Figure 1.

Exercise induces SPM biosynthesis and mitochondrial respiration in macrophages. (A) Experimental scheme outlining the isolation of PM from exercise-trained mice and subsequent assessment of mitochondrial respiratory parameters via extracellular flux (XF) analysis, as well as extraction and quantification of lipid mediators in the cell-free lavage fluid via SPE and HPLC-MS/MS, respectively. (B) Partial Least Squares-Discriminant Analysis (PLS-DA) and (D) heatmap of peritoneal lipid mediator metabololipidomics following four weeks of voluntary wheel running (Exe) or sedentarism (Sed). (C) Quantification of RvE1, PGJ₂, 20-OH LTB₄, 5S,15S-diHETE and ratio of RvE1 and RvD1 to leukotrienes (LTs; LTB₄, 6-trans LTB₄, and 6-trans-12-epi LTB₄). (E) Cellular respiration was assessed by recording oxygen consumption rate (OCR) of peritoneal macrophages (PM) isolated from exercise and sedentary mice. (F) Derived mitochondrial respiratory parameters calculated from the mitochondrial stress assay. Data expressed as mean ± SEM, n = 4 for Sed mice, n = 3 for Exe mice. ∗P < 0.05, ∗∗P < 0.01, two-tailed Student's t-test.