title: High-frequency, low-magnitude vibration does not prevent bone loss resulting from muscle disuse in mice following botulinum toxin injection.
abstract: High-frequency, low-magnitude vibration enhances bone formation ostensibly by mimicking normal postural muscle activity. We tested this hypothesis by examining whether daily exposure to low-magnitude vibration (VIB) would maintain bone in a muscle disuse model with botulinum toxin type A (BTX). Female 16-18 wk old BALB/c mice (N = 36) were assigned to BTX-VIB, BTX-SHAM, VIB, or SHAM. BTX mice were injected with BTX (20 µL; 1 U/100 g body mass) into the left hindlimb posterior musculature. All mice were anaesthetized for 20 min/d, 5 d/wk, for 3 wk, and the left leg mounted to a holder. Through the holder, VIB mice received 45 Hz, ± 0.6 g sinusoidal acceleration without weight bearing. SHAM mice received no vibration. At baseline and 3 wk, muscle cross-sectional area (MCSA) and tibial bone properties (epiphysis, metaphysis and diaphysis) were assessed by in vivo micro-CT. Bone volume fraction in the metaphysis decreased 12 ± 9% and 7 ± 6% in BTX-VIB and BTX-SHAM, but increased in the VIB and SHAM. There were no differences in dynamic histomorphometry outcomes between BTX-VIB and BTX nor between VIB and SHAM. Thus, vibration did not prevent bone loss induced by a rapid decline in muscle activity nor produce an anabolic effect in normal mice. The daily loading duration was shorter than would be expected from postural muscle activity, and may have been insufficient to prevent bone loss. Based on the approach used in this study, vibration does not prevent bone loss in the absence of muscle activity induced by BTX.
authors.affiliation: Faculty of Kinesiology, University of Calgary, Calgary, Canada.
authors.forename: Sarah L
authors.initials: SL
authors.lastname: Manske
authors.forename: Craig A
authors.initials: CA
authors.lastname: Good
authors.forename: Ronald F
authors.initials: RF
authors.lastname: Zernicke
authors.forename: Steven K
authors.initials: SK
authors.lastname: Boyd
mesh_terms: D000818:Animals; D001851:Bone Diseases, Metabolic / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D019274:Botulinum Toxins, Type A / Q000009:adverse effects* / Q000494:pharmacology; D005260:Female; D051379:Mice; D008807:Mice, Inbred BALB C; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D020966:Muscular Disorders, Atrophic / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D009498:Neurotoxins / Q000009:adverse effects* / Q000494:pharmacology; D026741:Physical Therapy Modalities; D013977:Tibia / Q000473:pathology / Q000503:physiopathology; D014732:Vibration
chemical_list: D009498:Neurotoxins; D019274:Botulinum Toxins, Type A