5 resultados para Muscle trigger points
em BORIS: Bern Open Repository and Information System - Berna - Suiça
Resumo:
Liegt die Ursache von Schmerzen oder Funktionseinbussen im Schulterbereich selbst, können diese mit einer präzisen klinischen Untersuchung in den meisten Fällen einer bestimmten anatomischen Struktur zugeordnet werden. Vorwiegend im Bild, mit nur knappem Text, werden die einzelnen Tests dargestellt. Dabei wurde zur besseren Merkfähigkeit die jeweils getestete Struktur mit eingezeichnet. Auch die häufigsten in der Praxis vorkommenden Trigger-Punkte mit der entsprechenden pseudoradikulären Symptomatik werden dargestellt. Ziel dieses Artikels ist die Erleichterung der täglichen Arbeit in der Praxis bei häufigen Schulterproblemen.
Resumo:
Long-term disturbance of the calcium homeostasis of motor endplates (MEPs) causes necrosis of muscle fibers. The onset of morphological changes in response to this disturbance, particularly in relation to the fiber type, is presently unknown. Omohyoid muscles of mice were incubated for 1-30 minutes in 0.1 mM carbachol, an acetylcholine agonist that causes an inward calcium current. In these muscles, the structural changes of the sarcomeres and the MEP sarcoplasm were evaluated at the light- and electron-microscopic level. Predominantly in type I fibers, carbachol incubation resulted in strong contractures of the sarcomeres underlying the MEPs. Owing to these contractures, the usual beret-like form of the MEP-associated sarcoplasm was deformed into a mushroom-like body. Consequently, the squeezed MEPs partially overlapped the adjacent muscle fiber segments. There are no signs of contractures below the MEPs if muscles were incubated in carbachol in calcium-free Tyrode's solution. Carbachol induced inward calcium current and produced fiber-type-specific contractures. This finding points to differences in the handling of calcium in MEPs. Possible mechanisms for these fiber-type-specific differences caused by carbachol-induced calcium entry are assessed.
Optimizing human in vivo dosing and delivery of β-alanine supplements for muscle carnosine synthesis
Resumo:
Interest into the effects of carnosine on cellular metabolism is rapidly expanding. The first study to demonstrate in humans that chronic β-alanine (BA) supplementation (~3-6 g BA/day for ~4 weeks) can result in significantly augmented muscle carnosine concentrations (>50%) was only recently published. BA supplementation is potentially poised for application beyond the niche exercise and performance-enhancement field and into other more clinical populations. When examining all BA supplementation studies that directly measure muscle carnosine (n=8), there is a significant linear correlation between total grams of BA consumed (of daily intake ranges of 1.6-6.4 g BA/day) versus both the relative and absolute increases in muscle carnosine. Supporting this, a recent dose-response study demonstrated a large linear dependency (R2=0.921) based on the total grams of BA consumed over 8 weeks. The pre-supplementation baseline carnosine or individual subjects' body weight (from 65 to 90 kg) does not appear to impact on subsequent carnosine synthesis from BA consumption. Once muscle carnosine is augmented, the washout is very slow (~2%/week). Recently, a slow-release BA tablet supplement has been developed showing a smaller peak plasma BA concentration and delayed time to peak, with no difference in the area under the curve compared to pure BA in solution. Further, this slow-release profile resulted in a reduced urinary BA loss and improved retention, while at the same time, eliciting minimal paraesthesia symptoms. However, our complete understanding of optimizing in vivo delivery and dosing of BA is still in its infancy. Thus, this review will clarify our current knowledge of BA supplementation to augment muscle carnosine as well as highlight future research questions on the regulatory points of control for muscle carnosine synthesis.
Resumo:
Skeletal muscle complaints are a common consequence of cholesterol-lowering therapy. Transverse tubular (T-tubular) vacuolations occur in patients having statin-associated myopathy and, to a lesser extent, in statin-treated patients without myopathy. We have investigated quantitative changes in T-tubular morphology and looked for early indicators of T-tubular membrane repair in skeletal muscle biopsy samples from patients receiving cholesterol-lowering therapy who do not have myopathic side effects. Gene expression and protein levels of incipient membrane repair proteins were monitored in patients who tolerated statin treatment without myopathy and in statin-naive subjects. In addition, morphometry of the T-tubular system was performed. Only the gene expression for annexin A1 was up-regulated, whereas the expression of other repair genes remained unchanged. However, annexin A1 and dysferlin protein levels were significantly increased. In statin-treated patients, the volume fraction of the T-tubular system was significantly increased, but the volume fraction of the sarcoplasmic reticulum remained unchanged. A complex surface structure in combination with high mechanical loads makes skeletal muscle plasma membranes susceptible to injury. Ca(2+)-dependent membrane repair proteins such as dysferlin and annexin A1 are deployed at T-tubular sites. The up-regulation of annexin A1 gene expression and protein points to this protein as a biomarker for T-tubular repair.
Resumo:
BACKGROUND Pelvic floor muscle training is effective and recommended as first-line therapy for female patients with stress urinary incontinence. However, standard pelvic floor physiotherapy concentrates on voluntary contractions even though the situations provoking stress urinary incontinence (for example, sneezing, coughing, running) require involuntary fast reflexive pelvic floor muscle contractions. Training procedures for involuntary reflexive muscle contractions are widely implemented in rehabilitation and sports but not yet in pelvic floor rehabilitation. Therefore, the research group developed a training protocol including standard physiotherapy and in addition focused on involuntary reflexive pelvic floor muscle contractions. METHODS/DESIGN The aim of the planned study is to compare this newly developed physiotherapy program (experimental group) and the standard physiotherapy program (control group) regarding their effect on stress urinary incontinence. The working hypothesis is that the experimental group focusing on involuntary reflexive muscle contractions will have a higher improvement of continence measured by the International Consultation on Incontinence Modular Questionnaire Urinary Incontinence (short form), and - regarding secondary and tertiary outcomes - higher pelvic floor muscle activity during stress urinary incontinence provoking activities, better pad-test results, higher quality of life scores (International Consultation on Incontinence Modular Questionnaire) and higher intravaginal muscle strength (digitally tested) from before to after the intervention phase. This study is designed as a prospective, triple-blinded (participant, investigator, outcome assessor), randomized controlled trial with two physiotherapy intervention groups with a 6-month follow-up including 48 stress urinary incontinent women per group. For both groups the intervention will last 16 weeks and will include 9 personal physiotherapy consultations and 78 short home training sessions (weeks 1-5 3x/week, 3x/day; weeks 6-16 3x/week, 1x/day). Thereafter both groups will continue with home training sessions (3x/week, 1x/day) until the 6-month follow-up. To compare the primary outcome, International Consultation on Incontinence Modular Questionnaire (short form) between and within the two groups at ten time points (before intervention, physiotherapy sessions 2-9, after intervention) ANOVA models for longitudinal data will be applied. DISCUSSION This study closes a gap, as involuntary reflexive pelvic floor muscle training has not yet been included in stress urinary incontinence physiotherapy, and if shown successful could be implemented in clinical practice immediately. TRIAL REGISTRATION NCT02318251 ; 4 December 2014 First patient randomized: 11 March 2015.