The brain-derived neurotrophic factor (BDNF) is a protein mainly synthetized in the neurons. Early evidence showed that BDNF participates in cognitive processes as measured at the hippocampus. This neurotrophin is as a reliable marker of brain function; moreover, recent studies have demonstrated that BDNF participates in physiological processes such as glucose homeostasis and lipid metabolism. The BDNF has been also studied using the exercise paradigm to determine its response to different exercise modalities; therefore, BDNF is considered a new member of the exercise-related molecules. The high-intensity interval training (HIIT) is an exercise protocol characterized by low work volume performed at a high intensity [i.e., ≥80% of maximal heart rate (HRmax)]. Recent evidence supports the contention that HIIT elicits higher fat oxidation in skeletal muscle than other forms of exercise. Similarly, HIIT is a good stimulus to increase maximal oxygen uptake (VO2max). Few studies have investigated the impact of HIIT on the BDNF response. The present work summarizes the effects of acute and long-term HIIT on BDNF.

Background: Brain-derived neurotrophic factor (BDNF) increases neuronal viability and cognitive function, peripheral lipid metabolism and skeletal muscle repair. The primary purpose of this study was to determine the effect of short-term highintensity interval training (HIIT) on serum BDNF concentrations in healthy young women. Methods: Seventeen women (age:22 ± 1 years); body mass index (BMI:24.2 ± 2.2 kg/m²), body fat percentage (% fat:25.8 ± 4.7) participated in the study. Participants were randomly assigned to a control (n = 8) or HIIT group (n = 9). All participants performed a graded exercise test (GXT) on an electronically-braked cycle ergometer to determine maximal aerobic power (MAP, Watts). HIIT was performed three days per week for four weeks. Each HIIT session consisted of three to five cycling bouts of 30 s each at 80% MAP, followed by four-minutes of recovery at 40% MAP. Forty-eight hours after the last bout of exercise, both groups performed a follow-up GXT. Non-fasting blood samples were collected before and immediately after each GXT. Mixed factorial (2 groups x 4 measures, and 2 groups x 2 measures) ANOVA was used to assess BDNF concentrations, performance and anthropometric variables. Results: Serum BDNF concentrations in the HIIT group (21.9 ± 1.3 ng/mL) increased compared to control (19.2 ± 2.8 ng/mL) (∼12%, P < 0.05) following HIIT. In contrast, circulating BDNF concentrations were reduced following the GXT (P < 0.05). The MAP and % Fat did not change with HIIT. Conclusions: Twelve sessions of HIIT increases circulating BDNF concentrations in healthy young women despite no change in physical performance or % fat.

BackgroundPhysical exercise improves glucose metabolism and insulin sensitivity. Brain-derived neurotrophic factor (BDNF) enhances insulin activity in diabetic rodents. Because physical exercise modifies BDNF production, this study aimed to investigate the effects of chronic exercise on plasma BDNF levels and the possible effects on insulin tolerance modification in healthy rats.MethodsWistar rats were divided into five groups: control (sedentary, C); moderate- intensity training (MIT); MIT plus K252A TrkB blocker (MITK); high-intensity training (HIT); and HIT plus K252a (HITK). Training comprised 8 weeks of treadmill running. Plasma BDNF levels (ELISA assay), glucose tolerance, insulin tolerance, and immunohistochemistry for insulin and the pancreatic islet area were evaluated in all groups. In addition, Bdnf mRNA expression in the skeletal muscle was measured.Principal FindingsChronic treadmill exercise significantly increased plasma BDNF levels and insulin tolerance, and both effects were attenuated by TrkB blocking. In the MIT and HIT groups, a significant TrkB-dependent pancreatic islet enlargement was observed. MIT rats exhibited increased liver glycogen levels following insulin administration in a TrkB-independent manner.Conclusions/SignificanceChronic physical exercise exerted remarkable effects on insulin regulation by inducing significant increases in the pancreatic islet size and insulin sensitivity in a TrkB-dependent manner. A threshold for the induction of BNDF in response to physical exercise exists in certain muscle groups. To the best of our knowledge, these are the first results to reveal a role for TrkB in the chronic exercise-mediated insulin regulation in healthy rats.

Chronic fructose ingestion is linked to the global epidemic of metabolic syndrome (MetS), and poses a serious threat to brain function. We asked whether a short period (one week) of fructose ingestion potentially insufficient to establish peripheral metabolic disorder could impact brain function. We report that the fructose treatment had no effect on liver/body weight ratio, weight gain, glucose tolerance and insulin sensitivity, was sufficient to reduce several aspects of hippocampal plasticity. Fructose consumption reduced the levels of the neuronal nuclear protein NeuN, Myelin Basic Protein, and the axonal growth-associated protein 43, concomitant with a decline in hippocampal weight. A reduction in peroxisome proliferator-activated receptor gamma coactivator-1 alpha and Cytochrome c oxidase subunit II by fructose treatment is indicative of mitochondrial dysfunction. Furthermore, the GLUT5 fructose transporter was increased in the hippocampus after fructose ingestion suggesting that fructose may facilitate its own transport to brain. Fructose elevated levels of ketohexokinase in the liver but did not affect SIRT1 levels, suggesting that fructose is metabolized in the liver, without severely affecting liver function commensurable to an absence of metabolic syndrome condition. These results advocate that a short period of fructose can influence brain plasticity without a major peripheral metabolic dysfunction.

These results indicate that high-intensity chronic exercise reduces BDNF protein level in fast muscles and increases Bdnf mRNA levels in slow muscles.