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Copenhagen Muscle Research Centre, August Krogh Institute, University of Copenhagen, DK-2100 Copenhagen Ø, Denmark
Received 6 February 1996; accepted in final form 3 July 1996.
Asp, Sven, and Erik A. Richter. Decreased insulin
action on muscle glucose transport after eccentric contractions in rats. J. Appl. Physiol. 81(5):
1924-1928, 1996.
We have recently shown that eccentric
contractions (Ecc) of rat calf muscles cause muscle damage and
decreased glycogen and glucose transporter GLUT-4 protein content in
the white (WG) and red gastrocnemius (RG) but not in the soleus (S) (S. Asp, S. Kristiansen, and E. A. Richter. J. Appl.
Physiol. 79: 1338-1345, 1995). To study whether
these changes affect insulin action, hindlimbs were perfused at three different insulin concentrations (0, 200, and 20,000 µU/ml) 2 days
after one-legged eccentric contractions of the calf muscles. Compared
with control, basal glucose transport was slightly higher (P < 0.05) in Ecc-WG and -RG,
whereas it was lower (P < 0.05) at
both submaximal and maximal insulin concentrations in the Ecc-WG and at
maximal concentrations in the Ecc-RG. In the Ecc-S, the glucose
transport was unchanged in hindquarters perfused in the absence or
presence of a submaximal stimulating concentration of insulin, whereas
it was slightly (P < 0.05) higher
during maximal insulin stimulation compared with control S. At the end
of perfusion the glycogen concentrations were lower in both
Ecc-gastrocnemius muscles compared with control muscles at all insulin
concentrations. Fractional velocity of glycogen synthase increased
similarly with increasing insulin concentrations in Ecc- and control WG
and RG. We conclude that insulin action on glucose transport but not
glycogen synthase activity is impaired in perfused muscle exposed to
prior eccentric contractions.
skeletal muscle; insulin resistance
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