Stretching and electrical stimulation reduce the accumulation of MyoD, myostatin and atrogin-1 in denervated rat skeletal muscle

Abstract

Denervation causes muscle atrophy and incapacity in humans. Although electrical stimulation (ES) and stretching (St) are commonly used in rehabilitation, it is still unclear whether they stimulate or impair muscle recovery and reinnervation. The purpose of this study was to evaluate the effects of ES and St, alone and combined (ES + St), on the expression of genes that regulate muscle mass (MyoD, Runx1, atrogin-1, MuRF1 and myostatin), on muscle fibre cross-sectional area and excitability, and on the expression of the neural cell adhesion molecule (N-CAM) in denervated rat muscle. ES, St and ES + St reduced the accumulation of MyoD, atrogin-1 and MuRF1 and maintained Runx1 and myostatin expressions at normal levels in denervated muscles. None of the physical interventions prevented muscle fibre atrophy or N-CAM expression in denervated muscles. In conclusion, although ES, St and ES + St changed gene expression, they were insufficient to avoid muscle fibre atrophy due to denervation.

Serum myostatin levels are independently associated with skeletal muscle wasting in patients with heart failure

“…[9,24,25] Previous animal study reported that myostatin levels were increased in muscle atrophy due to denervation (a model of disuse), and stretching and electrical stimulation to muscle, which mimic exercise training, decreased myostatin levels. [26] Therefore, serum myostatin levels depend on the various conditions including severity of HF and treatment including exercise therapy. In the present study, all patients with HF were already compensated and about 70% of HF patients performed exercise training when they tested.…”

Effects of electrical stimulation and stretching on the adaptation of denervated skeletal muscle: implications for physical therapy

“…A series of studies from our laboratory and from collaborators have investigated the effects of ES on the adaptation of denervated muscle in animal models 32,[39][40][41][42][43] . The use of animal models allows a greater control over the variables and avoids important ethical issues involved in this type of study in humans.…”

Effect of tibiotarsal joint inflammation on gene expression and cross-sectional area in rat soleus muscle

“…The cycling conditions for the target genes have been previously described [31][32][33] . Data were analyzed using the comparative cycle threshold (Ct) method described by the manufacturer; GAPDH was the control gene.…”