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The study is divided in to two parts, the first dealing with the cell and the molecular biology of muscle in terms of growth and the second deals with physiological mechanism involved in the alteration of size of the human muscle mass. This study would benefit physicians, physiotherapist and kinesiologists.

Purpose: Aggressive play in professional soccer, punished by referees with fouls and cards, carries increased injury risk. We compared fouls and cards in the English Premier League (EPL) with the next three divisions of English soccer over 17 seasons (2000/01–2016/17), to determine whether previously observed differences with other top European leagues are unique to the EPL or are characteristic of English professional soccer overall. Methods: Data from individual matches were obtained through online sources and season averages for each league were compared. Fouls and cards were also compared between home and away teams. Correlations with final league positions were examined. Results: Numbers of fouls and yellow cards per match did not substantially differ between leagues, with average differences of 3–3.8% and 6.1–14.0% (effect sizes (ηp2) < 0.01). Away teams consistently committed more fouls and yellow card offences than home teams in each league. Results were similar though less consistent for red cards. Number and rate of cards awarded to the opposition exhibited strongest correlations with final league position across leagues. Conclusions: Our results suggest similar rates of aggressive play among the top English soccer leagues, possibly due to standardized refereeing style. Consequently, contact injuries rates may be higher in English soccer. [ABSTRACT FROM AUTHOR]

Key points: Breast cancer 1 early onset gene codes for the DNA repair enzyme, breast cancer type 1 susceptibility protein (BRCA1). The gene is prone to mutations that cause a loss of protein function.BRCA1/Brca1 has recently been found to regulate several cellular pathways beyond DNA repair and is expressed in skeletal muscle.Skeletal muscle specific knockout of Brca1 in mice caused a loss of muscle quality, identifiable by reductions in muscle force production and mitochondrial respiratory capacity.Loss of muscle quality was associated with a shift in muscle phenotype and an accumulation of mitochondrial DNA mutations.These results demonstrate that BRCA1 is necessary for skeletal muscle function and that increased mitochondrial DNA mutations may represent a potential underlying mechanism. Recent evidence suggests that the breast cancer 1 early onset gene (BRCA1) influences numerous peripheral tissues, including skeletal muscle. The present study aimed to determine whether induced‐loss of the breast cancer type 1 susceptibility protein (Brca1) alters skeletal muscle function. We induced genetic ablation of exon 11 in the Brca1 gene specifically in the skeletal muscle of adult mice to generate skeletal muscle‐specific Brca1 homozygote knockout (Brca1KOsmi) mice. Brca1KOsmi exhibited kyphosis and decreased maximal isometric force in limb muscles compared to age‐matched wild‐type mice. Brca1KOsmi skeletal muscle shifted toward an oxidative muscle fibre type and, in parallel, increased myofibre size and reduced capillary numbers. Unexpectedly, myofibre bundle mitochondrial respiration was reduced, whereas contraction‐induced lactate production was elevated in Brca1KOsmi muscle. Brca1KOsmi mice accumulated mitochondrial DNA mutations and exhibited an altered mitochondrial morphology characterized by distorted and enlarged mitochondria, and these were more susceptible to swelling. In summary, skeletal muscle‐specific loss of Brca1 leads to a myopathy and mitochondriopathy characterized by reductions in skeletal muscle quality and a consequent kyphosis. Given the substantial impact of BRCA1 mutations on cancer development risk in humans, a parallel loss of BRCA1 function in patient skeletal muscle cells would potentially result in implications for human health. Key points: Breast cancer 1 early onset gene codes for the DNA repair enzyme, breast cancer type 1 susceptibility protein (BRCA1). The gene is prone to mutations that cause a loss of protein function.BRCA1/Brca1 has recently been found to regulate several cellular pathways beyond DNA repair and is expressed in skeletal muscle.Skeletal muscle specific knockout of Brca1 in mice caused a loss of muscle quality, identifiable by reductions in muscle force production and mitochondrial respiratory capacity.Loss of muscle quality was associated with a shift in muscle phenotype and an accumulation of mitochondrial DNA mutations.These results demonstrate that BRCA1 is necessary for skeletal muscle function and that increased mitochondrial DNA mutations may represent a potential underlying mechanism. [ABSTRACT FROM AUTHOR]

