There are hundreds of studies showing the insulin response post workout by card, carb+protein, protein and protein alone. Tipton made a career on it. Increases in GLUT4 expression is insulin independent initially but subsides quickly and its also biphasic which means there is a insulin dependent phase as well.
Also, 80g is what the guy was using.
You seem to be saying exactly what I did on page 1. To put it simply, as I states earlier, you are trying to use a sledghammer to open a door thats already open.
Yeah AA says it now..but he didn't then. That is until I got him to look at it from a different perspective.
Regulation of GLUT4 protein and glycogen synthase during muscle glycogen synthesis after exercise.
Ivy JL1, Kuo CH.
Author information
Abstract
The pattern of muscle glycogen synthesis following its depletion by exercise is biphasic. Initially, there is a rapid, insulin independent increase in the muscle glycogen stores. This is then followed by a slower insulin dependent rate of synthesis. Contributing to the rapid phase of glycogen synthesis is an increase in muscle cell membrane permeability to glucose, which serves to increase the intracellular concentration of glucose-6-phosphate (G6P) and activate glycogen synthase. Stimulation of glucose transport by muscle contraction as well as insulin is largely mediated by translocation of the glucose transporter isoform GLUT4 from intracellular sites to the plasma membrane. Thus, the increase in membrane permeability to glucose following exercise most likely reflects an increase in GLUT4 protein associated with the plasma membrane. This insulin-like effect on muscle glucose transport induced by muscle contraction, however, reverses rapidly after exercise is stopped. As this direct effect on transport is lost, it is replaced by a marked increase in the sensitivity of muscle glucose transport and glycogen synthesis to insulin. Thus, the second phase of glycogen synthesis appears to be related to an increased muscle insulin sensitivity. Although the cellular modifications responsible for the increase in insulin sensitivity are unknown, it apparently helps maintain an increased number of GLUT4 transporters associated with the plasma membrane once the contraction-stimulated effect on translocation has reversed. It is also possible that an increase in GLUT4 protein expression plays a role during the insulin dependent phase.