Abstract
The purpose of this study was to investigate the intensity-specific regenerative effects of microcurrent therapy on gastrocnemius muscle atrophy induced by cast-immobilization in rabbits. Fifteen rabbits were randomly allocated to 3 groups after cast removal: cast-immobilization and sham microcurrent therapy for 2 weeks (group 1); cast-immobilization and microcurrent therapy (25 μA) for 2 weeks (group 2); cast-immobilization and microcurrent therapy (5,000 μA) for 2 weeks (group 3). Clinical parameters [calf circumference, compound muscle action potential (CMAP) of the tibial nerve, thickness of gastrocnemius muscle], cross sectional area of gastrocnemius muscle fibres, and immunohistochemistry was evaluated. The clinical parameters representing mean atrophic changes in group 2 were significantly lower than those in group 3. The cross sectional area of the gastrocnemius muscle fibres and immunohistochemical parameters in group 2 were significantly greater than those in group 3. The results showed that low-intensity microcurrent therapy can more effectively promote regeneration in atrophied gastrocnemius muscle than high-intensity microcurrent therapy.
Highlights
Skeletal muscle dysfunction and atrophy limit quality of life and daily living activities in patients apart from the underlying disease conditions[1]
Given the paucity of data and uncertainty about the effective intensity in treatment, we aimed to investigate the regenerative effects of different intensities of Microcurrent therapy (MT) on gastrocnemius (GCM) muscle atrophy induced by Immobilisation by cast (IC) in rabbits
The most significant finding of the present study is the greater regenerative effect seen in atrophied GCM muscle in group 2 than in groups 1 and 3, suggesting that low-intensity (25 mA) MT could minimize the detrimental effects induced by 2-week IC as compared to no MT or high-intensity (5,000 mA) MT
Summary
Skeletal muscle dysfunction and atrophy limit quality of life and daily living activities in patients apart from the underlying disease conditions[1]. Deconditioning and reduced muscle activity are estimated to be the most relevant factors, which lead to muscle atrophy and loss of function in patients[1–2]. Treating soft tissue and bone injuries by immobilisation may result in skeletal muscle atrophy and decreased functional performance[3–4]. Tion causes significant muscle remodelling including loss of myofibrillar proteins, changes in metabolic enzyme activities, and vascular and neural alterations[5]. The rapid loss in myofibrillar proteins during immobilisation is induced by a transient decrease in protein synthesis, followed by increased protein degradation, resulting in net protein loss[6]. Regardless of the cause of muscle atrophy, effective skeletal muscle recovery appears to be dependent on protein synthesis
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