Changes in skeletal muscle size, fibre-type composition and capillary supply after chronic venous occlusion in rats.
OBJECTIVE
We have previously shown that surgical occlusion of some veins from skeletal muscle results in muscle hypertrophy without mechanical overloading in the rat. The present study investigated the changes in muscle-fibre composition and capillary supply in hypertrophied muscles after venous occlusion in the rat hindlimb.


METHODS
Sixteen male Wistar rats were randomly assigned into two groups: (i) sham operated (sham-operated group; n = 7); (ii) venous occluded for 2 weeks (2-week-occluded group; n = 9). At the end of the experimental period, specimens of the plantaris muscle were dissected from the hindlimbs and subjected to biochemical and histochemical analyses.


RESULTS
Two weeks after the occlusion, both the wet weight of plantaris muscle relative to body weight and absolute muscle weight showed significant increases in the 2-week-occluded group ( approximately 15%) when compared with those in the sham-operated group. The concentrations of muscle glycogen and lactate were higher in the 2-week-occluded group, whereas staining intensity of muscle lipid droplets was lower in the 2-week-occluded group than those in the sham-operated group. The percentage of type I muscle fibre decreased, whereas that of type IIb fibre increased in the 2-week-occluded group when compared with the sham-operated group. Although the expression of vascular endothelial growth factor-188 mRNA increased, the number of capillaries around the muscle fibres tended to decrease (P = 0.07).


CONCLUSIONS
Chronic venous occlusion causes skeletal muscle hypertrophy with fibre-type transition towards faster types and changes in contents of muscle metabolites.
Kawada
S
S
Department of Human and Engineered Environmental Studies, Graduate School of Frontier Sciences, The University of Tokyo, Chiba Prefecture, Japan. kawada@k.u-tokyo.ac.jp
Ishii
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N
D000818:Animals; D001391:Azo Compounds; D002908:Chronic Disease; D003251:Constriction, Pathologic; D006984:Hypertrophy; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000502:physiology*; D018995:Myosin Heavy Chains / Q000737:chemistry / Q000378:metabolism; D020033:Protein Isoforms; D051381:Rats; D017208:Rats, Wistar; D013194:Staining and Labeling; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D014680:Veins
D001391:Azo Compounds; C497444:Hif1a protein, rat; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D020033:Protein Isoforms; D042461:Vascular Endothelial Growth Factor A; D018995:Myosin Heavy Chains; C011049:oil red O