Changes in the mechanical characteristics of the knee musculature in professional female volleyball players

The technical efficiency in volleyball is closely related to the ability to perform displacements or jump (1). Therefore, it is necessary that precise, individualized, and localized evaluation of the muscles frequently involved in volleyball practice be studied (2,3). The aim of this study was to analyze the neuromuscular changes of the knee musculature in professional volleyball players using Tensiomyography (TMG) and jump tests.

Design of a myofascial therapy protocol for the treatment of hemophilic arthropathy of the knee and ankle

Hemophilic arthropathy limits daily life activities of patients with hemophilia, presenting with clinical manifestations such as chronic pain, limited mobility, or muscular atrophy. Although physical therapy is considered essential for these patients, few clinical studies have demonstrated the efficacy and safety of the various physiotherapy techniques. Physical therapy may be useful for treating hemophilic arthropathy by applying safe and effective techniques. However, it is necessary to create protocols for possible treatments to avoid the risk of bleeding in these patients. This article describes the musculoskeletal pathology of hemophilic arthropathy and characteristics of fascial therapy. This systematic protocol for treatment by fascial therapy of knee and ankle arthropathy in patients with hemophilia provides an analysis of the techniques that, depending on their purpose and methodology, can be used in these patients. Similarly, the protocol's applicability is analyzed and the steps to be followed in future research studies are described. Fascial therapy is a promising physiotherapy technique for treating fascial tissue and joint contractures in patients with hemophilic arthropathy. More research is needed to assess the efficacy and safety of this intervention in patients with hemophilia, particularly with randomized multicenter clinical trials

Phenotype consequences of myophosphorylase dysfunction: insights from the McArdle mouse model

McArdle disease, caused by inherited deficiency of the enzyme muscle glycogen phosphorylase (GP-MM), is arguably the paradigm of exercise intolerance. The recent knock-in (p.R50X/p.R50X) mouse disease model allows an investigation of the phenotypic consequences of muscle glycogen unavailability and the physiopathology of exercise intolerance. We analysed, in 2-month-old mice [wild-type (wt/wt), heterozygous (p.R50X/wt) and p.R50X/p.R50X)], maximal endurance exercise capacity and the molecular consequences of an absence of GP-MM in the main glycogen metabolism regulatory enzymes: glycogen synthase, glycogen branching enzyme and glycogen debranching enzyme, as well as glycogen content in slow-twitch (soleus), intermediate (gastrocnemius) and glycolytic/fast-twitch (extensor digitorum longus; EDL) muscles.