The Effect of High Intensity Interval Exercise on Postprandial Triacylglycerol and Leukocyte Activation – Monitored for 48h Post Exercise

Postprandial phenomenon are thought to contribute to atherogenesis alongside activation of the immune system. A single bout of high intensity interval exercise attenuates postprandial triacylglycerol (TG), although the longevity and mechanisms underlying this observation are unknown. The aims of this study were to determine whether this attenuation in postprandial TG remained 2 days after high intensity interval exercise, to monitor markers of leukocyte activation and investigate the underlying mechanisms. Eight young men each completed two three day trials. On day 1: subjects rested (Control) or performed 5 x 30 s maximal sprints (high intensity interval exercise). On day 2 and 3 subjects consumed high fat meals for breakfast and 3 h later for lunch. Blood samples were taken at various times and analysed for TG, glucose and TG-rich lipoprotein (TRL)-bound LPL-dependent TRL-TG hydrolysis (LTTH). Flow cytometry was used to evaluate granulocyte, monocyte and lymphocyte CD11b and CD36 expression. On day 2 after high intensity interval exercise TG area under the curve was lower (P<0.05) (7.46±1.53 mmol/l/7h) compared to the control trial (9.47±3.04 mmol/l/7h) with no differences during day 3 of the trial. LTTH activity was higher (P<0.05) after high intensity interval exercise, at 2 hours of day 2, compared to control. Granulocyte, monocyte and lymphocyte CD11b expression increased with time over day 2 and 3 of the study (P<0.0001). Lymphocyte and monocyte CD36 expression decreased with time over day 2 and 3 (P<0.05). There were no differences between trials in CD11b and CD36 expression on any leukocytes. A single session of high intensity interval exercise attenuated postprandial TG on day 2 of the study, with this effect abolished by day 3.The reduction in postprandial TG was associated with an increase in LTTH. High intensity interval exercise had no effect on postprandial responses of CD11b or CD36.