Study found that six minutes of high-intensity exercise might prevent beginning of Alzheimer’s disease

According to new study, six minutes of high-intensity exercise can lengthen the lifetime of a healthy brain and prevent the onset of neurodegenerative illnesses like Alzheimer’s and Parkinson’s. A brief but intensive bout of cycling enhances the synthesis of a specialised protein that is crucial for brain development, learning, and memory, and may protect the brain against age-related cognitive decline, according to new study published in The Journal of Physiology. This exercise insight is part of a larger effort to find non-pharmacological methods to healthy ageing that are accessible, egalitarian, and inexpensive to anybody.

Brain-derived neurotrophic factor (BDNF) is a specialised protein that promotes neuroplasticity (the ability of the brain to build new connections and pathways) and neuron survival. Animal studies have demonstrated that increasing the availability of BDNF promotes memory formation and storage, improves learning, and improves general cognitive function. These important responsibilities, as well as its apparent neuroprotective properties, have sparked interest in BDNF for ageing research.

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.”

In comparison to one day of fasting with or without a lengthy session of gentle activity, they discovered that quick but vigorous exercise was the most efficient strategy to raise BDNF. When compared to fasting (no change in BDNF concentration) or extended exercise, BDNF rose four to five-fold (396 pg L-1 to 1170 pg L-1) (slight increase in BDNF concentration, 336 pg L-1 to 390 pg L-1).

The source of these discrepancies is unknown, and additional study is required to understand the processes at work. One theory is linked to the cerebral substrate switch and glucose metabolism, which is the brain’s principal fuel source.

The cerebral substrate switch occurs when the brain moves from one preferred fuel source to another in order to meet the body’s energy demands, such as metabolising lactate rather than glucose during exercise. The brain’s conversion from glucose to lactate activates pathways that result in higher BDNF levels in the blood.

The observed rise in BDNF after exercise might be attributed to an increase in the number of platelets (the smallest blood cell), which contain high quantities of BDNF. Exercise has a greater affect on platelet concentrations in the blood than fasting and boosts them by 20%.

The study included 12 physically active volunteers (six males and six females aged 18 to 56 years). The balanced ratio of male and female participants was intended to create a more accurate portrayal of the population rather than to highlight gender inequalities. More study is being conducted to investigate the impact of calorie restriction and exercise on BDNF and the cognitive advantages.

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.”