9- and 13-Hydroxy-octadecadienoic acids (9Â +Â 13 HODE) are inversely related to granulocyte colony stimulating factor and IL-6 in runners after 2Â h running

This study utilized a pro-inflammatory exercise mode to explore potential linkages between increases in 9- and 13-hydroxy-octadecadienoic acid (9 + 13 HODE) and biomarkers for inflammation, oxidative stress, and muscle damage. Male (N = 10) and female (N = 10) runners ran at ∼70% VO2max for 1.5 h followed by 30 min of downhill running (−10%). Blood samples were taken pre-run and immediately-, 1-h-, and 24-h post-run, and analyzed for 9 + 13 HODE, F2-isoprostanes, six cytokines, C-reactive protein (CRP), creatine kinase (CK), and myoglobin (MYO). Gender groups performed at comparable relative heart rate and oxygen consumption levels during the 2-h run. All outcome measures increased post-run (time effects, P ⩽ 0.001), with levels near pre-run levels by 24 h except for CRP, CK, MYO, and delayed onset of muscle soreness (DOMS). Plasma 9 + 13 HODE increased 314 ± 38.4% post-run (P < 0.001), 77.3 ± 15.8% 1-h post-run (P < 0.001), and 40.6 ± 16.4% 24-h post-exercise (P = 0.024), and F2-isoprostanes increased 50.8 ± 8.9% post-run (P < 0.001) and 19.0 ± 5.3% 1-h post-run (P = 0.006). Post-run increases were comparable between genders for all outcomes except for 9 + 13 HODE (interaction effect, P = 0.024, post-run tending higher in females), IL-10 (P = 0.006, females lower), and DOMS (P = 0.029, females lower). The pre-to-post-run increase in 9 + 13 HODEs was not related to other outcomes except for plasma granulocyte colony stimulating factor (GCSF) (r = −0.710, P < 0.001) and IL-6 (r = −0.457, P = 0.043). Within the context of this study, exercise-induced increases in 9 + 13 HODEs tended higher in females, and were not related to increases in F2-isoprostanes, muscle damage, or soreness. The negative relationships to GCSF and IL-6 suggest a linkage between 9 + 13 HODES and exercise-induced neutrophil chemotaxis, degranulation, and inflammation.