The higher your BS the fewer glucose transporter molecules on your cells, and the more insulin is needed to increase the number of transporter molecules. Exercise will also increase glucose transport in muscle cells.
If you BG is high and not responding you can take a short walk and bring it down with the original correction factor.
Mike
Just to agree with Mikey. For me, exercise is a more effective blood sugar reducer than insulin. And insulin’s effectiveness seems to be turbocharged by exercise.
And I second the idea of a short walk - it doesn’t have to be particularly strenuous - but something that elevates your pulse maybe 15%.
This is kind of a crazy thing! But it makes sense if you think about why it works this way.
GLUT4 is the primary insulin-regulated transport of glucose into the cells. For a non-diabetic, the normal time of higher blood sugar is after eating. During this time, the body wants to bank that extra glucose as fat and also into the liver for storage.
Makes sense, right? Because we did not always have grocery stores and Kwik-E-Marts and Grubhub, we did not always have a reliable source of food. So after feeding, the body would want to stash some of that food away for times when there was nothing available.
So after eating, our body would save some of that for times of scarcity. To do this, the body down-regulates GLUT4 when our blood sugar is high. This reduces the amount of glucose being taken into the cells, and more of it goes to the liver and goes to fat storage. That way it can be saved for a rainy day.
Makes perfect sense for a non-diabetic!
But for the rest of us, when our BG is high and GLUT4 is down-regulated, it does not make as much sense. When our BG is high, we want the cells to take the glucose out of our blood. But it takes more insulin to make this happen.
Or maybe when a particular cell doesn’t need and can’t use any more glucose the chemical reactions in the cell lower the GLUT4.
If that didn’t happen what would happen to the valuable glucose? Nothing.
It’s pretty much essential to our survival that glucose that cannot be used by an individual cell isn’t used by that cell.
So what happens to excess glucose? It goes into muscle and liver cells and is converted to glycogen; this is a rapid reaction that happens over minutes, but there aren’t that many cells and the muscle cells necessarily shut down too. The liver cells are the last resort, when they are maxed out, what happens to the glucose?
For non-diabetics, what happens to glucose depends on a number of things. The first thing is the I:G ratio. That’s insulin to glucagon ratio.
A low I:G ratio (more glucagon than insulin in the blood) means the person’s BG is low. During this time, less will be stored and more will be released into the blood to counter the low BG. That causes the mobilization of stored nutrients, increases glycogenolysis (the breakdown of stored glycogen into glucose) and gluconeogenesis (the creation of glucose from non-carb sources). It also promotes the breakdown of fat tissue into free fatty acids for energy.
A high I:G ratio (more insulin than glucagon) is pretty much the opposite. We store glucose as glycogen, it moves into the cells and undergoes glycolysis (the conversion of glucose into energy), we reduce the creation of glucose, and we don’t breakdown fat.
All of this makes sense if you think of it in terms of a non-diabetic. When do they have a lot of insulin? After eating, when plenty of carbs are available.
Depending on the carb source - fructose vs glucose - the amount of carbs available, the demand of working muscle, the amount of glycogen currently stored in the liver, and the I:G ratio (also the same as BG for the most part), glucose will end up as liver glycogen, in muscle cells as muscle glycogen for future use, used immediately by working muscles, or left in the blood to raise low BG.
You asked, “The liver cells are the last resort, when they are maxed out, what happens to the glucose?”
Well, I got great news for you. It gets turned into fat! 
(As long as you have sufficient insulin to store it as fat. If you don’t have sufficient insulin, you end up peeing it out and damaging your kidneys. Kind of a lose-lose scenario.)
I asked in the context of a few hours; we don’t care about days. What happens in hours is the latter; we excrete it. No choice.
I’ve suffered from T1 since I was about 12. In all that time I’ve never put on fat. My control was not good; I don’t mean I didn’t have enough insulin, I went low enough times. I mean it was all over the place. If your hypothesis was correct I wouldn’t have a problem building fat.
Rather, I suggest, putting on weight involves an intimate relationship between the liver, a fully functioning pancreas, and the fat cells; the liver acts as a storage cell, sucking up glucose, then releases it gradually over time to build fat and the pancreas releases insulin to cover it. That fails in me because the lack of overall regulation means that even though my liver keeps on releasing glucose (I have the autoimmune variant; I still have alpha cells) I don’t have the continuous insulin supply to allow the fat cells to work.
One of the attractions, or not, of automatic control of insulin is that it gives the possibility that autoimmune T1s might actually be able to get fat. We can run a dangerously high basal because the autocorrect will handle it.
My fundamental hypothesis:
While a cell contains glycogen it does not require insulin to acquire glucose for cellular function.