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Recovery from traumatic muscle injuries is typically prolonged and incomplete, leading to impaired muscle and joint function. We sought to determine whether mechanical stimulation via whole-body low-intensity vibration (LIV) could (1) improve muscle regeneration and (2) reduce muscle fibrosis following traumatic injury. C57BL/6J mice were subjected to a laceration of the gastrocnemius muscle and were treated with LIV (0.2 g at 90 Hz or 0.4 g at 45 Hz for 30 min/day) or non-LIV sham treatment (controls) for seven or 14 days. Muscle regeneration and fibrosis were assessed in hematoxylin and eosin or Masson’s trichrome stained muscle cryosections, respectively. Compared to non-LIV control mice, the myofiber cross-sectional area was larger in mice treated with each LIV protocol after 14 days of treatment. Minimum fiber diameter was also larger in mice treated with LIV of 90 Hz/0.2 g after 14 days of treatment. There was also a trend toward a reduction in collagen deposition after 14 days of treatment with 45 Hz/0.4 g (p = 0.059). These findings suggest that LIV may improve muscle healing by enhancing myofiber growth and reducing fibrosis. The LIV-induced improvements in muscle healing suggest that LIV may represent a novel therapeutic approach for improving the healing of traumatic muscle injuries.

Aim Investigate the immediate effect of low intensity vibration on skin blood flow and its underlying control mechanisms in healthy human participants. Materials and methods One-group pre-post design in a university laboratory setting. Nine adults underwent two bouts of 10-minute vibration (30Hz, peak acceleration 0.4g). Outcome measures include skin blood flow, and skin temperature on the right foot. To examine the control mechanisms underlying the vibration-induced blood flow response, SHORT-TIME Fourier analyses were computed to obtain the spectral densities for three frequency bands: metabolic (0.0095–0.02Hz), neurogenic (0.02–0.06Hz), and myogenic (0.06–0.15Hz). Non-parametric Friedman’s tests were computed to compare changes of the outcome measures and control mechanisms over the course of vibration. Results Vibration increased skin blood flow during both bouts of vibration, however the effect did not last after vibration was terminated. Myogenic spectral density increased during both bouts of vibration, whereas the metabolic and neurogenic spectral densities increased only during the 2nd bout of vibration. Interestingly, only the metabolic spectral density remained elevated after vibration ended. Conclusion Low intensity vibration produced acute increases in skin blood flow mediated in part by vascular control mechanisms of myogenic origin. Further investigation is warranted to determine whether low intensity vibration induces similar increases in skin blood flow in populations prone to developing chronic non-healing wounds, such as spinal cord injury and diabetes.

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., Our findings demonstrate that muscle cells can directly transduce LIV signals into increased growth and differentiation, and this effect is associated with increased Akt signaling.