same meal to stimulate protein synthesis.
The CHRONOS project aims to provide a device to detect earlier the motor decline, by developing a precise quantitative device measuring "Motor Functional Age" (MFA) of young, middle-aged and old people, thus preventing future functional motor loss for healthy aging. The MFA might be different from the Chronological Age (CA), depending on lifestyle, physical activity, and medical condition. Thus, this device will permit monitoring, adaptation and new design of a variety of personalized therapies for healthy aging including physical exercise, medication and nutritional interventions to reduce the MFA toward or less than the CA. The device combines data processing software that estimates the MFA by assessing muscle aging using a non-invasive multichannel electromyographical technique coupled to accelerometry sensors for motion evaluation. These data will provide with a built-in clinical database of subjects from different age categories (25-75 years old).
The purpose of this study was to determine the effects of L-leucine (LEU) or different protein supplements standardized to LEU (~3.0 g/serving) on changes in body composition, strength, and histological attributes in skeletal muscle and adipose tissue. Seventy-five untrained, college-aged males (mean±SE; age=21±1 yr, body mass=79.2±0.3 kg) were randomly assigned to an isocaloric, lipid-, and organoleptically-matched maltodextrin placebo (PLA, n=15), LEU (n=14), whey protein concentrate (WPC, n=17), whey protein hydrolysate (WPH, n=14), or soy protein concentrate (SPC, n=15) group. Participants performed whole-body resistance training three days per week for 12 weeks while consuming supplements twice daily. Skeletal muscle and subcutaneous (SQ) fat biopsies were obtained at baseline (T1) and ~72 h following the last day of training (T39). Tissue samples were analyzed for changes in type I and II fiber cross sectional area (CSA), non-fiber specific satellite cell count, and SQ adipocyte CSA. On average, all supplement groups including PLA exhibited similar training volumes and experienced statistically similar increases in total body skeletal muscle mass determined by dual x-ray absorptiometry (+2.2 kg; time p=0.024) and type I and II fiber CSA increases (+394 µm2 and +927 µm2; time p<0.001 and 0.024, respectively). Notably, all groups reported increasing Calorie intakes ~600-800 kcal/d from T1 to T39 (time p<0.001), and all groups consumed at least 1.1 g/kg/d of protein at T1 and 1.3 g/kg/d at T39. There was a training, but no supplementation, effect regarding the reduction in SQ adipocyte CSA (-210 µm2; time p=0.001). Interestingly, satellite cell counts within the WPC (p<0.05) and WPH (p<0.05) groups were greater at T39 relative to T1. In summary, LEU or protein supplementation (standardized to LEU content) does not provide added benefit in increasing whole-body skeletal muscle mass or strength above PLA following 3 months of training in previously untrained college-aged males that increase Calorie intakes with resistance training and consume above the recommended daily intake of protein throughout training. However, whey protein supplementation increases skeletal muscle satellite cell number in this population, and this phenomena may promote more favorable training adaptations over more prolonged periods.
The investigator showed that a night of sleep deprivation halved the duration of an inspiratory endurance test and that this loss of endurance could be secondary to a lack of activation of the pre-motor cortex. However, the inspiratory endurance test is associated with a feeling of dyspnea that could lead to premature arrest, and the inspiratory drive is complex, both automatic and voluntary. The investigator can reproduce this results on a simpler drive. During the execution of an exercise involving repeated contractions of the hand it is possible to record the activation of the pre-motor cortex corresponding to the phase of preparation of the movement. The amplitude of these premotor potentials is proportional to the developed motive force. The purpose of this study is to assess the impact of sleep deprivation on the muscular endurance of non-dominant in healthy subjects. Hypothesis: Sleep deprivation causes a decrease in manual motor endurance by decreasing cortical pre-motor control. Main objective: To compare the motor endurance of healthy subjects after a night's sleep and after a sleepless night. Secondary objective: To compare the amplitude of premature cortical control at the beginning of the endurance test after a night's sleep and after a sleepless night.
Tendons are essential structures for transmitting muscle forces to skeletal structures. A stiffer tendon will transmit muscle force faster, and then allow faster movement. Moreover, tendons are a living tissue and respond to mechanical forces by changing their metabolism as well as their structural and mechanical properties. The aim of the present study is to answer essential questions remaining unanswered that are necessary in order to optimize physical activity with ageing in humans, and thus improve quality of life in elderly. The main questions are: What is the minimal training intensity leading to tendon adaptations? What is the time-course of tendon adaptations? Does the same loading protocol lead to similar tendon adaptations for different tendons (Achilles vs Patellar) and does the same training program lead to identical tendon adaptations with age (25yrs vs 75yrs)? To answer these questions, tendon architecture and mechanical properties will be investigated in humans of different age and applying different training intensities. The kinematic of the tendon adaptations due to these different training characteristics will also be investigated. The training protocol will be applied on plantar flexors and knee extensors. MRI and ultrasound techniques as well as the use of ankle and knee ergometers will allow the quantification of possible modifications in tendon architecture and mechanical properties (tendon stiffness and Young's Modulus). This will be assessed in vivo, using ultrasound images to assess tendon displacement during an incremental maximal contraction.
The purpose of this Proof of Concept study is to determine the effects of BYM338 on skeletal muscle volume, mass, and strength and patient function (gait speed) in non-demented elderly adults with sarcopenia and mobility limitations. In addition, this study will generate data on the safety, tolerability, and pharmacokinetics of BYM338 in older adults and its response on additional physical function measures in this population. Furthermore, the extended study duration will provide information on the stability of BYM-induced changes in skeletal muscle and patient function in this subgroup of the older population.
The investigators here propose to perform a prospective randomized intervention trial in post-menopausal women to investigate the endocrine network, which contributes to the changes in skeletal muscle mass during weight loss.
The investigators here propose to perform a collaborative clinical research effort including a randomized controlled trial investigating the mechanisms of weight maintenance and their relation to a lifestyle intervention in children, adolescents and adults. The detailed investigation and analysis of the variability and dynamics of the endocrine circuits responding to a negative energy balance and weight loss will be accompanied and enhanced by specific clinical projects targeting peripheral and central-nervous aspects of hormonal counter-regulation after weight loss. Mechanisms of endocrine counter-regulation and potential therapeutic approaches will be studied.