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

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

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

source: The Physiological Society

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

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

This insight into exercise is part of a drive to develop accessible, equitable, and affordable non-pharmacological approaches that everyone can adopt to promote healthy aging.

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

Animal studies show that increasing the availability of BDNF promotes the formation and storage of memories, improves learning, and generally increases 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 the brain’s capacity that people can use to naturally increase BDNF to support healthy aging.”

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

  • Fasting 20 hours
  • Light exercise (90 minutes of low-intensity cycling)
  • High-intensity exercise (six minutes of intense cycling)
  • Combined fasting and exercise

They found that short but vigorous exercise was the most effective way to increase BDNF compared to a day of fasting with or without a sustained session of light exercise. BDNF increased four- to fivefold (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 up to 390 pg L-1).

The reason for these differences is not yet known and more research is needed to understand the mechanisms involved. One hypothesis has to do with switching the cerebral substrate and metabolism of glucose, the main fuel source for the brain.

Cerebral substrate switching is when the brain switches its favorite fuel source with another to ensure that the body’s energy needs are met, for example metabolizing lactate rather than glucose during exercise. The brain’s transition from consuming glucose to lactate initiates pathways that lead to increased levels of BDNF in the blood.

They found that short but vigorous exercise was the most effective way to increase BDNF compared to a day of fasting with or without a sustained session of light exercise. Image is in the public domain

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

Twelve physically active participants (six men, six women aged between 18 and 56 years) took part in the study. The balanced ratio of male and female participants was intended to provide a better representation of the population rather than showing gender differences.

Additional research is warranted to further investigate the effects of calorie restriction and exercise to disentangle the impact on BDNF and cognitive benefits.

Travis Gibbons noted, “We are now studying how fasting for longer durations, such as up to three days, affects BDNF. We are curious whether vigorous exercise at the beginning of the fast accelerates the beneficial effects of the fast.

“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.”

About this exercise and dementia research news

Author: Press office
source: The Physiological Society
Contact: Press Office – The Physiological Society
Image: Image is in the public domain

See also

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

Original research: Closed access.
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 disparate stressors is their ability to steer the brain away from exclusively glucose metabolism. This cerebral substrate switch is implicated in the regulation of brain-derived neurotrophic factor (BDNF), a protein involved in neuroplasticity, learning, and memory, and may underlie some of these neuroprotective effects.

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

A subsequent study isolated the influence of cerebrovascular shear stress on circulating BDNF. Fasting for 20 hours lowers glucose and increases ketones (P ≤ 0.0157), but no effect on BDNF (P ≥ 0.4637). Light cycling at 25% of peak oxygen uptake (${dot V_{{{rm{O}}_{rm{2}}}{rm{peak}}}}$) increased serum BDNF by 6 ± 8% (regardless of fed or fasted) and is mediated by a 7 ± 6% increase in platelets (P < 0.0001).

Plasma BDNF increased from 336 pg l−1 [46,626] up to 390 pg l−1 [127,653] with a 90 minute light cycle (P = 0.0128). Six 40-second intervals at 100% of ${dot V_{{{rm{O}}_{rm{2}}}{rm{peak}}}}$ also increased plasma and serum BDNF as platelet BDNF ratio was 4- to 5-fold greater than mild exercise (P ≤ 0.0044). Plasma BDNF correlated with circulating lactate during the high-intensity intervals (r = 0.47, P = 0.0057), but not during light exercise (P = 0.7407).

Changes in cerebral shear stress—whether occurring naturally during exercise or induced experimentally with inhaled CO2 – does not correspond to changes in BDNF (P ≥ 0.2730).

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


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