Acute effects of two different work-to-rest ratio of high-intensity interval training on brain-derived neurotrophic factor in untrained young men.

Aerobic exercise could produce a positive effect on the brain by releasing brain-derived neurotrophic factor (BDNF). In untrained healthy humans there seems to be a linear correlation between exercise duration and the positive effect of acute aerobic exercise on brain-derived neurotrophic factor levels. Therefore, we performed two different duration of high-intensity interval training protocols (HIIT), both known to improve cardiovascular fitness, to determine whether then have a similar efficacy in affecting brain-derived neurotrophic factor levels. 12 untrained young males (aged 23.7 ± 1.8 years), participated in a randomized controlled cross-over trial. They underwent two different work-to-rest ratio high-intensity interval training protocols: high-intensity interval training 1 (30 min, 15 intervals of 1 min efforts at 85%-90% VO2max with 1 min of active recovery at 50%-60% VO2max) and HIIT2 (30 min, 10 intervals of 2 min efforts at 85%-90% VO2max with 1 min of active recovery at 50%-60% VO2max). Serum cortisol, brain-derived neurotrophic factor were collected at baseline, immediately following intervention, and 30 min into recovery for measurements using a Sandwich ELISA method, blood lactate was measured by using a portable lactate analyzer. Our results showed that the similar serum brain-derived neurotrophic factor change in both high-intensity interval training protocols, with maximal serum brain-derived neurotrophic factor levels being reached toward the end of intervention. There was no significant change in serum brain-derived neurotrophic factor from baseline after 30 min recovery. We then showed that both high-intensity interval training protocols significantly increase blood lactate and serum cortisol compared with baseline value (high-intensity interval training < 0.01; high-intensity interval training 2 < 0.01), with high-intensity interval training 2 reaching higher blood lactate levels than high-intensity interval training 1 ( = 0.027), but no difference was observed in serum cortisol between both protocols. Moreover, changes in serum brain-derived neurotrophic factor did corelate with change in blood lactate (high-intensity interval training 1 = 0.577, < 0.05; high-intensity interval training 2 = 0.635, < 0.05), but did not correlate with the change in serum cortisol. brain-derived neurotrophic factor levels in untrained young men are significantly increased in response to different work-to-rest ratio of high-intensity interval training protocols, and the magnitude of increase is exercise duration independent. Moreover, the higher blood lactate did not raise circulating brain-derived neurotrophic factor. Therefore, given that prolonged exercise causes higher levels of cortisol. We suggest that the 1:1work-to-rest ratio of high-intensity interval training protocol might represent a preferred intervention for promoting brain health.