Publication | Closed Access
Disuse deterioration of human skeletal muscle challenged by resistive exercise superimposed with vibration: evidence from structural and proteomic analysis
68
Citations
37
References
2014
Year
Musculoskeletal ScienceMuscle FunctionResistive ExerciseCytoskeletonMechanotransductionCellular PhysiologyMuscle AtrophyMuscle PhysiologyKinesiologyMuscle InjurySkeletal MuscleExerciseBiomechanicsApplied PhysiologyMolecular SignalingMechanobiologyHealth SciencesMolecular PhysiologyMusculoskeletal FunctionRehabilitationNeuromuscular PhysiologyCell BiologyDisuse DeteriorationHuman Skeletal MusclePhysiologyExercise PhysiologyPresent Bed RestDifferential ProteomicsMedicine
In the present bed rest (BR) study, 23 volunteers were randomized into 3 subgroups: 60 d BR control (Ctr); BR with resistive exercise (RE; lower-limb load); and resistive vibration exercise (RVE; RE with superimposed vibration). The aim was to analyze by confocal and electron microscopy the effects of vibration on myofibril and filament integrity in soleus (Sol) and vastus lateralis (VL) muscle; differential proteomics of contractile, cytoskeletal, and costameric proteins (TN-C, ROCK1, and FAK); and expression of PGC1α and atrophy-related master genes MuRF1 and MuRF2. RVE (but not RE) preserved myofiber size and phenotype in Sol and VL by overexpressing MYBPC1 (42%, P ≤ 0.01), WDR1 (39%, P ≤ 0.01), sarcosin (84%, P ≤ 0.01), and CKM (20%, P ≤ 0.01) and prevented myofibrillar ultrastructural damage as detectable by MuRF1 expression. In Sol, cytoskeletal and contractile proteins were normalized by RVE, and TN-C increased (59%, P ≤ 0.01); the latter also with RE (108%, P ≤ 0.01). In VL, the outcomes of both RVE (acting on sarcosin and desmin) and RE (by way of troponinT-slow and MYL2) were similar. RVE appears to be a highly efficient countermeasure protocol against muscle atrophy and ultrastructural and molecular dysregulation induced by chronic disuse.
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