Literature DB >> 15677735

High-frequency, low-magnitude vibrations suppress the number of blood vessels per muscle fiber in mouse soleus muscle.

Walter L Murfee1, Laura A Hammett, Caroline Evans, Liqin Xie, Maria Squire, Clinton Rubin, Stefan Judex, Thomas C Skalak.   

Abstract

Extremely low-magnitude (0.3 g), high-frequency (30-90 Hz), whole body vibrations can stimulate bone formation and are hypothesized to provide a surrogate for the oscillations of muscle during contraction. Little is known, however, about the potential of these mechanical signals to stimulate adaptive responses in other tissues. The objective of this study was to determine whether low-level mechanical signals produce structural adaptations in the vasculature of skeletal muscle. Eight-week-old male BALB/cByJ (BALB) mice were divided into two experimental groups: mice subjected to low-level, whole body vibrations (45 Hz, 0.3 g) superimposed on normal cage activities for 15 min/day (n = 6), and age-matched controls (n = 7). After the 6-wk experimental protocol, sections from end and mid regions of the soleus muscles were stained with lectin from Bandeiraea Simplicifolia, an endothelial cell marker, and smooth muscle (SM) alpha-actin, a perivascular cell marker. Six weeks of this low-level vibration caused a 29% decrease in the number of lectin-positive vessels per muscle fiber in the end region of the soleus muscle, indicating a significant reduction in the number of capillaries per muscle fibers. Similarly, these vibrations caused a 36% reduction in SM alpha-actin-positive vessels per muscle fiber, indicating a reduction in the number of arterioles and venules. The decreases in lectin- and SM alpha-actin-positive vessels per muscle fiber ratios were not significant in the mid muscle sections. These results demonstrate the sensitivity of the vasculature in mouse skeletal muscle to whole body, low-level mechanical signals.

Entities:  

Keywords:  Non-programmatic

Mesh:

Year:  2005        PMID: 15677735     DOI: 10.1152/japplphysiol.01135.2004

Source DB:  PubMed          Journal:  J Appl Physiol (1985)        ISSN: 0161-7567


  21 in total

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Journal:  Calcif Tissue Int       Date:  2010-06-09       Impact factor: 4.333

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