Decreased muscle GLUT-4 and contraction-induced glucose transport after eccentric contractions
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Decreased muscle GLUT-4 and contraction-induced glucose transport after eccentric contractions. / Kristiansen, S; Asp, Svend; Richter, Erik A.
In: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Vol. 271, No. 2, 1996, p. R477-R482.Research output: Contribution to journal › Journal article › peer-review
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TY - JOUR
T1 - Decreased muscle GLUT-4 and contraction-induced glucose transport after eccentric contractions
AU - Kristiansen, S
AU - Asp, Svend
AU - Richter, Erik A.
PY - 1996
Y1 - 1996
N2 - Eccentric exercise causes muscle damage and decreased muscle glycogen and glucose transporter isoform (GLUT-4) protein content. We investigated whether the contraction-induced increase in skeletal muscle glucose transport and muscle performance is affected by prior eccentric contractions. The calf muscles from rats were stimulated for eccentric (EC) or concentric (CC) contractions or were passively stretched (ST). Muscles from unstimulated control (CT) rats were also studied. Two days later, all rats had their isolated hindlimbs perfused either at rest or during 15 min of isometric muscle contractions. EC rats had a significantly lower total GLUT-4 protein content in the white gastrocnemius (GW) muscle (55%) and red gastrocnemius (GR) muscle (34%) compared with muscle from the CT, ST, and CC rats. In contrast, GLUT-1 protein content was approximately twofold higher in the GW muscle in EC rats than in CT rats. In the GW and GR muscle, prior eccentric exercise decreased contraction-induced stimulation of glucose transport compared with CT, ST, and CC rats despite no difference in tension development and oxygen uptake among the groups. There was no change in total GLUT-4 content and glucose transport in the soleus (S) muscle among the four group. It is concluded that the GLUT-4 and GLUT-1 protein contents in fast-twitch muscle are decreased and increased, respectively, 2 days after eccentric contractions. The functional consequence of these changes appears to be decreased contraction-induced increase in skeletal muscle glucose transport.
AB - Eccentric exercise causes muscle damage and decreased muscle glycogen and glucose transporter isoform (GLUT-4) protein content. We investigated whether the contraction-induced increase in skeletal muscle glucose transport and muscle performance is affected by prior eccentric contractions. The calf muscles from rats were stimulated for eccentric (EC) or concentric (CC) contractions or were passively stretched (ST). Muscles from unstimulated control (CT) rats were also studied. Two days later, all rats had their isolated hindlimbs perfused either at rest or during 15 min of isometric muscle contractions. EC rats had a significantly lower total GLUT-4 protein content in the white gastrocnemius (GW) muscle (55%) and red gastrocnemius (GR) muscle (34%) compared with muscle from the CT, ST, and CC rats. In contrast, GLUT-1 protein content was approximately twofold higher in the GW muscle in EC rats than in CT rats. In the GW and GR muscle, prior eccentric exercise decreased contraction-induced stimulation of glucose transport compared with CT, ST, and CC rats despite no difference in tension development and oxygen uptake among the groups. There was no change in total GLUT-4 content and glucose transport in the soleus (S) muscle among the four group. It is concluded that the GLUT-4 and GLUT-1 protein contents in fast-twitch muscle are decreased and increased, respectively, 2 days after eccentric contractions. The functional consequence of these changes appears to be decreased contraction-induced increase in skeletal muscle glucose transport.
KW - Animals
KW - Biological Transport
KW - Electric Stimulation
KW - Glucose
KW - Glucose Transporter Type 1
KW - Glucose Transporter Type 4
KW - Hindlimb
KW - Isometric Contraction
KW - Male
KW - Monosaccharide Transport Proteins
KW - Muscle Contraction
KW - Muscle Proteins
KW - Muscle, Skeletal
KW - Rats
KW - Rats, Wistar
M3 - Journal article
C2 - 8770151
VL - 271
SP - R477-R482
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 2
ER -
ID: 154748459