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      Low-Magnitude, High-Frequency Vibration Fails to Accelerate Ligament Healing but Stimulates Collagen Synthesis in the Achilles Tendon

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          Abstract

          Background

          Low-magnitude, high-frequency vibration accelerates fracture and wound healing and prevents disuse atrophy in musculoskeletal tissues.

          Purpose

          To investigate the role of low-magnitude, high-frequency vibration as a treatment to accelerate healing of an acute ligament injury and to examine gene expression in the intact Achilles tendon of the injured limb after low-magnitude, high-frequency vibration.

          Study Design

          Controlled laboratory study.

          Methods

          Complete surgical transection of the medial collateral ligament (MCL) was performed in 32 Sprague-Dawley rats, divided into control and low-magnitude, high-frequency vibration groups. Low-magnitude, high-frequency vibration started on postoperative day 2, and rats received vibration for 30 minutes a day for 12 days. All rats were sacrificed 2 weeks after the operation, and their intact and injured MCLs were biomechanically tested or used for histological analysis. Intact Achilles tendons from the injured limb were evaluated for differences in gene expression.

          Results

          Mechanical testing revealed no differences in the ultimate tensile load or the structural stiffness between the control and vibration groups for either the injured or intact MCL. Vibration exposure increased gene expression of collagen 1 alpha (3-fold), interleukin 6 (7-fold), cyclooxygenase 2 (5-fold), and bone morphogenetic protein 12 (4-fold) in the intact Achilles tendon when compared with control tendons ( P < .05).

          Conclusion

          While no differences were observed in the mechanical or histological properties of the fully transected MCL after low-magnitude, high-frequency vibration treatment, significant enhancements in gene expression were observed in the intact Achilles tendon. These included collagen, several inflammatory cytokines, and growth factors critical for tendons.

          Clinical Relevance

          As low-magnitude, high-frequency vibration had no negative effects on ligament healing, vibration therapy may be a useful tool to accelerate healing of other tissues (bone) in multitrauma injuries without inhibiting ligament healing. Additionally, the enhanced gene expression in response to low-magnitude, high-frequency vibration in the intact Achilles tendon suggests the need to further study its potential to accelerate tendon healing in partial injury or repair models.

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          Most cited references 45

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          Mechanical regulation of signaling pathways in bone.

          A wide range of cell types depend on mechanically induced signals to enable appropriate physiological responses. The skeleton is particularly dependent on mechanical information to guide the resident cell population towards adaptation, maintenance and repair. Research at the organ, tissue, cell and molecular levels has improved our understanding of how the skeleton can recognize the functional environment, and how these challenges are translated into cellular information that can site-specifically alter phenotype. This review first considers those cells within the skeleton that are responsive to mechanical signals, including osteoblasts, osteoclasts, osteocytes and osteoprogenitors. This is discussed in light of a range of experimental approaches that can vary parameters such as strain, fluid shear stress, and pressure. The identity of mechanoreceptor candidates is approached, with consideration of integrins, pericellular tethers, focal adhesions, ion channels, cadherins, connexins, and the plasma membrane including caveolar and non-caveolar lipid rafts and their influence on integral signaling protein interactions. Several mechanically regulated intracellular signaling cascades are detailed including activation of kinases (Akt, MAPK, FAK), β-catenin, GTPases, and calcium signaling events. While the interaction of bone cells with their mechanical environment is complex, an understanding of mechanical regulation of bone signaling is crucial to understanding bone physiology, the etiology of diseases such as osteoporosis, and to the development of interventions to improve bone strength. Copyright © 2012 Elsevier B.V. All rights reserved.
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            Mechanical signals as anabolic agents in bone.

