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

Summary: Researchers report that six minutes of high-intensity exercise on a regular basis can slow brain aging and delay the onset of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. High-intensity exercise increases production of BDNF, a protein involved in memory, learning, and brain plasticity, which may protect the brain from age-related cognitive decline.

Source: The physiological society

Six minutes of high-intensity exercise could extend the lifespan of a healthy brain and delay the onset of neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease.

New research published in The Journal of Physiology shows that a short but intense cycle increases the production of a specialized protein essential for brain formation, learning and memory, and may protect the brain from age-related cognitive decline.

This idea of ​​exercise is part of the desire to develop accessible, equitable and affordable non-pharmacological approaches that everyone can adopt to promote healthy aging.

The specialized protein called brain-derived neurotrophic factor (BDNF) promotes neuroplasticity (the brain’s ability to form new connections and pathways) and the survival of neurons.

Animal studies have shown that increasing the availability of BDNF encourages the formation and storage of memories, enhances learning, and improves overall cognitive performance. These key roles and its apparent neuroprotective qualities have led to interest in BDNF for aging research.

Lead author Travis Gibbons from the University of Otago, New Zealand, said: “BDNF has shown great promise in animal models, but pharmaceutical interventions have so far failed to safely harness the protective power of BDNF in humans.

“We saw the need to explore non-pharmacological approaches that can preserve brain capacity that humans can use to naturally increase BDNF to aid in healthy aging.”

To distinguish the influence of fasting and exercise on BDNF production, researchers at the University of Otago, New Zealand, compared the following factors to study isolated and interactive effects:

• Fast for 20 hours
• Light exercise (90 minutes of low intensity cycling)
• High-intensity exercise (six minutes of vigorous cycling)
• Fasting and exercise combined

They found that brief but vigorous exercise was the most effective way to increase BDNF compared to a day of fasting with or without a long bout of light exercise. BDNF increased four to five times (396 pg L-1 at 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 at 390 pg L-1).

The cause of these differences is not yet known and further research is needed to understand the mechanisms involved. One hypothesis relates to the change in brain substrate and the metabolism of glucose, the brain’s main fuel source.

Brain substrate switching occurs when the brain changes its preferred fuel source to another to ensure that the body’s energy demands are met, for example by metabolizing lactate rather than glucose during exercise. The brain’s transition from consuming glucose to lactate initiates pathways that lead to high levels of BDNF in the blood.

The observed increase in BDNF during exercise could be due to the increase in the number of platelets (the smallest blood cell), which store large amounts of BDNF. The concentration of platelets circulating in the blood is more strongly influenced by exercise than by fasting and increases by 20%.

Twelve physically active participants (six men, six women, ages 18-56) participated in the study. The balanced ratio of male and female participants was intended to provide a better representation of the population rather than to indicate gender differences.

Further research is underway to further investigate the effects of calorie restriction and exercise to distinguish influence on BDNF and cognitive benefits.

Travis Gibbons noted, “We are currently investigating how fasting for longer durations, such as up to three days, influences BDNF. We are curious whether intensive exercise at the start of a fast accelerates the beneficial effects of fasting.

“Fasting and exercise are rarely studied together. We believe that fasting and exercise can be used together to optimize BDNF production in the human brain.

Author: Press office
Source: The physiological society
Contact: Press Office – The Physiological Society
Picture: Image is in public domain

Original research: Access closed.
“Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans” by Travis Gibbons et al. Journal of Physiology

Summary

Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans

Intermittent fasting and exercise provide neuroprotection against age-related cognitive decline. A link between these two seemingly separate stressors is their ability to steer the brain away from exclusive glucose metabolism. This brain substrate shift has been implicated in the upregulation of brain-derived neurotrophic factor (BDNF), a protein involved in neuroplasticity, learning, and memory, and may underlie some of these neuroprotective effects.

We examined the isolated and interactive effects of (1) 20-h fasting, (2) 90-min light exercise, and (3) high-intensity exercise on peripheral venous BDNF in 12 human volunteers.

A follow-up study isolated the influence of cerebrovascular shear stress on circulating BDNF. Fasting for 20 h decreased blood sugar and increased ketone bodies (P ≤ 0.0157) but had no effect on BDNF (P ≥ 0.4637). The light cycle at 25% of maximum oxygen consumption (${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$) increased serum BDNF by 6 ± 8% (regardless of diet or fasting) and was mediated by a 7 ± 6% increase in platelets (P < 0.0001).

Plasma BDNF was increased by 336 pg l−1 [46,626] at 390 pg l−1 [127,653] per 90 min of light cycling (P = 0.0128). Six 40-s intervals at 100% ${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$ also increased plasma and serum BDNF as the BDNF per platelet ratio 4-5 times higher than light exercise (P ≤ 0.0044). Plasma BDNF was correlated with circulating lactate during high-intensity intervals (r = 0.47, P = 0.0057), but not during light exercise (P = 0.7407).

Changes in brain shear stress – whether naturally occurring during exercise or experimentally induced with inspired CO2 – did not match BDNF changes (P ≥ 0.2730).

BDNF responses to low-intensity exercise are mediated by an increase in circulating platelets, and increasing exercise duration or intensity is required to release free BDNF.