Molecular Signalling Responses to High-Intensity Interval Exercise: Effects of Carbohydrate Availability

Abstract

Manipulating carbohydrate (CHO) availability has been shown to alter acute exercise-induced changes in metabolic gene transcription and training-induced changes in oxidative capacity. The present study examined the effect of CHO availability on signalling pathways linked to mitochondrial biogenesis in response to high-intensity interval exercise (HIE). We hypothesized that reduced CHO availability would augment phosphorylation of AMP-activated protein kinase (AMPK), calcium/calmodulin-dependent kinase II (CaMKII), and p38 mitogen-activated protein kinase (p38) in response to HIE. Ten active men performed two experimental trials in random order, separated by 2:1 wk. During each trial, subjects performed two HIE sessions separated by 3 h (AM and PM sessions). Exercise sessions consisted of 5 x 4 min cycling bouts at a workload that elicited approximately 90% V02peak, with 2 min rest periods. Between sessions, subjects ingested -1.2 g CHO/kg b.w./h (HI-HI) or a taste-matched, non-energetic placebo (HI-LO). Muscle biopsies and blood samples were obtained before (Pre) and after (Post) the AM and PM HIE sessions. AMPK, CaMKII, and p38 MAPK phosphorylation increased from AM Pre to AM Post (p<0.01). During the PM exercise session, p38 phosphorylation increased in the HI-LO condition (-4.5-fold, p<0.001), whereas the HI-HI condition remained unchanged. PM HIE significantly increased CaMKII phosphorylation independent of condition, while no exercise or condition-mediated AMPK effects were observed. In summary, restricting CHO availability following an acute session of HIE augmented the exercise-induced increase in p38 phosphorylation during a subsequent HIE session. It remains to be determined whether chronic changes in p38 MAPK signalling are mechanistically linked to altered skeletal muscle remodelling observed after CHO-restricted exercise training.