IntroductionWe developed a novel adaptation of blood flow restriction exercise, cyclical blood flow restriction exercise (C‐BFRE), as a method to potentially augment the cardio‐protective effects associated with conventional exercise (CE) and remote ischemic preconditioning (RIPC). As the cytokines IL‐6 and IL‐10 have been implicated in mediating the acute cardio‐protection associated with both exercise training and RIPC when performed independently, we hypothesized that C‐BFRE would augment the systemic release of these factors compared to an acute bout of either CE or RIPC alone.Methods13 young healthy subjects (6M/7F, age 28±2 y) completed 3 experimental sessions separated by at least 1 month each. Aerobic exercise was performed via 40‐min of treadmill walking at 65–70% HRmax with (C‐BFRE) and without (CE) application of bilateral thigh cuffs inflated to 220 mmHg (4 × 5‐min inflation periods followed by 5‐min reperfusion periods). RIPC consisted of 4 × 5‐min thigh cuff inflation periods (220 mmHg) followed by 5‐min reperfusion periods in the absence of exercise. Venous blood samples (via an antecubital vein) were collected at baseline and immediately following completion of each protocol for analysis of IL‐6 and IL‐10 via multiplex ELISA.ResultsPlasma IL‐6 increased from baseline following CE (Pre, 0.26 ± 0.03 vs. Post, 0.40 ± 0.07 pg/ml; P=0.03) but not with C‐BFRE (Pre, 0.28 ± 0.05 vs. Post, 0.34 ± 0.07 pg/ml; P=0.75) or RIPC (Pre, 0.31 ± 0.04 vs. Post, 0.32 ± 0.03 pg/ml; P=1.0). There were no changes in plasma IL‐10 from pre‐ to post‐intervention for any of the three conditions (P=0.42 for main effect of time).DiscussionContrary to our hypothesis, we observed no change in plasma IL‐10 or IL‐6 with application of acute C‐BFRE. These findings suggest that the model of C‐BFRE utilized in this study does not augment the release of these cytokines in young healthy individuals. This may be due to the timing of the blood samples, the use of a standard occlusive pressure across all subjects, and the young, healthy subjects tested in this study. Future work should delineate the inflammatory response induced by C‐BFRE at more extended recovery time points, with use of individualized occlusive pressures, and in more clinically relevant populations in both acute and long term settings.Support or Funding InformationFunding for this study was provided, in part, by training fellowships awarded to Justin Sprick through a NIH‐supported Neurobiology of Aging Training Grant (T32 AG020494, PI: Singh, M), and a Ruth L. Kirchstein NRSA F31 Predoctoral Fellowship (1F31HL134242‐01A1; PI: Sprick, JD), a UNTHSC Faculty Research Pilot Grant (PI: Rickards, CA), and a Texas Chapter of the American College of Sports Medicine (TACSM) Student Research Development Award (PI: Sprick, JD).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.