Background: Alzheimer’s disease (AD) is the most common and irreversible neurodegenerative
disorder, and amyloid peptide plays a central role in its pathogenesis. Physical training contributes
as a beneficial adaptation to AD. However, these effects may be underestimated because much of
the literature used fixed training prescription variables (intensity and volume) throughout the protocol.
Moreover, researchers poorly understand whether chronic high-intensity interval training (HIIT) exerts
similar effects on the brain tissue of individuals with AD.
Objective: This study evaluated the effect of 8 minutes of HIIT with incremental overload in an AD
Methods: Forty male Wistar rats were divided into four groups: an untrained Sham group, Sham
trained group, Aβ1-42 (Alzheimer’s) untrained group, and Aβ1-42 (Alzheimer’s) trained group (n=10 rats
per group). Animals underwent stereotactic surgery and received a hippocampal injection of Aβ1-42 or a
saline solution. Seven days after surgery, two weeks of treadmill adaptation followed by a maximal
running test (MRT) was performed. Then, animals were subjected to eight weeks of HIIT. Rats were
sacrificed 24 h after the behavioral tests (open field and Morris water maze), hippocampal tissue was
extracted to analyze the redox balance and BDNF/TrkB pathway, and neuritic plaques (NP) were
detected by evaluating silver impregnation.
Results: The AD trained group presented a physical capacity amelioration every two weeks and
locomotor, learning, and memory improvements (p<0.05). These effects were accompanied by
increased CAT and SOD levels, followed by decreased lipid peroxidation (p<0.05). Furthermore,
increased activation of the BDNF/TrkB (p<0.05) pathway and decreased NP was observed.
Conclusion: Based on these results, MRT was essential for an excellent chronic training protocol prescription
and overload adjustment. Therefore, 8 minutes of HIIT daily for 8 weeks may reduce behavioral
deficits by promoting a positive redox balance and increased activity of the BDNF/TrkB pathway
that may contribute to NP attenuation.