Skeletal muscle hypertrophy after chronic restriction of venous blood flow in rats.
OBJECTIVE
Some previous studies have shown that resistance exercise training with venous occlusion causes an enhanced hypertrophy in human muscles. To investigate the effects of blood flow on muscular size at either cellular or subcellular level, we developed an animal model in which several veins from hindlimb muscles of the rat are surgically crush-occluded.


METHODS
Twenty-four male Wister rats were randomly assigned into either a group for sham operation (sham group) or a group for venous occlusion (experimental group; N = 12 for each group). Fourteen days after the operation, plantaris, soleus, gastrocnemius, extensor digitorum longus, and tibialis anterior muscles were dissected from hindlimbs and subjected to morphological and biochemical analyses.


RESULTS
Fourteen days after the operation, the muscles expect for soleus showed similar increases in wet weight/body weight (by 7-12%) as compared with the sham-operated group (P < 0.05). Further analyses on the plantaris muscle showed increases in muscle dry weight/ body weight (by 10%) and the concentrations of myofibrillar protein (by 23%), glycogen (by 93%) and lactate (by 23%) after the operation (P < 0.05). Mean fiber cross-sectional area was larger by 34% in the experimental group than in the sham-operated group (P < 0.01). The content of HSP-72 increased, whereas that of myostatin protein decreased (P < 0.01). The expression of nitric oxide synthase-1 (NOS-1) mRNA increased (P < 0.01), whereas that of IGF-1 mRNA showed no significant change (P = 0.36). Although the muscle nitric oxide (NO) concentration tended to increase, but the change was not significant (P = 0.10).


CONCLUSIONS
Changes in muscle blood flow may affect the muscular size through actions of HSP-72, myostatin, and NOS-1.
Kawada
Shigeo
S
Institute of Environmental Studies, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa-shi, Chiba Prefecture, Japan. kawada@k.u-tokyo.ac.jp
Ishii
Naokata
N
D000818:Animals; D001483:Base Sequence; D003251:Constriction, Pathologic; D017931:DNA Primers; D006003:Glycogen / Q000378:metabolism; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000378:metabolism; D006984:Hypertrophy; D007564:Japan; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D055435:Myostatin; D019001:Nitric Oxide Synthase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D016212:Transforming Growth Factor beta / Q000378:metabolism
D017931:DNA Primers; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; C525911:MSTN protein, human; C525913:Mstn protein, rat; D055435:Myostatin; D016212:Transforming Growth Factor beta; D019344:Lactic Acid; D006003:Glycogen; D019001:Nitric Oxide Synthase