Abstract
Macrophage accumulation in response to decreasing myonuclei may be the major mechanism underlying immobilization-induced muscle fibrosis in muscle contracture, an intervention strategy suppressing these lesions is necessary. Therefore, this research investigated the effect of belt electrode-skeletal muscle electrical stimulation (B-SES), a new electrical stimulation device, to the macrophage accumulation via myonuclei decrease in immobilization-induced muscle fibrosis. 18 Wistar male rats were divided into the control group, immobilization group (with plaster cast fixation to immobilize the soleus muscles in a shortened position for 2 weeks), and B-SES group (with muscle contractile exercise through B-SES during the immobilization period). B-SES stimulation was performed at a frequency of 50 Hz and an intensity of 4.7 mA, muscle contractile exercise by B-SES was applied to the lower limb muscles for 20 minutes/session (twice a day) for 2 weeks (6 times/week). The bilateral soleus muscles were used for histological, immunohistochemical, biochemical, and molecular biological analyses. The number of myonuclei was significantly higher in the B-SES group than in the immobilization group, and there was no significant difference between the B-SES and control groups. The cross-sectional area of type I and II myofibers in the immobilization and B-SES groups was significantly lower than that in the control group, and the cross-sectional area of type I myofibers in the B-SES group was higher than that in the immobilization group. However, Atrogin-1 and MuRF-1 mRNA expression in the immobilization and B-SES groups was significantly higher than those in the control group. Additionally, the number of macrophages, IL-1β, TGF-β1, and α-SMA mRNA expression, and hydroxyproline expression was significantly lower in the control and B-SES groups than those in the immobilization group. This research surmised that muscle contractile exercise through B-SES prevented immobilization-induced muscle fibrosis, and this alteration suppressed the development of muscle contracture.
Highlights
Muscle contracture, caused by immobilization of joints through excessive rest, limits daily activities and interferes with rehabilitation [1]
The number of myonuclei was significantly higher in the belt electrode-skeletal muscle electrical stimulation (B-SES) group than in the immobilization group, and there was no significant difference between the B-SES and control groups
This research surmised that muscle contractile exercise through B-SES prevented immobilization-induced muscle fibrosis, and this alteration suppressed the development of muscle contracture
Summary
Muscle contracture, caused by immobilization of joints through excessive rest, limits daily activities and interferes with rehabilitation [1]. Reduced muscle extensibility decreases joint mobility, contributing to muscle contracture. Muscle fibrosis induced by collagen overexpression was the main cause of reduced muscle extensibility [2]. Previous research has shown that myonuclei are removed from the cytoplasm during muscle atrophy [4]. A study by Reilly and Franklin suggested that the unnecessary cytoplasm generated by decreasing myonuclei was eliminated under muscle atrophy conditions [5]. Macrophages play a key role in the clearance of unnecessary muscle cytoplasm [6]. From these previous studies, the macrophage accumulation in response to decreasing myonuclei may be the major mechanism underlying muscle fibrosis. Our laboratory hypothesized that an intervention strategy suppressing these lesions is necessary to prevent immobilization-induced muscle fibrosis
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