Skeletal muscle contraction rapidly increases the translocation of glucose transporters (GLUTs) to facilitate the transport of glucose across the cell membrane. The prevailing concept holds that sarcoplasmatic reticulum (SR) Ca2+ release is neccesary and sufficient to cause a substantial feed-forward increase in glucose transport, with subsequent fine-tuning by feed-back signals relating to the muscle work-load. In the work presented here, a series of experiments were performed in incubated mouse muscles to scrutinize this model. Our data challenge the current Ca2+-centric paradigm by showing that increased cytosolic Ca2+ coming from the SR was unable to stimulate glucose transport in the absence of signals relating to ATP turnover and mechanical stress. Conversely, artificial activation of AMPK and mechanical stress-signaling elicited a full contraction-mimicking glucose transport-response without increasing Ca2+ signaling. These results call for a major reconsideration of the current working model describing glucose uptake in contracting skeletal muscle and may provide a useful framework for future investigations.