Abstract
The objective of the study was to determine if low intensity, high frequency vibration training impacted the musculoskeletal system in a mouse model of Duchenne muscular dystrophy, relative to healthy mice. Three-week old wildtype (n = 26) and mdx mice (n = 22) were randomized to non-vibrated or vibrated (45 Hz and 0.6 g, 15 min/d, 5 d/wk) groups. In vivo and ex vivo contractile function of the anterior crural and extensor digitorum longus muscles, respectively, were assessed following 8 wks of vibration. Mdx mice were injected 5 and 1 days prior to sacrifice with Calcein and Xylenol, respectively. Muscles were prepared for histological and triglyceride analyses and subcutaneous and visceral fat pads were excised and weighed. Tibial bones were dissected and analyzed by micro-computed tomography for trabecular morphometry at the metaphysis, and cortical geometry and density at the mid-diaphysis. Three-point bending tests were used to assess cortical bone mechanical properties and a subset of tibiae was processed for dynamic histomorphometry. Vibration training for 8 wks did not alter trabecular morphometry, dynamic histomorphometry, cortical geometry, or mechanical properties (P≥0.34). Vibration did not alter any measure of muscle contractile function (P≥0.12); however the preservation of muscle function and morphology in mdx mice indicates vibration is not deleterious to muscle lacking dystrophin. Vibrated mice had smaller subcutaneous fat pads (P = 0.03) and higher intramuscular triglyceride concentrations (P = 0.03). These data suggest that vibration training at 45 Hz and 0.6 g did not significantly impact the tibial bone and the surrounding musculature, but may influence fat distribution in mice.
Highlights
Duchenne muscular dystrophy (DMD) is an X-chromosomelinked disease characterized by progressive muscle weakness [1,2,3]
Preliminary data suggest that bone size is reduced in various skeletal sites in boys with DMD [11,12], and those data are supported by reports that that these patients have low bone mass across their lifespan [4,13]
This is supported by evidence that the discrepancies in bone mass between boys with DMD and their age-matched peers are accentuated with age, especially following the loss of ambulation where skeletal regions such as the hip and calcaneus experience dramatic bone loss [4,13]
Summary
Duchenne muscular dystrophy (DMD) is an X-chromosomelinked disease characterized by progressive muscle weakness [1,2,3]. Compromised bone strength in DMD is multi-factorial, likely including effects of failure to accumulate peak bone strength during growth as well as declines in bone health secondary to the muscle disease. Paralleling suboptimal attainment of bone strength, continual declines in muscle function associated with disease progression (i.e., reduced magnitude and frequency of muscle-induced mechanical loads) likely initiates disuse-mediated bone remodeling. This is supported by evidence that the discrepancies in bone mass between boys with DMD and their age-matched peers are accentuated with age, especially following the loss of ambulation where skeletal regions such as the hip and calcaneus experience dramatic bone loss [4,13]. Effective bone-sparing interventions are warranted to thwart declines in bone health of boys with DMD in effort to preserve bone strength and prevent fractures
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
