Do blood glucose "spikes" contribute to insulin resistance, or is prolonged elevation required?
Great Question.

The biggest problem is persistent insulin signaling from prolonged excessive high blood glucose over time. The reason being that it is this kind of signaling that results in insulin insensitivity due to down-regulation of the insulin receptors. 

Any bolus of carbohydrates > ~ 25grams in a sitting is going to bump up blood sugar at a fast enough rate to warrant the release of insulin to help lower blood sugar levels.  This can be mitigated by an excessive amount of fat along with the carbohydrates, thus slowing down the spike.


  Your question: 1) Is it true that high blood glucose is normalized substantially more rapidly in people who have depleted their glycogen, or who have higher energy needs?


So this is a little confounded by several variables.  The thought process is that people that have less glycogen or higher energy needs, don't have insulin insensitivity; thus the same amount of insulin would do a better job of shuttling glucose into cells.  We know that consistent exercise increases insulin sensitivity, as does lack of persistent insulin signaling (such as comes from being in a glycogen depleted state).  So the answer to your question is generally YES for these reasons.


  2) Does repeated exposure to high levels of blood glucose contribute to IR by itself, or are high and prolonged levels of blood glucose required?


What we know from epi studies suggests that it isn't insulin spikes.  It is prolonged insulin signaling that causes insulin insensitivity through down-regulation of insulin receptors.  

If you are fuel deprived, or only getting what you need from your food, insulin spikes are normal and transient and don't cause this IR.

Persistent insulin signaling causes many many side effects. Insulin is mitogenic,  has downstream pro-inflammatory cascades, and the insulin insensitivity that results is a major player in non-alchololic fatty liver disease.

Some references for these thoughts and further reading:


This one gives evidence of reduced IR activity, not
downreglation 
Insulin signaling and NAFLD
Exercise and Insulin Sensitivity