“…The main finding of this study was that experimentally-induced pain, i.e., acute pain, did not affect the levels of sAA, which seems to be in contrast to previous studies [ 20 , 21 , 22 , 23 ]. However, in contrast to the previous studies [ 5 , 8 , 20 , 21 , 22 , 23 ], this study used a short lasting, high intensity pain model [ 35 , 36 , 37 , 38 ]. This could have resulted in a pain state that was too short-lasting to activate the ANS, resulting in a secretion of sAA.…”