title: Low amplitude, high frequency strains imposed by electrically stimulated skeletal muscle retards the development of osteopenia in the tibiae of hindlimb suspended rats.
abstract: The purpose of this study was to determine the extent to which high frequency, low amplitude skeletal muscle contractions, induced using electrical stimulation, could prevent or retard disuse osteopenia. Ten minutes of 30 Hz electrical stimulation was delivered, 5 days a week, during a 4 week rat-hindlimb suspension protocol. Each pulse generated a peak compressive dynamic strain on the tibia of approximately 200 microepsilon. We hypothesized that the electrical stimulation protocol would significantly reduce the loss of tibial bone mineral density compared to the contralateral control tibia that did not receive electrical stimulation. Compared to the contralateral control limb, the tibia of the stimulated limb had significantly higher bone mineral density and enhanced newly formed bone in the tibial diaphysis. The diaphysis, specifically the posterior bone cortex, of the tibia of the limb receiving the stimulation also demonstrated substantially larger mineral-binding fluorochrome biomarker within the osteocyte lacunae and canalicular volumes. Although the protocol did not prevent disuse osteopenia the evidence suggests that it was effective at reducing the extent of the osteopenia. One possibility for this outcome may be the insensitivity of bone to static, compared to dynamic compressive loads. In the present study there was a considerable static component to the compressive loads that accounted for a large component of the peak load generated by the stimulated skeletal muscle. Nevertheless, the results provide impetus for further development of the methods by which muscle contraction-induced loading of bone can be clinically exploited.
authors.affiliation: Department of Biomedical Engineering, The Cleveland Clinic Foundation, USA.
authors.forename: Ronald J
authors.initials: RJ
authors.lastname: Midura
authors.forename: Charles J
authors.initials: CJ
authors.lastname: Dillman
authors.forename: Mark D
authors.initials: MD
authors.lastname: Grabiner
mesh_terms: D000818:Animals; D015519:Bone Density; D001851:Bone Diseases, Metabolic / Q000209:etiology / Q000473:pathology* / Q000517:prevention & control* / Q000534:rehabilitation; D019245:Compressive Strength; D004548:Elasticity; D004558:Electric Stimulation / Q000379:methods; D004599:Electric Stimulation Therapy / Q000379:methods*; D005260:Female; D019417:Hindlimb Suspension / Q000009:adverse effects / Q000379:methods; D040542:Mechanotransduction, Cellular; D009119:Muscle Contraction; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology*; D020966:Muscular Disorders, Atrophic / Q000150:complications / Q000503:physiopathology* / Q000534:rehabilitation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013314:Stress, Mechanical; D013977:Tibia / Q000473:pathology* / Q000503:physiopathology*; D016896:Treatment Outcome