Increased mammographic density, caused by increased extracellular collagen matrix deposition in the breast, is associated with a 4-6 fold increased risk in the incidence of breast cancer. Interestingly, changes in the composition of the extracellular matrix can also alter various metabolic pathways in cancer cells. Here we investigate the role of collagen matrix density in regulating the metabolic pathways utilized by mammary carcinoma cells. We find changes in functional metabolism of mammary carcinoma cells in response to changes in collagen matrix density. Further, mammary carcinoma cells grown in high density collagen matrices display decreased glucose metabolism via the tricarboxylic acid (TCA) cycle compared to cells cultured in low density collagen matrices. Despite decreased glucose entry into the TCA cycle, levels of glucose uptake are not different between high and low density matrices. Interestingly, under high density conditions the contribution of glutamine as a fuel source to drive the TCA cycle is significantly enhanced. This study highlights the broad importance of the collagen microenvironment in modulating metabolic shifts of cancer cells. While changes in the composition of the tumor microenvironment can alter the metabolism of mammary carcinoma cells, the interaction between the microenvironment and tumor cells can have larger impacts on the ability of tumor cells to proliferate. While the recurrence risk in patients with definitively treated breast cancer is highest in the first five years after treatment, some patients have late recurrence of metastatic disease many years after definitive treatment. This has led to the recognition of a dormant tumor cell population that can exist in definitively treated cancer patients. Here we show that placing dormant tumor cells into an aged microenvironment is able to reactivate dormant tumor cells. Interestingly, this reactivation of dormant tumor cells is due to a combination of decreased immune surveillance in aged animals coupled with increased fibrosis at the metastatic site. In addition we identify an intracellular pathway regulated by the transcription factor Macc1 which plays a role in regulating the metastatic potential of mammary carcinoma cells. These studies provide important insight into both intra and extracellular cues responsible for metastasis and tumor dormancy.