Cancer cells undergo metabolic changes that affect their proliferation. Far less is known about the effect of metabolic changes on cancer cell invasion and metastasis. β-adrenoceptor signalling drives the spread of cancer. However, little is known about how β-agonism affects cancer cell metabolism. To address this, an untargeted metabolomics approach was used to explore the effects of β-agonism on the metabolome of breast cancer cells. It was predicted that β-adrenoceptor signalling would cause the cancer cells to become more glycolytic, which would result in an acidic environment that has been associated with cancer progression. However, it was found that βAR signalling induced a partial reversal of the Warburg effect in cancer cells. This was linked to increased activity of the TCA cycle and increased intake of essential amino acids. Increased levels of glycolytic intermediates may be associated with biosynthesis of macromolecules through these pathways. Future studies are evaluating the molecular mechanisms of these effects and investigating if β-adrenoceptor regulation of metabolism contributes to cancer cell invasion. Drugs that block β-adrenoceptor signalling are currently being trialled as adjuvant cancer therapy. β-adrenoceptor regulation of metabolism may provide biomarkers for aggressive cancer and be used to identify successful response to beta-blockade.