You are asking a black and white question with answer likely being something blurred in the middle. AMPK responds to energetic stress, which is clearly induced by exercise in muscle, thus AMPK is activated during exercise. Is it a master regulator? This part is challenging to address because the experimental approaches often used to determine a mechanism equate to hitting a fly with a sledge hammer. It would be naive to think that AMPK is not regulating a number of critical mechanisms in response to the exercise bout, but I find it unlikely that AMPK acts as a master regulator of all exercise-induced adaptations. My reason for arguing this is that it makes more sense to me that cells have redundant pathways that control the same pathways because it gives the cell more flexibility to control or modulate the activation or deactivation of various mechanisms in response to a stress. Thus I find it unlikely that by itself AMPK acts as master regulator of exercise adaptation, but I do think it does contribute and is important to exercise response. There is evidence for this when AMPK activity is abolished or reduced you still retain some form adaptation to exercise---the response is not completely lost.

Seems to be a nice paper, thanks for sharing! Agree with Espen.

But then is PGC-1alpha dispensable, this recent work suggests that it is at least in some exercises and in in these mice ;) http://www.ncbi.nlm.nih.gov/pubmed/22848618

Thanks for the great response Espen. I agree, I think all too often that redundancy is interpretated as not-important. But as you say its much more likely that our cells evolved to be flexible and building redundancy into regulatory pathways would be a good way to acheive this flexibility. Perhaps we need to abondon the concept of master regulator :-)

Thanks for the paper Juha, and good point.