The effect of two intensities resistance training on muscle growth regulatory myokines in sedentary young women
Introduction
The skeletal muscles are vitally important for preserving and developing health. In this respect, muscle is considered as an important endocrine organ (Broholm and Pedersen, 2010). More than 40% of body weight of a normal person is skeletal muscle that includes a major part of the body's metabolism; therefore, most metabolic diseases are related to muscles, directly or indirectly (Broholm and Pedersen, 2010, Roca-Rivada et al., 2012). A sedentary lifestyle is the most important factor in muscle atrophy in healthy and mature individuals (Pedersen and Febbraio, 2012); therefore, atrophy and muscle development depend on the balance between developer and inhibitor factors of muscle growth. According to research, Myostatin (GDF-8) and Follistatin are the most important inhibitors and developers of muscle growth (Migliaccio et al., 2014, Juhas and Bursac, 2014). Myostatin, a cytokinetic inhibitor factor of muscle growth, was introduced in 1997 by Mc Pherrone (Kandarian and Jackman, 2006). This cytokines is a new member of the large family of TGF-β1. Myostatin is primarily released by muscle cells and, in smaller amounts, by various tissues such as brain and fat tissue (Juhas and Bursac, 2014, Lutosławska et al., 2012) and is responsible for inhibiting the hypertrophic growth of muscle cells and preventing cell proliferation (growth inhibition of Hyperiolasic) (Lee et al., 2010). Myostatin functions may be influenced by interactive factors such as Follistatin, FLRG2, GASP-13 and Myostatin receptors (Activin IIb). Among these, Follistatin is the most important inhibitor factor (McPherron and Lee, 2002).
Follistatin is a glycoprotein which is released in almost all tissues of mammals and, in particular, by skeletal muscles. The most important task of Follistatin is neutralizing functions of the TGF-β family proteins, including Myostatin. In the presence of Follistatin, Myostatin is not able to bind to self-receptors and its function will be impaired (Juhas and Bursac, 2014, Bradley et al., 2008). In addition, the type of training and energy intensity involved in activities can cause different adaptations in muscle through different changes in muscle growth regulation factors (Elkina et al., 2011). In general, most studies show that resistance training (after one session or a prolonged period) reduces the level of Myostatin (Elkina et al., 2011, Fedoruk and Rupert, 2008) and increases Follistatin expression (Hiroki et al., 2011, Hittel et al., 2010), however there are also conflicting results (Bradley et al., 2008, Hiroki et al., 2011).
Resistance training increases muscle growth factors and inhibits negative adjustment factors by increasing the muscle hypertrophy and hyperplasia (Bellamy et al., 2014, Sharp et al., 2014). However, it is known that exercise pattern and intensity in resistance training as well as the role of gender are very effective for the development of muscle (Saini et al., 2009). According to different hormonal and metabolic characteristics and patterns of gain power, muscle mass is naturally less in adult women than in adult men (Juhas and Bursac, 2014, Gundersen, 2016). Nevertheless, more research has been done on males (Allen et al., 2011, Schoenfeld, 2010), and different patterns and different intensities of resistance training exercises have been less studied. On the other hand, deleting the Myostatin gene in animals doubled muscle growth, while in animals that received Follistatin, the muscle growth increased fourfold. Therefore, Follistatin, in addition to its effect on the Myostatin, can affect the other members of the TGF-β family (Bradley et al., 2008, Elkina et al., 2011). Thus, the positive and negative regulatory factor interactions in muscle growth also seem useful.
Section snippets
Subjects
This semi-experimental research included two phases which were performed before and after 8 weeks in two experimental groups. A total of 24 sedentary young women aged over 20 years (mean age 24.42 ± 2.95 years, and mean body mass index 23.77 ± 1.54 kg/m2) were recruited for this study. All of the volunteers completed the exercise program during 8 weeks. Based on the demographic and medical records questionnaires, the subjects had not done regular exercise over the prior six months and did not
Results
As seen in Table 1, in the low-intensity RT group, no significant changes were observed in Follistatin serum (P = 0.649), whereas it increased significantly (P = 0.040) in the high intensity RT group. Nevertheless, the variance between groups in Follistatin was not significant (P = 0.086).
In the high intensity RT group, Myostatin serum decreased significantly (P = 0.041), whereas the ratio of Follistatin to Myostatin increased dramatically (P = 0.951). In this case, the variance between the
Discussion and conclusion
Statistical analysis showed that eight weeks of high intensity resistance training significantly increased both Follistatin and the ratio of Follistatin to Myostatin. It also significantly reduced the amount of Myostatin in sedentary young women. Raue et al. (2006) reported that one high-intensity resistance training session caused a 50% reduction in Myostatin mRNA levels in young and old women (Moienneia and Attarzadeh Hosseini, 2016). Kim et al. (2005) examined the effect of a resistance
Conclusion
Overall, according to our findings, it seems that low-intensity resistance training does not provide adequate mechanism to enable the most important factors of Myostatic and myogenic in sedentary women. Moreover, high intensity resistance training develops their muscular tissue through increasing the Follistatin levels and decreasing the Myostatin levels in sedentary women, and probably by enabling the powerful mechanisms of protein synthesis and breakdown of fatty tissue.
Acknowledgement
This study is derived from the research project No. 40389, which was supported by the Research Council of Ferdowsi University of Mashhad.
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