Six minutes of high-intensity exercise could delay the onset of Alzheimer’s disease


High-intensity exercise for six minutes could increase the longevity of a healthy brain and postpone the beginning of neurodegenerative diseases like Parkinson’s and Alzheimer’s. A brief but vigorous cycling session promotes the production of a specialised protein that is crucial for brain development, learning, and memory and may shield the brain from age-related cognitive decline, according to new research published in The Journal of Physiology. This understanding of exercise is a component of the effort to create non-pharmacological, non-discriminatory, and economical ways that anybody can use to promote good ageing.
Brain-derived neurotrophic factor (BDNF), a specialised protein, encourages neuroplasticity (the capacity of the brain to develop new connections and pathways), as well as the survival of neurons. According to research conducted on animals, BDNF availability increases memory formation and storage, improves learning, and generally improves cognitive performance. The importance of BDNF for ageing research is a result of these crucial roles as well as its apparent neuroprotective properties. Lead author Travis Gibbons from University of Otago, New Zealand said: “BDNF has shown great promise in animal models, but pharmaceutical interventions have thus far failed to safely harness the protective power of BDNF in humans. We saw the need to explore non-pharmacological approaches that can preserve the brain’s capacity which humans can use to naturally increase BDNF to help with healthy ageing.”
They found that brief but vigorous exercise was the most efficient way to increase BDNF compared to one day of fasting with or without a lengthy session of light exercise. BDNF increased by four to five-fold (396 pg L-1 to 1170 pg L-1) more compared to fasting (no change in BDNF concentration) or prolonged activity (slight increase in BDNF concentration, 336 pg L-1 to 390 pg L-1).

More research is required to fully understand the mechanisms at play because the reason for these discrepancies is still unknown. One theory relates to glucose metabolism, the brain’s main fuel source, and the cerebral substrate switch. The cerebral substrate switch occurs when the brain moves from one preferred fuel source to another in order to meet the body’s energy requirements, such as when lactate is metabolised during exercise instead of glucose. When the brain switches from ingesting glucose to lactate, several pathways are set off, which raise the blood levels of BDNF.
The increased quantity of platelets, the smallest blood cell, which are known to contain high amounts of BDNF, may be the cause of the BDNF rise that has been reported during exercise. More platelets are circulating in the blood, and their concentration is higher.

Further research is underway to delve deeper into the effects of calorie restriction and exercise to distinguish the influence on BDNF and the cognitive benefits.
Travis Gibbons said: “We are now studying how fasting for longer durations, for example up to three days, influences BDNF. We are curious whether exercising hard at the start of a fast accelerates the beneficial effects of fasting. Fasting and exercise are rarely studied together. We think fasting and exercise can be used in conjunction to optimise BDNF production in the human brain.”