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Original Studies |
Departments of Internal Medicine (M.K., K.F.P., R.B., D.L., G.I.S.) and Diagnostic Radiology (T.P., D.L.R.) and the Howard Hughes Medical Institute (G.I.S.), Yale University School of Medicine, New Haven, Connecticut 06536; and the Division of Endocrinology and Metabolism, Department of Internal Medicine III (M.R.), University of Vienna, Vienna, Austria
Address all correspondence and requests for reprints to: Gerald I. Shulman, M.D., Ph.D., Howard Hughes Medical Institute Research Laboratories, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, P.O. Box 9812, New Haven, Connecticut 06536-8012. E-mail: gerald.shulman{at}yale.edu
Depletion of muscle glycogen is considered a limiting performance
factor during prolonged exercise, whereas the role of the
intramyocellular lipid (IMCL) pool is not yet fully understood. We
examined 1) intramyocellular glycogen and lipid utilization during
prolonged exercise, 2) resynthesis of muscle glycogen and lipids during
recovery, and 3) changes in glycogen content between nonexercising and
exercising muscles during recovery. Subjects ran on a treadmill at
submaximal intensity until exhaustion. Glycogen concentrations were
assessed in thigh, calf, and nonexercising forearm muscle, and IMCL
content was measured in soleus muscle using magnetic resonance
spectroscopy techniques. At the time of exhaustion, glycogen depletion
was 2-fold greater in calf than in thigh muscles, but a significant
amount of glycogen was left in both leg muscles. The glycogen
concentration in nonexercising forearm muscle decreased during the
initial 5 h of recovery to 73% of the baseline value. During the
exercise, the IMCL content decreased to 67% and subsequently during
recovery increased to 83% of the baseline value. In summary, we found
during prolonged running 1) significantly greater muscle glycogen
utilization in the calf muscle group than in the thigh muscle group, 2)
significant utilization of IMCL in the soleus muscle, and 3) a decrease
in glycogen content in nonexercising muscle and an increase in glycogen
content in recovering muscles during the postexercise phase. These
latter data are consistent with the hypothesis that there is transfer
of glycogen by the glucose
lactate and the glucose
alanine cycle
from the resting muscle (forearm) to recovering muscles (thigh and
calf) after running exercise .
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