Given that the latter is fundamental for contraction-induced stimulation of MPS following RE [26, 38] and that LGSI-driven insulin resistance is attributed to impaired activation of the IRS1-PI3K-PDK1-Akt signaling pathway [26, 39], we assume that the blunted rpS6 phosphorylation in ESI dictates reduced responsiveness of the PI3K/Akt/mTOR/S6K1 signal transduction pathway as a consequence of the coexistence of chronic LGSI and insulin resistance. Here, MTOR is linked to Insulin resistance.