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Six minutes of daily high-intensity exercise may 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 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: The Physiological Society

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

New research published in The Journal of Physiology shows that a short but intense cycle increases 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 insight into exercise is part of the effort to develop accessible, equitable, and accessible 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 neuron survival.

Animal studies have shown that increased BDNF availability stimulates memory formation and storage, 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 of the University of Otago, New Zealand stated: “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 might preserve brain capacity that humans can use to naturally increase BDNF to help with healthy aging.”

To disentangle 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:

  • 20 hour fast
  • Light exercise (90-minute 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 efficient 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 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).

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

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

This is a drawing of a person running
They found that brief but vigorous exercise was the most efficient way to increase BDNF compared to a day of fasting with or without a long bout of light exercise. The image is in the public domain

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

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

More research is underway to delve into the effects of caloric restriction and exercise to distinguish the influence on BDNF and cognitive benefits.

Travis Gibbons noted: “We are now studying how fasting for longer periods, for example up to three days, influences BDNF. We are curious to know whether intense exercise at the beginning 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.”

About this exercise and dementia research news

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

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“20 h fasting does not affect exercise-induced increases in circulating BDNF in humans” by Travis Gibbons et al. Journal of Physiology


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

Intermittent fasting and exercise provide neuroprotection against age-related cognitive decline. One link between these two seemingly distinct stressors is their ability to divert the brain exclusively from glucose metabolism. This brain substrate switch 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-hour fasting, (2) 90-minute 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. The 20 h fast decreased glucose and increased ketones (P ≤ 0.0157), but had no effect on BDNF (P ≥ 0.4637). Light cycling at 25% of maximal oxygen uptake (${dot V_{{{rm{O}}_{rm{2}}}{rm{peak}}}}$) increased serum BDNF by 6 ± 8% (regardless of whether fed or fasted) and was mediated by a 7 ± 6% increase in platelets (P < 0.0001).

Plasma BDNF increased from 336 pg l−1 [46,626] for 390 pg l−1 [127,653] for 90 min of light cycling (P = 0.0128). Six 40-second intervals at 100% ${dot V_{{{rm{O}}_{rm{2}}}{rm{peak}}}}$ increase in plasma and serum BDNF, as well as the ratio of BDNF per platelet 4 to 5 times more 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 – naturally occurring during exercise or experimentally induced with inspired COtwo – did not correspond with changes in BDNF (P ≥ 0.2730).

BDNF responses to low-intensity exercise are mediated by increases in circulating platelets, and it is necessary to increase exercise duration or particularly intensity to release free BDNF.