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Journal of Applied Physiology, Vol 62, Issue 6 2180-2186, Copyright © 1987 by American Physiological Society
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R. W. Tsika, R. E. Herrick and K. M. Baldwin
The purpose of this study was to investigate the role of chronic weight-bearing activity as the primary inducer of compensatory muscle growth and changes in myosin isoform expression in rodent fast-twitch plantaris muscle. Thus, female rats were subjected to the independent and simultaneous exposure of functional overload (induced via synergist removal) and hindlimb unweighting (suspension) for 6 wk. Groups (n = 7/group) consisted of normal-control (NC); overload (OV); normal-suspension (N-SUS); and overload-suspension (OV-SUS). Body weight of both suspension groups was significantly less than both the NC and OV groups (P less than 0.001). Compared with the NC group, normalized plantaris weight (mg/g body wt) of both the OV and OV-SUS groups was greater, whereas that of the N-SUS was lower (P less than 0.001). However, normalized plantaris weight was greater in OV compared with OV-SUS by 35% (P less than 0.001). Myofibril protein content (mg/g) and Ca2+-regulated myofibril adenosinetriphosphatase (ATPase) specific activity were similar for all groups except that ATPase was lower in the OV group compared with the other groups (P less than 0.05). Native myosin isoform analysis revealed a significant increase in the expression of slow and intermediate myosin and the repression of fast myosin 1 (Fm1) in OV compared with NC. This shift in expression was not as pronounced in the OV-SUS group. Interestingly, only traces of slow myosin were observed in the N-SUS group compared with the other groups. These results suggest that weight bearing is an essential component of the overload model for inducing significant increases in both muscle mass and slow myosin isoform expression. Second, lack of weight bearing, while not markedly affecting fast myosins, appears to repress the expression of slow myosin.
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