S. Kristiansen et al., ECCENTRIC CONTRACTIONS DECREASE GLUCOSE-TRANSPORTER TRANSCRIPTION RATE, MESSENGER-RNA, AND PROTEIN IN SKELETAL-MUSCLE, American journal of physiology. Cell physiology, 41(5), 1997, pp. 1734-1738
We have recently shown that eccentric contractions (ECs; forced length
ening of active muscle) elicit a delayed decrease in glucose transport
er (GLUT-I) protein content in rat skeletal muscle and a decrease in s
ubsequent contraction-stimulated glucose transport. Here, we investiga
te whether this decrease in total GLUT-4 protein after prior ECs is du
e to changes in GLUT-4 gene transcription rate and GLUT-I mRNA. level.
Furthermore, the effect of prior ECs on sarcolemmal GLUT-4 protein co
ntent in plasma membrane (PM) vesicles isolated from contraction-stimu
lated muscle was determined. Rat gastrocnemius muscle was electrically
stimulated for ECs, and the contralateral muscle served as unstimulat
ed control (UC). Two days later, the total GLUT-4 protein content was
decreased by 50% (P < 0.05) and 32% (P < 0.05) in the white and red ga
strocnemius muscle, respectively. Furthermore, the GLUT-I mRNA concent
ration was decreased by 41% (P < 0.05) in both the white and red gastr
ocnemius muscle. Moreover, the GLUT-4 transcription rate, determined b
y nuclear run-on analysis, was decreased by 75% (P < 0.05) in mixed EC
gastrocnemius muscle compared with UC muscle. PM vesicles were isolat
ed from EC and UC muscle after 15 min of isometric contractions. The P
M GLUT-4 protein content was reduced by 51% (P < 0.05) in EC muscle co
mpared with UC muscle. In conclusion, 2 days after ECs, the GLUT-4 tra
nscription rate, GLUT-I mRNA, and GLUT-I protein content were decrease
d in rat skeletal muscle. Moreover, the PM GLUT-I protein content in c
ontraction-stimulated muscle was decreased. We suggest that eccentric
muscle contractions decrease muscle GLUT-I transcription rate, resulti
ng in a lower GLUT-I protein content, which in turn decreases the numb
er of GLUT-4 transporters translocated to the sarcolemma, ultimately l
eading to decreased contraction-induced muscle glucose transport.