Spangenburg, Espen E., Jay H. Williams, Roland R. Roy, and Robert J. Talmadge. Skeletal muscle calcineurin: influence of phenotype adaptation and atrophy. Am J Physiol Regulatory Integrative Comp Physiol 280: R1256-R1260, 2001.--Calcineurin (CAN) has been implicated as a signaling molecule that can transduce physiological stimuli (e.g., contractile activity) into molecular signals that initiate slow-fiber phenotypic gene expression and muscle growth. To determine the influence of muscle phenotype and atrophy on CaN levels in muscle, the levels of soluble CaN in rat muscles of varying phenotype, as assessed by myosin heavy chain (MHC)-isoform proportions, were determined by Western blotting. CaN levels were significantly greater in the plantaris muscle containing predominantly fast (IIx and IIb) MHC isoforms, compared with the soleus (predominantly type I MHC) or vastus intermedius (VI, contains all 4 adult MHC isoforms). Three months after a complete spinal cord transection (ST), the CaN levels in the VI muscle were significantly reduced, despite a significant increase in fast MHC isoforms. Surprisingly, the levels of CaN in the VI were highly correlated with muscle mass but not MHC isoform proportions in ST and control rats. These data demonstrate that CaN levels in skeletal muscle are highly correlated to muscle mass and that the normal relationship with phenotype is lost after ST. calcium; calmodulin; myosin heavy chain; nuclear factor of activated T cells

Current trends suggest professional soccer is becoming less aggressive, with England often argued to have the most aggressive of the top European leagues. The purpose of this study was to investigate differences in fouls and cards as indicators of aggressive play in the first divisions of England, France, Germany, Italy, and Spain over the past decade. Number of fouls per match and per yellow card has decreased in all leagues since 2007/08, though attempted tackles per foul has not changed or has increased. A lack of substantial rule changes suggests players have become less aggressive in tackling as opposed to referees becoming more lenient. Total number of fouls and cards per match were consistently lower in the English Premier League, however attempted tackles per foul was higher. The data also demonstrate the notions of home advantage and potentially referee bias, since referees tended to call more fouls and award more cards to away teams. Lastly, number of attempted tackles per foul and yellow cards received exhibited the strongest correlations with final league position across the leagues. In conclusion, our data support that elite European soccer has become less aggressive and the English Premier League is the most aggressive league. [ABSTRACT FROM AUTHOR]

Investigating the extremes of the continuum of paracrine functions in CD34-/CD31+ CACs across diverse populations. Am J Physiol Heart Circ Physiol 312: H162-H172, 2017. First published October 28, 2016; doi:10.1152/ajpheart.00342.2016.--Paracrine function of circulating angiogenic cells (CACs) is thought to contribute to vascular maintenance. We previously identified S100A8 and S100A9 secreted from physically inactive individuals' CD34-/CD31+ CACs as negative regulators of capillary-like network formation. The purpose of this study was to investigate further the extremes of the continuum of CAC paracrine actions using two distinctly different groups representing "healthy" and "impaired" CAC function. We aimed to determine how capillary-like network formation in human umbilical vein endothelial cells (HUVECs) is affected by S100A8 and S100A9 in concentrations secreted by CACs from different ends of the health spectrum. CD34-/CD31+ CACs were isolated and cultured from 10 impaired function individuals defined as older (50-89 yr), non-ST-elevation myocardial infarction patients and 10 healthy individuals defined as younger (18-35 yr), healthy individuals, and conditioned media (CM) was generated. CM from the impaired function group's CACs significantly diminished network formation compared with CM from the healthy group (P<0.05). We identified elevations in S100A8, S100A9, and S100A8/A9 in the CM from the impaired function group (P<0.05). Pretreatment of HUVECs with inhibitors to a known S100A8 and S100A9 receptor, Toll-like receptor 4 (TLR4), but not receptor for advanced glycation end products, improved HUVEC network formation (P<0.05) compared with CM alone in the impaired function conditions. Exposure of HUVECs to the TLR4 signaling inhibitor also blocked recombinant S100A8- and S100A9-mediated reductions in network formation. Collectively, the results suggest that the mechanisms behind impaired CAC CD34-/CD31+ CM-mediated reductions in capillary-like network formation involve secretion of S100A8 and S100A9 and binding of these proteins to TLR4 receptors on HUVECs. [ABSTRACT FROM AUTHOR]