90% of our glycogen is stored in the liver and 10% in muscle. Each gram of glycogen comes with 4 grams of water. Hence, we can not store too much in muscle. Also muscle lacks glucose-6-phosphatase., Hence, muscle glycogen breakdown does not produce glucose, but makes lactate. Too much muslce glycogen breakdown will produce excess amount of lactic acid.

Muscle can increase its capacity to store glycogen - it just requires mechanical stimulation. This increases insulin sensitivity. Glycogen is obviously not toxic.

It depends on the metabolic homeostasis in body. For example, if you think of a person with high adipose tissue (Obese individual) most likely there will be imbalance in metabolism as well as the excessive fatty acids in the circulation from adipose tissue (due to reduced capacity to store the fatty acids) which are taken up by the muscles for the energy purposes that leads to increase in lipid toxicity and causes insulin resistance. This phenomena is also known as "Metabolic flexibility".

Here is the attachment of the paper which might be helpful.

May I suggest my 2012 paper, were we investigated some of the molecular mechanisms behind bed rest induced insulin resistance. After bed rest the subjects had elevated glycogen. but they were still able to increase GS activity, but at o lower level than before bed rest

Article GLUT4 and Glycogen Synthase Are Key Players in Bed Rest–Indu...

Never read about the toxicity of glycogen in the skeletal muscle. In insulin resistance, uptake of glucose by the skeletal muscle is reduced, thus leading to reduction in glycogen synthesis.

This is an indication of insulin resistance in skeletal muscle that reduces glucose uptake and thus reduced glycogen storage....this is the story

90% of our glycogen is stored in the liver and 10% in muscle. Each gram of glycogen comes with 4 grams of water. Hence, we can not store too much in muscle. Also muscle lacks glucose-6-phosphatase., Hence, muscle glycogen breakdown does not produce glucose, but makes lactate. Too much muslce glycogen breakdown will produce excess amount of lactic acid.

Another interesting point to note is that due to lack of insulin (or in insulin resistance) GSK-3 beta is not phosphorylated (hence stays active) and can phosphorylate and inactivate glycogen synthase resulting in reduced glycogen synthesis.

Please note GSK-3 and glycogen synthase are inhibited by phosphorylation unlike most protein kinases.

The attached article may be of interest.

It seems you are asking two very different questions, one catabolic (glycolysis) and the other anabolic (glycogen synthesis).

It would appear that the only way for skeletal muscle, or any cell for that matter, to experience glycogen toxicity (I think you mean glucose toxicity) would mean that the cells normal ability to regulate glucose uptake has been compromised. The only way this could happen, in my opinion, is one of two ways: (1) the cell has more mitochondria therefore increasing the need for both energy and oxygen; which has been seen in athletes through increased capillary beds; or, (2) the cell has lost the ability to reduce the rate of glucose uptake.

The latter has already been evidenced in Diabetes. For example, hyperglycemia selectively causes damage to specific cell-types; those that are unable to decrease the rate of glucose transported inside the cell (Kaiser, et al., 1993; Heilig, et al., 1995). Specifically, these cells include the capillary endothelial cells of the retina, mesanglial cells in renal glomerulus, and neurons and Schwann cells of peripheral nerves (Brownlee, 2004). Each cell-type is representative of microvascular complications in diabetes; retinopathy, nephropathy, and neuropathy.

Increased circulating glucose levels combined with insulin resistant adipose tissue and muscle cells results in an interesting mix - altered metabolism of both carbohydrates and lipids. Logically, glycogen synthesis would make sense as a next step however with defective signal transduction GLUT 4 is never initiated thereby leaving the cell to believe it's in a fasting state.