Skeletal Muscle Mass ...

Discussion in 'Men's Health Forum' started by Michael Scally MD, Oct 19, 2018.

  1. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Wackerhage H, Schoenfeld BJ, Hamilton DL, Lehti M, Hulmi JJ. Stimuli and sensors that initiate skeletal muscle hypertrophy following resistance exercise. Journal of Applied Physiology 2018. https://doi.org/10.1152/japplphysiol.00685.2018

    One of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a mTORC1-mediated increase of muscle protein synthesis is the key, but not sole, mechanism by which resistance exercise causes muscle hypertrophy. Whilst much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive.

    For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as "hypertrophy stimulus", and the sensor of such a signal as "hypertrophy sensor". In this review we discuss our current knowledge of specific mechanical stimuli, damage/injury-associated and metabolic stress-associated triggers as potential hypertrophy stimuli.

    Mechanical signals are the prime hypertrophy stimuli candidates and a Filamin-C-BAG3-dependent regulation of mTORC1, Hippo and autophagy signalling is a plausible albeit still incompletely characterised hypertrophy sensor. Other candidate mechanosensing mechanisms are nuclear deformation-initiated signalling or several mechanisms related to costameres, which are the functional equivalents of focal adhesions in other cells.

    Whilst exercise-induced muscle damage is probably not essential for hypertrophy, it is still unclear whether and how such muscle damage could augment a hypertrophic response. Interventions that combine blood flow restriction and especially low load resistance exercise suggest that resistance exercise-regulated metabolites could be hypertrophy stimuli but this is based on indirect evidence and metabolite candidates are poorly characterised.
     
  2. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    McCarthy JJ, Murach KA. Chapter 24 - Anabolic and Catabolic Signaling Pathways That Regulate Skeletal Muscle Mass. In: Bagchi D, Nair S, Sen CK, eds. Nutrition and Enhanced Sports Performance (Second Edition): Academic Press; 2019:275-90. https://www.sciencedirect.com/science/article/pii/B9780128139226000242

    Skeletal muscle mass is primarily dictated by the balance between the rates of protein synthesis and degradation. Over the last decade, significant progress has been made in defining the anabolic and catabolic signaling pathways that control skeletal muscle mass through the regulation of protein synthesis and degradation.

    The purpose of this review is to briefly describe known and emerging signaling pathways involved in the regulation of skeletal muscle mass. Two important themes have come to light:

    (1) the degree of cross talk between and among anabolic and catabolic signaling pathways involved in the control of skeletal muscle hypertrophy and atrophy and

    (2) the balance between anabolism and catabolism that is required to facilitate a proper hypertrophic response.

    A more in-depth understanding of the anabolic and catabolic signaling pathways that regulate skeletal muscle mass will provide a critical foundation for the development of more effective training programs and nutritional aids to enhance athletic performance.
     
  3. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Role of Mammalian Target of Rapamycin in Muscle Growth

    Increase in muscle mass, or hypertrophy, in adults comes as a result of an increase in the size, as opposed to the number, of prenatally formed skeletal muscle fibers. The mammalian target of rapamycin (mTOR) coordinately regulates various steps of muscle development and pathways mediating hypertrophy, which are influenced by mechanical stress, physical activity, availability of nutrients, and growth factors.

    Skeletal muscle hypertrophy largely depends on protein turnover, defined as balance between protein synthesis and degradation. Activation of mTOR signaling positively affects processes of protein transcription and translation and inhibits autophagy, leading to increase in size of muscle fibers. In this review we describe both the upstream components of the signaling pathways, which activate mTOR, and the downstream targets that affect muscle growth.

    We focus on the most recent progress in the understanding of mTOR signaling mechanisms, which regulate skeletal muscle hypertrophy and atrophy, and the cross-regulation between the two systems.

    Panzhinskiy E, Culver B, Ren J, Bagchi D, Nair S. Chapter 22 - Role of Mammalian Target of Rapamycin in Muscle Growth. In: Bagchi D, Nair S, Sen CK, eds. Nutrition and Enhanced Sports Performance (Second Edition): Academic Press; 2019:251-61. https://www.sciencedirect.com/science/article/pii/B9780128139226000229
     

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  4. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Genetics and Sprint, Strength, and Power Performance: Candidate Gene Versus Genome-Wide Association Study Approaches

    The ability of skeletal muscles to produce force at a high velocity is crucial for success in sprint, strength, and power performance. There are many factors that influence sprint, strength, and power performance and genetics is one of them. Without the appropriate genetic makeup, the chance of success as an elite athlete is reduced.

    Several different genetic variants (i.e., polymorphisms) have been linked with power and sprint performance lately both using candidate gene and genome-wide sequencing approaches. It has become clear that athletic performance is influenced by many genes, with small contributions from each genetic variant.

    This chapter is an update of the chapter published in the first edition and is summarizing the knowledge to date in the field of genetics and sprint, strength, and power performance and highlighting future directions for the field.

    While there has been considerable growth in basic knowledge and understanding of how genes are influencing sprint, strength, and power performance, we stress that there is no current clinical application for genetic testing in the area of exercise prescription.

    Jacques M, Eynon N, Hanson ED. Chapter 31 - Genetics and Sprint, Strength, and Power Performance: Candidate Gene Versus Genome-Wide Association Study Approaches. In: Bagchi D, Nair S, Sen CK, eds. Nutrition and Enhanced Sports Performance (Second Edition): Academic Press; 2019:371-83. https://www.sciencedirect.com/science/article/pii/B978012813922600031X
     

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