Abstract
The effect of a period of starvation followed by refeeding on skeletal muscle glycogen was investigated by the use of double-labelled radioactive glucose precursors in rats. Skeletal muscle glycogen, which is not depleted to anything like the extent of liver glycogen, shows a remarkable stability with respect to its overall molecular size distribution during starvation and subsequent refeeding. The experiments also indicate that there is a control mechanism in muscle tissue enabling the synthesis of lysosomal glycogen to be switched off during the initial part of the refeeding process. The results emphasise the inadequacy of the Cori cycle and a modified version is proposed.
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