Abstract

Recovery from traumatic muscle injuries is typically prolonged and incomplete. Our previous study demonstrated that whole‐body low‐intensity vibration (LIV) enhances healing in a mouse laceration model. We sought to determine whether locally applied LIV (a) improves muscle repair following injury in mice and (b) is directly transduced by cultured muscle cells, via increased IGF‐1 activity. C57BL/6J mice were subjected to laceration of the gastrocnemius muscle and were treated with LIV applied directly to the lower leg for 30 min/day or non‐LIV sham treatment (controls) for 7 or 14 days. LIV was also applied to differentiating myotubes in culture for 30 min/day for 3 or 6 days. Compared with control mice, LIV increased myofiber cross‐sectional area, diameter, and percent area of peripherally nucleated fibers, and decreased percent damaged area after 14 days of treatment. In cultured myotubes, LIV increased fusion and diameter compared with controls after 6 days of treatment. These LIV‐induced effects were associated with increased total Akt on day 7 in injured muscle and on day 3 in myotubes, whereas phosphorylated‐to‐total Akt ratio increased on day 14 in injured muscle and on day 6 in myotubes but were not associated with increased IGF‐1 levels at any time point. These changes were also associated with LIV‐induced suppression of FOXO1 and Atrogin‐1 gene expression at day 7 in injured muscle. These findings demonstrate that muscle cells can directly transduce LIV signals into increased growth and differentiation, and this effect is associated with increased Akt signaling.

Highlights

  • Traumatic muscle injuries are a devastating consequence of motor vehicle accidents, limb salvage surgeries (Turner & Badylak, 2012), and military combat (Covey, 2006)

  • We recently showed that low-intensity vibration (LIV;

  • Applied LIV induced larger myofiber size and improved muscle morphology, compared with injured, but sham-treated controls. These improvements in muscle healing were not associated with any changes in Insulin-like growth factor 1 (IGF-1) protein or mRNA expression

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Summary

Introduction

Traumatic muscle injuries are a devastating consequence of motor vehicle accidents, limb salvage surgeries (Turner & Badylak, 2012), and military combat (Covey, 2006). They are characterized by a significant loss of tissue and inadequate healing leading to impaired muscle function, joint stiffness, and loss of mobility (Bedair et al, 2007; Menetrey, Kasemkijwattana, Fu, Moreland, & Huard, 1999; Shen, Li, Tang, Cummins, & Huard, 2005; Vaittinen, Hurme, Rantanen, & Kalimo, 2002). The only current clinical option for traumatic muscle injury is autologous muscle transfer using muscle flaps or vascularized tissue (Whiteside, 2014) These surgical procedures, are technically difficult, have limited success, and result in donor site morbidity (Turner & Badylak, 2012). There is an urgent need for new therapies that can restore functional muscle tissue following traumatic injury

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