Label X Muscle - SLOW MUSCLE BUILDS AND LOW ENERGY(Hard to Gain Muscles) v1

Label X Muscle - SLOW MUSCLE BUILDS AND LOW ENERGY(Hard to Gain Muscles)

Nebulin and Lmod2 are critical for specifying thin-filament length in skeletal muscle

Regulating the thin-filament length in muscle is crucial for controlling the number of myosin motors that generate power. The giant protein nebulin forms a long slender filament that associates along the length of the thin filament in skeletal muscle with functions that remain largely obscure. Here nebulin’s role in thin-filament length regulation was investigated by targeting entire super-repeats in the Neb gene; nebulin was either shortened or lengthened by 115 nm. Its effect on thin-filament length was studied using high-resolution structural and functional techniques. Results revealed that thin-filament length is strictly regulated by the length of nebulin in fast muscles. Nebulin’s control is less tight in slow muscle types where a distal nebulin-free thin-filament segment exists, the length of which was found to be regulated by leiomodin-2 (Lmod2). We propose that strict length control by nebulin promotes high-speed shortening and that dual-regulation by nebulin/Lmod2 enhances contraction efficiency.

Adaptive Mechanisms of a Mouse Locomotor Muscles "M. Soleus" and "M. Edl" the Conditions of the Allergic Modification of the Organism

The relevance of the problem discussed in the article is connected to the fact that mandatory athletes’ vaccination before competitions leads to the change in the function of the muscular system, the mechanisms of which have not yet been fully clarified. The purpose of the article is to determine the mechanism of a mouse skeletal muscles adaptation (SM) ("fast" (in case of m.edl) and "slow" (in case of m.soleus) in case of allergic alteration. The following research methods were used in the presented work: registration of the constrictive function of the abovementioned muscles in vitro to the humoral constriction initiators (carbacholinum and KCI) and determination of malonyldialdehyde (MDA) level in them, just as the indicators of the oxidant and antioxidant equilibrium. It has been demonstrated that the change in the “slow” muscle strength correlates with the MDA level dynamics, evidently, reflects the adaptation processes during the allergic modification. "Fast" muscles turn out to be more sustainable to oxidative stress which is most probably achieved by the work of compensatory mechanisms and is expressed in quite minor changes in the MDA dynamics. The article can be used in the search of the new possibilities for the correction of the locomotor muscles function in the conditions of the allergy, аnd also while the therapeutic impact strategy is determined, taking into account their fiber composition.

miR-206 enforces a slow muscle phenotype

ABSTRACTStriated muscle is a highly specialized collection of tissues with contractile properties that vary according to functional needs. Although muscle fiber types are established postnatally, lifelong plasticity facilitates stimulus-dependent adaptation. Functional adaptation requires molecular adaptation, which is partially provided by miRNA-mediated post-transcriptional regulation. miR-206 is a muscle-specific miRNA enriched in slow muscles. We investigated whether miR-206 drives the slow muscle phenotype or is merely an outcome. We found that miR-206 expression increases in both physiological (including female sex and endurance exercise) and pathological conditions (muscular dystrophy and adrenergic agonism) that promote a slow phenotype. Consistent with that observation, the slow soleus muscle of male miR-206-knockout mice displays a faster phenotype than wild-type mice. Moreover, left ventricles of male miR-206 knockout mice have a faster myosin profile, accompanied by dilation and systolic dysfunction. Thus, miR-206 appears to be necessary to enforce a slow skeletal and cardiac muscle phenotype and to play a key role in muscle sexual dimorphisms.