To investigate the effects of temperature on Brassica napus (canola) resistance to Leptosphaeria maculans (LM), the causal agent of blackleg disease, metabolic profiles of LM infected resistant (R) and susceptible (S) canola cultivars at 21 °C and 28 °C were analyzed. Metabolites were detected in cotyledons of R and S plants at 48- and 120-h post-inoculation with LM using UPLC-QTOF/MS. The mock-inoculated plants were used as controls. Some of the resistance-related specific pathways, including lipid metabolism, amino acid metabolism, carbohydrate metabolism, and aminoacyl-tRNA biosynthesis, were down-regulated in S plants but up-regulated in R plants at 21 °C. However, some of these pathways were down-regulated in R plants at 28 °C. Amino acid metabolism, lipid metabolism, alkaloid biosynthesis, phenylpropanoid biosynthesis, and flavonoid biosynthesis were the pathways linked to combined heat and pathogen stresses. By using network analysis and enrichment analysis, these pathways were identified as important. The pathways of carotenoid biosynthesis, pyrimidine metabolism, and lysine biosynthesis were identified as unique mechanisms related to heat stress and may be associated with the breakdown of resistance against the pathogen. The increased susceptibility of R plants at 28 °C resulted in the down-regulation of signal transduction pathway components and compromised signaling, particularly during the later stages of infection. Deactivating LM-specific signaling networks in R plants under heat stress may result in compatible responses and deduction in signaling metabolites, highlighting global warming challenges in crop disease control.