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

2005 ◽  
Vol 98 (6) ◽  
pp. 2376-2380 ◽  
Author(s):  
Walter L. Murfee ◽  
Laura A. Hammett ◽  
Caroline Evans ◽  
Liqin Xie ◽  
Maria Squire ◽  
...  

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) α-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 α-actin-positive vessels per muscle fiber, indicating a reduction in the number of arterioles and venules. The decreases in lectin- and SM α-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.

2015 ◽  
Author(s):  
Stella Maris Lins Terena ◽  
Kristianne Porta Santos Fernandes ◽  
Sandra Kalil ◽  
Agnelo Neves Alves ◽  
Raquel Agnelli Mesquita Ferrari

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10388
Author(s):  
Miloš Kalc ◽  
Ramona Ritzmann ◽  
Vojko Strojnik

Background Whole body vibrations have been used as an exercise modality or as a tool to study neuromuscular integration. There is increasing evidence that longer WBV exposures (up to 10 minutes) induce an acute impairment in neuromuscular function. However, the magnitude and origin of WBV induced fatigue is poorly understood. Purpose The study aimed to investigate the magnitude and origin of neuromuscular fatigue induced by half-squat long-exposure whole-body vibration intervention (WBV) with sets of different duration and compare it to non-vibration (SHAM) conditions. Methods Ten young, recreationally trained adults participated in six fatiguing trials, each consisting of maintaining a squatting position for several sets of the duration of 30, 60 or 180 seconds. The static squatting was superimposed with vibrations (WBV30, WBV60, WBV180) or without vibrations (SHAM30, SHAM60, SHAM180) for a total exercise exposure of 9-minutes in each trial. Maximum voluntary contraction (MVC), level of voluntary activation (%VA), low- (T20) and high-frequency (T100) doublets, low-to-high-frequency fatigue ratio (T20/100) and single twitch peak torque (TWPT) were assessed before, immediately after, then 15 and 30 minutes after each fatiguing protocol. Result Inferential statistics using RM ANOVA and post hoc tests revealed statistically significant declines from baseline values in MVC, T20, T100, T20/100 and TWPT in all trials, but not in %VA. No significant differences were found between WBV and SHAM conditions. Conclusion Our findings suggest that the origin of fatigue induced by WBV is not significantly different compared to control conditions without vibrations. The lack of significant differences in %VA and the significant decline in other assessed parameters suggest that fatiguing protocols used in this study induced peripheral fatigue of a similar magnitude in all trials.


2014 ◽  
Vol 35 (6) ◽  
pp. 425-435 ◽  
Author(s):  
Åsa Beijer ◽  
Hans Degens ◽  
Tobias Weber ◽  
André Rosenberger ◽  
Sebastian Gehlert ◽  
...  

2006 ◽  
Vol 21 (9) ◽  
pp. 1464-1474 ◽  
Author(s):  
Vicente Gilsanz ◽  
Tishya AL Wren ◽  
Monique Sanchez ◽  
Frederick Dorey ◽  
Stefan Judex ◽  
...  

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
James Nelson McKeehen ◽  
Kristen A Baltgalvis ◽  
Jarrod A Call ◽  
Sarah M Greising ◽  
Susan A Novotny ◽  
...  

2012 ◽  
Vol 302 (3) ◽  
pp. E365-E373 ◽  
Author(s):  
Richard A. M. Jonkers ◽  
Marlou L. Dirks ◽  
Christine I. H. C. Nabuurs ◽  
Henk M. De Feyter ◽  
Stephan F. E. Praet ◽  
...  

Lack of physical activity has been related to an increased risk of developing insulin resistance. This study aimed to assess the impact of chronic muscle deconditioning on whole body insulin sensitivity, muscle oxidative capacity, and intramyocellular lipid (IMCL) content in subjects with paraplegia. Nine subjects with paraplegia and nine able-bodied, lean controls were recruited. An oral glucose tolerance test was performed to assess whole body insulin sensitivity. IMCL content was determined both in vivo and in vitro using1H-magnetic resonance spectroscopy and fluorescence microscopy, respectively. Muscle biopsy samples were stained for succinate dehydrogenase (SDH) activity to measure muscle fiber oxidative capacity. Subcellular distributions of IMCL and SDH activity were determined by defining subsarcolemmal and intermyofibrillar areas on histological samples. SDH activity was 57 ± 14% lower in muscle fibers derived from subjects with paraplegia when compared with controls ( P < 0.05), but IMCL content and whole body insulin sensitivity did not differ between groups. In muscle fibers taken from controls, both SDH activity and IMCL content were higher in the subsarcolemmal region than in the intermyofibrillar area. This typical subcellular SDH and IMCL distribution pattern was lost in muscle fibers collected from subjects with paraplegia and had changed toward a more uniform distribution. In conclusion, the lower metabolic demand in deconditioned muscle of subjects with paraplegia results in a significant decline in muscle fiber oxidative capacity and is accompanied by changes in the subcellular distribution patterns of SDH activity and IMCL. However, loss of muscle activity due to paraplegia is not associated with substantial lipid accumulation in skeletal muscle tissue.


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