Fibroblasts play a pivotal role in cancer progression. In prostate cancer, fibroblasts have been shown to induce growth and increase metastatic potential. To further understand how fibroblasts respond to hypoxic tumor microenvironments that are frequently observed in prostate cancer, we have characterized the effects of hypoxia on normal and cancer associated prostate fibroblast (PCAF) metabolomics and invasion using 1H MRS/I. We found that hypoxia increased matrix degradation by normal fibroblasts. Furthermore, hypoxia metabolically reprogrammed normal prostate fibroblasts to mimic the metabolic pattern of PCAFs, highlighting the potential role of hypoxia in the transition of normal fibroblasts to CAFs.