China
Africa
Explore chapters and articles related to this topic
Tissue Structure and Function
Published in Joseph W. Freeman, Debabrata Banerjee, Building Tissues, 2018
Joseph W. Freeman, Debabrata Banerjee
The myofibers are embedded in a matrix of collagen. At either end of the muscle belly, the matrix becomes the tendon that connects the muscle to bone (Figure 4.32). The tissue gradually increases in collagen content and decreases in muscle content until it becomes the tendon (Figure 4.32). The change happens gradually, so the tendon and muscle are considered to be one unit. It is believed that the number of muscle fibers in a human is fixed early on in his or her life. Myofibers are regulated by myostatin, a cytokine that is synthesized in muscle cells (and circulates as a hormone later in life). Myostatin suppresses skeletal muscle development.
Is Supraphysiological Enhancement Possible, and What are the Downsides?
Published in Steven Kornguth, Rebecca Steinberg, Michael D. Matthews, Neurocognitive and Physiological Factors During High-Tempo Operations, 2018
Myostatin regulates the utilization of satellite cells to create new muscle cells and the myostatin gene presents a target for improvement on nature through genetic selection or engineering. This follows logically from the observations that a mutational deletion of the gene that codes for myostatin has intriguing consequences to human performance with tiny “Hercules” babies with great muscle mass (Schuelke et al. 2004). There is a version of cattle with mutations in the myostatin gene that are now being bred for their great mass and leanness (McPherron and Lee 1997). With such emerging discoveries, Aldous Huxley’s Brave New World depiction of manipulating embryos to create a force of optimized manual laborers appears to be within reach. The amount of coal or gravel that an individual can shovel is largely dependent on the individual’s mass of working muscle and on the amount of food energy they are provided (Spurr 1986); thus, a deficient myostatin gene, especially on a genetic background for a large skeletal frame might optimize a specifically cultivated herd of human laborers for a nation where people are more abundant and affordable than earth moving equipment and other technologies. The question of interest to physiologists is what deficiency or compensation occurs in the absence of myostatin. One hypothesis is that in the absence of a functioning myostatin, the unrestrained use of satellite cells may cause a depletion that leads to accelerated loss of muscle mass (and bone) later in life when cells can no longer be replaced. If this is the case, the cultivated laborers might have only a relatively short work life; these overly specialized strong mutants would be at a marked disadvantage against a normal military opponent with greater mobility, energy efficiency, and higher thermotolerance. Further investigations into the myostatin gene may lead to new treatments for age-related sarcopenia and be a great benefit to the ageing population and for individuals with muscle wasting diseases (Gonzalez-Cadavid et al. 1998). Based on recent history with performance enhancing drugs, there will be little or no lag time between the first emergence of a new promising treatment for muscle wasting and the widespread repurposing of that treatment to strength athletes and body builders.
Resistance training attenuates circulating FGF-21 and myostatin and improves insulin resistance in elderly men with and without type 2 diabetes mellitus: A randomised controlled clinical trial
Published in European Journal of Sport Science, 2021
Fatemeh Shabkhiz, Mousa Khalafi, Sara Rosenkranz, Pouran Karimi, Kamilia Moghadami
One potential contributor to both sarcopenia and insulin resistance in aging and T2D is myostatin. myostatin is a member of the transforming growth factor-beta (TGF-β) superfamily of secreted growth factors, with well-known inhibitory effects on skeletal muscle growth and strength, and stimulatory effects on insulin resistance (Camporez et al., 2016). myostatin is mainly produced in skeletal muscle in an autocrine/paracrine manner via binding to Activin receptor type IIA and IIB (ActRIIA and ActRIIB), and increases the activity of the ubiquitin–proteasome system resulting in muscle atrophy (Rodriguez et al., 2014). In addition, myostatin negatively regulates the activity of the Akt pathway, and leads to muscle atrophy (Rodriguez et al., 2014). myostatin was also shown to be negatively associated with insulin sensitivity (Amor et al., 2019), and previous studies have reported that treatment with an anti-Myostatin antibody improved muscle insulin sensitivity as well as increased muscle mass and muscle strength in old mice (Camporez et al., 2016).
Gene doping: Present and future
Published in European Journal of Sport Science, 2020
Rebeca Araujo Cantelmo, Alessandra Pereira da Silva, Celso Teixeira Mendes-Junior, Daniel Junqueira Dorta
The glycosylation patterns (post-translational modification) of EPO proteins resulting from an endogenous gene and an artificially introduced gene have been shown to be different, which brings an expectation for target detection (Haisma & de Hon, 2006; Lasne et al., 2004; Ye et al., 1999). In the case of the myostatin gene, a study with rats provided very interesting results: liquid chromatography coupled to high-resolution mass spectrometry (LC-HRMS) helped to identify the introduced genetic material (small interfering RNA – siRNA) in urine samples after a single intravenous administration (Thevis, Kuuranne, Geyer, & Schänzer, 2014; Thomas et al., 2013).