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

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

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

Abstract: Researchers report that six minutes of regular high-intensity exercise 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 involved in memory, learning and brain plasticity, which may protect the brain from age-related cognitive decline.

Source: 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 Journal of Physiology shows that short but intense cycling increases the production of a specialized protein that is essential for brain formation, learning and memory, and may protect the brain from age-related cognitive decline.

This exercise insight is part of an effort to develop accessible, equitable, and affordable non-pharmacological approaches that anyone 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 have shown that increasing the availability of BDNF promotes memory formation and storage, improves learning, and generally improves cognitive performance. These key roles and its apparent neuroprotective qualities have led to interest in BDNF in aging research.

Lead author Travis Gibbons of 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 a need to explore non-pharmacological approaches that can preserve the brain’s capacity that people can use to naturally increase BDNF to aid in healthy aging.”

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

  • Fasting for 20 hours
  • Light exercise (90-minute low-intensity cycling)
  • High-intensity exercise (six-minute vigorous cycling)
  • A combination of 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 long session of light exercise. BDNF increased four to fivefold (396 pg L-1 to 1170 pages L-1) more compared to fasting (no changes in BDNF concentration) or prolonged activity (slight increase in BDNF concentration, 336 pg L-1 up to 390 pg L-1).

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

Brain substrate switching occurs when the brain switches its preferred fuel source to another to ensure the body’s energy needs are met, for example by metabolizing lactate instead of glucose during exercise. The brain’s switch from consuming glucose to lactate triggers pathways that result in elevated levels of BDNF in the blood.

Six minutes of high-intensity exercise a day could delay the onset of Alzheimer’s disease
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 long session of light exercise. The image is in the public domain

The observed increase in BDNF during exercise could be due to an increased number of platelets (the smallest blood cells) that store large amounts of BDNF. The concentration of platelets circulating in the blood is more strongly influenced by exercise than by starvation and increases by 20%.

Twelve physically active participants (six men, six women aged 18 to 56) took part in the research. The balanced ratio of male and female participants was intended to ensure a better representation of the population and not to indicate gender differences.

Further research is underway to investigate the effects of caloric restriction and exercise in more depth to differentiate the impact on BDNF and cognitive benefits.

Travis Gibbons noted, “We are now studying how longer periods of fasting, for example up to three days, affect BDNF. We are interested in whether strenuous exercise at the beginning of fasting accelerates the beneficial effects of fasting.

“Fasting and exercise are rarely studied together. We think 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: Physiological Society
Contact: Press Office – The Physiological Society
Picture: The image is in the public domain

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Original research: Closed access.
A 20-hour fast does not affect exercise-induced increases in circulating BDNF in humans” Travis Gibbons et al. Journal of Physiology


Abstract

A 20-hour fast does not affect exercise-induced increases in circulating BDNF in humans

Intermittent fasting and exercise provide neuroprotection against age-related cognitive decline. The link between these two seemingly disparate stressors is their ability to divert the brain from exclusively metabolizing glucose. This change in brain substrate is involved 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 examined the isolated and interactive effects of (1) 20-hour fasting, (2) 90-minute light exercise, and (3) high-intensity exercise on peripheral venous BDNF in 12 human volunteers.

A subsequent study isolated the effect of cerebrovascular shear stress on circulating BDNF. Fasting for 20 hours reduced glucose and increased ketones (P ≤ 0.0157), but had no effect on BDNF (P ≥ 0.4637). Light cycling at 25% peak oxygen intake (${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$) increased serum BDNF by 6 ± 8% (regardless of food or fasting) and was mediated by an increase in platelets of 7 ± 6% (P < 0.0001).

BDNF in plasma increased from 336 pg l-1 [46,626] up to 390 pages l-1 [127,653] 90 minutes of light cycle (P = 0.0128). Six 40 s intervals at 100% of ${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$ increased both plasma and serum BDNF since the ratio of BDNF per platelet is 4 to 5 times higher than that of 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 cerebral shear stress—whether occurring naturally during exercise or induced by experimentally inspired CO2 – did not correspond to changes in BDNF (P ≥ 0.2730).

BDNF responses to low-intensity exercise are mediated by increases in circulating platelets, and release of free BDNF requires an increase in either exercise duration or specific intensity.

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