            Aging and a sedentary lifestyle conspire to reduce bone quantity and quality, decrease muscle mass and strength, and undermine postural stability, culminating in an elevated risk of skeletal fracture. Concurrently, a marked reduction in the available bone-marrow-derived population of mesenchymal stem cells (MSCs) jeopardizes the regenerative potential that is critical to recovery from musculoskeletal injury and disease. A potential way to combat the deterioration involves harnessing the sensitivity of bone to mechanical signals, which is crucial in defining, maintaining and recovering bone mass. To effectively utilize mechanical signals in the clinic as a non-drug-based intervention for osteoporosis, it is essential to identify the components of the mechanical challenge that are critical to the anabolic process. Large, intense challenges to the skeleton are generally presumed to be the most osteogenic, but brief exposure to mechanical signals of high frequency and extremely low intensity, several orders of magnitude below those that arise during strenuous activity, have been shown to provide a significant anabolic stimulus to bone. Along with positively influencing osteoblast and osteocyte activity, these low-magnitude mechanical signals bias MSC differentiation towards osteoblastogenesis and away from adipogenesis. Mechanical targeting of the bone marrow stem-cell pool might, therefore, represent a novel, drug-free means of slowing the age-related decline of the musculoskeletal system.
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              Hormonal responses to whole-body vibration in men.

              The aim of this study was to evaluate the acute responses of blood hormone concentrations and neuromuscular performance following whole-body vibration (WBV) treatment. Fourteen male subjects [mean (SD) age 25 (4.6) years] were exposed to vertical sinusoidal WBV, 10 times for 60 s, with 60 s rest between the vibration sets (a rest period lasting 6 min was allowed after 5 vibration sets). Neuromuscular performance tests consisting of counter-movement jumps and maximal dynamic leg presses on a slide machine, performed with an extra load of 160% of the subjects body mass, and with both legs were administered before and immediately after the WBV treatment. The average velocity, acceleration, average force, and power were calculated and the root mean square electromyogram (EMGrms) were recorded from the vastus lateralis and rectus femoris muscles simultaneously during the leg-press measurement. Blood samples were also collected, and plasma concentrations of testosterone (T), growth hormone (GH) and cortisol (C) were measured. The results showed a significant increase in the plasma concentration of T and GH, whereas C levels decreased. An increase in the mechanical power output of the leg extensor muscles was observed together with a reduction in EMGrms activity. Neuromuscular efficiency improved, as indicated by the decrease in the ratio between EMGrms and power. Jumping performance, which was measured using the counter-movement jump test, was also enhanced. Thus, it can be argued that the biological mechanism produced by vibration is similar to the effect produced by explosive power training (jumping and bouncing). The enhancement of explosive power could have been induced by an increase in the synchronisation activity of the motor units, and/or improved co-ordination of the synergistic muscles and increased inhibition of the antagonists. These results suggest that WBV treatment leads to acute responses of hormonal profile and neuromuscular performance. It is therefore likely that the effect of WBV treatment elicited a biological adaptation that is connected to a neural potentiation effect, similar to those reported to occur following resistance and explosive power training. In conclusion, it is suggested that WBV influences proprioceptive feedback mechanisms and specific neural components, leading to an improvement of neuromuscular performance. Moreover, since the hormonal responses, characterised by an increase in T and GH concentration and a decrease in C concentration, and the increase in neuromuscular effectiveness were simultaneous but independent, it is speculated that the two phenomena might have common underlying mechanisms.
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                Author and article information

                Journal
                101620522
                41944
                Orthop J Sports Med
                Orthop J Sports Med
                Orthopaedic journal of sports medicine
                2325-9671
                10 June 2015
                27 May 2015
                May 2015
                15 June 2015
                : 3
                : 5
                Affiliations
                []Department of Physical Therapy, School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana, USA.
                []Department of Orthopedics, University of North Carolina, Chapel Hill, North Carolina, USA.
                Author notes
                [* ]Address correspondence to William R. Thompson, DPT, PhD, 1140 West Michigan Street, CF322A, Indianapolis, IN 27599, USA ( thompwil@ 123456iu.edu )
                Article
                NIHMS698438
                10.1177/2325967115585783
                4467027
                © The Author(s) 2015

                This open-access article is published and distributed under the Creative Commons Attribution - NonCommercial - No Derivatives License ( http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits the noncommercial use, distribution, and reproduction of the article in any medium, provided the original author and source are credited. You may not alter, transform, or build upon this article without the permission of the Author(s).

                For reprints and permission queries, please visit SAGE’s Web site at http://www.sagepub.com/journalsPermissions.nav.

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