Most miRNAs are transcribed from DNA as long primary transcripts (pri-miRNA) which are processed by Drosha resulting in pre-miRNA hairpins with a length of about 70 nucleotides. After being transported from nucleus to the cytosol via Exportin-5 the hairpins are cleaved to form miRNA duplexes which again are cleaved to form the mature miRNAs. These short single-stranded miRNAs are incorporated into the RNA induced silencing complex (RISC) which regulates protein expression (Wessner et al., 2011).
To date, more than 700 human miRNAs have been identified (and the number is still increasing), possibly regulating 30 – 60% of protein-encoding genes (Friedman et al., 2009 & Griffiths-Jones et al., 2008). miRNAs usually are expressed in various cell types but interestingly, some miRNAs are expressed tissue-specific such as miR-1, miR-133a, and miR-206 in muscle (Lee et al., 2008).
(Eccentric) exercise-induced muscle damage involves a series of events starting with mechanical disruption of sarcomeres, followed by impaired excitation-contraction coupling and calcium signaling, and finally, activation of proteolytic pathways related to muscle fiber degradation and repair (Griffiths-Jones et al., 2008). Muscle damage coincides with ultra-structural changes in muscle architecture, loss of muscular strength and muscle soreness. miRNAs play important roles in the plasticity of skeletal muscle in response to hypertrophy but also atrophy signals, whereby local but also systemic inflammatory processes accompany the remodeling of skeletal muscle tissue. However, data especially derived from human studies are sparse, possibly due to the fact that skeletal muscle biopsies are not as easy to access and to investigate as blood.
Up to now, it is unproven whether miRNAs are involved in inflammatory processes within skeletal muscle tissue but a small number of striated muscle-specific miRNAs so-called MyomiRs have been identified and shown to have an important role in myogenesis, embryonic muscle growth and cardiac function and hypertrophy (Zhang et al., 2010). miR-206, a muscle-specific miRNA that is up-regulated by exercise in the intracellular space (Nielsen et al.2010) may be involved in tissue repair and adaptation.
Data defining circulating micro-RNA (c-miRNA) behavior in the settings of acute exercise bouts and sustained exercise training in healthy humans are lacking. Identification of miRNAs specifically regulated by exercise could reveal unique biomarkers of exercise physiology and would lend significant insight into the molecular control of exercise adaptation.
The purpose of this study was to assess miRNA-206 concentrations in basketball athletes at rest and after a proposed basketball game, before and after 12 weeks period of the training program.
Exercise training induces numerous muscular and cardiovascular changes including mitochondrial synthesis (Kiessling et al. 1973), myocardial remodeling (Baggish et al. 2008), and angiogenesis (Gute et al. 1996). Although such adaptations and their attendant impact on exercise capacity and health outcomes have been well documented, the cellular and molecular mechanisms leading to these changes remain incompletely understood (Baggish et al., 2011).
Recently, microRNA molecules (miRNAs) have been identified as essential intracellular mediators of processes inherent in exercise adaptation including angiogenesis (Zhang, 2010), inflammation (Davidson-Moncada et al. 2010), mitochondrial metabolism (Chan et al. 2009; Dang, 2010), cardiac/skeletal muscle contractile force generation, and tissue hypertrophy (Davidsen et al. 2011).