Schematic representation of the interconnection of the signaling pathways involved in the training of aerobic resistance and muscular strength and the adaptations generated by the two training modalities: (a) aerobic-resistance sports increase the oxygen consumption (O2 consumption). Due to the energy demand, the pathways are activated for the production of ATP, increasing the mitochondrial production of ROS, basically H2O2, increasing OS, with the consequent decrease of available ATP. The increase of ADP and AMP activate the energy sensor AMPK that, together with SIRT1, activates the PGC-1Œ±. These, upon interacting with other transcription factors, such as PPARγ, ERRŒ±, Nrf1, and Nrf2, induce adaptations to prolonged-duration training through the development of mechanisms, such as the oxidation of fatty acids, the formation of blood vessels, and mito... (b) Strength training plus other factors such as IGF-1, insulin, testosterone, and leucine stimulate the anabolizing pathway PI3K/Akt/mTOR. During physical work, this pathway is negatively regulated by AMPK through the mechanisms executed by Raptor, eEF2K, TSC2, and TIF-IA; on finalizing the exercise, the mechanisms are reverted, stimulating protein synthesis and muscular fibrogenesis. The pathway is reinforced by the post-training energy replacement of carbohydrates and the branched-chain amino acid, leucine, which exerts an effect on the activation of satellite cells and myogenesis. We find immersed, in the control of the pathway, Fox-O, a powerful inducer of muscular protein degradation, and myostatin, which negatively regulates the pathway. In counterpart, myostatin possesses the negative regulators p70S6K, 4E-BP1, and Mrf4 that, upon inhibiting it, promote the PI3K/Akt/mTOR pathway. In both exercise modalities, the interaction between the redox-dependent factors, PGC-1Œ± and Nfr2, converges, producing the different adaptat... (c) Representation of the nuclear transcription of PGC-1Œ± and the binding Ebox by USF-1 mediated by ROS. On the other hand, activation of the PI3K/Akt/mTOR pathway induces the re-organization of the actin filaments, depolymerizing the actin and forming a complex with Nrf2, which permits its later translocation to the nucleus for its binding to ARE and directing the...