The majority of sports rely on concurrent training (CT; e.g., the simultaneous training of strength and endurance). However, a phenomenon called "Concurrent training effect" (CTE), which is a compromise in adaptation resulting from concurrent training, appears to be mostly affected by the interference of the molecular pathways of the underlying adaptations from each type of training segments. Until now, it seems that the volume, intensity, type, frequency of endurance training, as well as the training history and background strongly affect the CTE. High volume, moderate, continuous and frequent endurance training, are thought to negatively affect the resistance training-induced adaptations, probably by inhibition of the Protein kinase B-mammalian target of rapamycin pathway activation, of the adenosine monophosphate-activated protein kinase (AMPK). In contrast, it seems that short bouts of high-intensity interval training (HIIT) or sprint interval training (SIT) minimize the negative effects of concurrent training. This is particularly the case when HIIT and SIT incorporated in cycling have even lower or even no negative effects, while they provide at least the same metabolic adaptations, probably through the peroxisome proliferator-activated receptor-γ coactivator (PGC-1a) pathway. However, significant questions about the molecular events underlying the CTE remain unanswered.
Keywords: adenosine monophosphate-activated protein kinase; concurrent exercise; mammalian target of rapamycin; peroxisome proliferator-activated receptor-γ coactivator.