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Tensiomyography is a non-invasive method to assess skeletal muscle contractile properties from the stimulated radial displacement. Many studies have used the rate of displacement (Vc) as an indirect measure of muscle contraction velocity. However, no standardised methodical approach exists to measure displacement and determine Vc. This review aimed to provide an overview of concepts to determine Vc and measurement protocols to foster the development of a standardised methodical approach. This review followed the Preferred Reporting Items for Systematic Reviews and meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guideline. Systematic searches were performed within five electronic databases and additional sources. The included 62 studies reported 10 different concepts to determine Vc, which we summarised in three groups. The determination concepts differed mainly regarding time intervals during the contraction phase considered and criteria used to define these intervals. Essential information on the equipment and raters, measurement setup, electrical stimulation procedure, and data analysis were frequently not reported. In conclusion, no consensus on how to determine Vc existed. Incomplete reporting of measurement protocols hindered study comparison, which obstructs developing a standardised approach. Therefore, we propose a new guideline for reporting measurement protocols, which covers the 1) equipment and rater, 2) measurement setup, including positioning of the subject, sensor and electrodes, 3) electrical stimulation, including initial stimulation amplitude, increment, and endpoint, and 4) data analysis, including selection criteria and number of analysed signals and a definition of derived parameters.

Despite more than four decades of research examining the physical demands of match-play, quantification of the customary training loads of adult male professional soccer players is comparatively recent. The training loads experienced by players during weekly micro-cycles are influenced by phase of season, player position, frequency of games, player starting status, player-specific training goals and club coaching philosophy. From a macronutrient perspective, the periodization of physical loading within (i.e., match versus training days) and between contrasting micro-cycles (e.g., 1, 2 or 3 games per week schedules) has implications for daily carbohydrate (CHO) requirements. Indeed, aside from the well-recognised role of muscle glycogen as the predominant energy source during match-play, it is now recognised that the glycogen granule may exert regulatory roles in activating or attenuating the molecular machinery that modulate skeletal muscle adaptations to training. With this in mind, the concept of CHO periodization is gaining in popularity, whereby CHO intake is adjusted day-by-day and meal-by-meal according to the fuelling demands and specific goals of the upcoming session. On this basis, the present paper provides a contemporary overview and theoretical framework for which to periodize CHO availability for the professional soccer player according to the \"fuel for the work\" paradigm.

1 H-MR spectroscopy of skeletal muscle provides insight into metabolism that is not available noninvasively by other methods. The recommendations given in this article are intended to guide those who have basic experience in general MRS to the special application of 1 H-MRS in skeletal muscle. The highly organized structure of skeletal muscle leads to effects that change spectral features far beyond simple peak heights, depending on the type and orientation of the muscle. Specific recommendations are given for the acquisition of three particular metabolites (intramyocellular lipids, carnosine and acetylcarnitine) and for preconditioning of experiments and instructions to study volunteers.

We recently reported that in addition to its classical cytoplasmic location, the fast skeletal muscle Troponin T3 (TnT3) shuttles to the nucleus, where it appears to perform nonclassical transcription regulatory functions. Importantly, changes in the composition of the nucleus-localized pool of TnT3 and its fragments contribute to age-dependent muscle damage and wasting. Here, using ChIP-Seq, we demonstrate that TnT3 associates with DNA consensus sequences including the TGCCT motif, which is required for p53 binding to the promoter area of p53-related genes. Gene set enrichment analysis further demonstrated that the p53 pathway was the most significantly enriched pathway among genes annotated to the TnT3 ChIP-Seq peaks. We further demonstrated a strong correlation (r = 0.78, P = 1 × 10-4) between the expression levels of TNNT3 and TP53-inducible ribonucleotide reductase regulatory subunit M2B (RRM2B) in skeletal muscle tissue of 21 lean non-diabetic human subjects and a significant (P < 0.05) reduction in the levels of both gene transcripts in the third age-tertile group [42.3-70 years of age (yoa)] as compared to the second age-tertile (31.3-42.3 yoa). Of note, both TNNT3 and RRM2B expression levels negatively associated with total body fat mass (each with r = 0.49, P < 0.05), whereas RRM2B positively correlated with pancreatic β cell function (rRRM2B~HOMA-B = 0.47, P = 0.047). This work suggests that reduced TNNT3 gene expression is another mechanism leading to reduced TnT3 and excitation-contraction coupling with aging. Consequently, TnT3 appears to contribute to age-related sarcopenia and possibly other age-related deficiencies such as muscle insulin resistance and β cell dysfunction by interacting with TnT3-binding sequences in the promoter area of p53-related genes, among others, and consequently modulating the transcriptional regulation of these target genes.

It is 30 yr since the British Journal of Anaesthesia published the first consensus protocol for the laboratory diagnosis of malignant hyperthermia susceptibility from the European Malignant Hyperthermia Group. This has subsequently been used in more than 10 000 individuals worldwide to inform use of anaesthetic drugs in these patients with increased risk of developing malignant hyperthermia during general anaesthesia, representing an early and successful example of stratified medicine. In 2001, our group also published a guideline for the use of DNA-based screening of malignant hyperthermia susceptibility. We now present an updated and complete guideline for the diagnostic pathway for patients potentially at increased risk of developing malignant hyperthermia. We introduce the new guideline with a narrative commentary that describes its development, the changes to previously published protocols and guidelines, and new sections, including recommendations for patient referral criteria and clinical interpretation of laboratory findings.

Skeletal muscle undergoes metabolic remodelling in response to environmental hypoxia, yet aspects of this process remain controversial. Broadly, environmental hypoxia has been suggested to induce: (i) a loss of mitochondrial density; (ii) a substrate switch away from fatty acids and towards other substrates such as glucose, amino acids and ketone bodies; and (iii) a shift from aerobic to anaerobic metabolism. There remains a lack of a consensus in these areas, most likely as a consequence of the variations in degree and duration of hypoxic exposure, as well as the broad range of experimental parameters used as markers of metabolic processes. To attempt to resolve some of the controversies, we performed a comprehensive review of the literature pertaining to hypoxia-induced changes in skeletal muscle energy metabolism. We found evidence that mass-specific mitochondrial function is decreased prior to mass-specific mitochondrial density, implicating intra-mitochondrial changes in the response to environmental hypoxia. This loss of oxidative capacity does not appear to be matched by a loss of glycolytic capacity, which on the whole is not altered by environmental hypoxia. Environmental hypoxia does however induce a selective attenuation of fatty acid oxidation, whilst glucose uptake is maintained or increased, perhaps to support glycolysis in the face of a downregulation of oxidative metabolism, optimising the pathways of ATP synthesis for the hypoxic environment.